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An open trial of cognitive therapy for chronic insomnia
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Behaviour Research and Therapy 45 (2007) 2491–2501 www.elsevier.com/locate/brat
Shorter communication
An open trial of cognitive therapy for chronic insomnia Allison G. Harveya,, Ann L. Sharpleyb, Melissa J. Reec, Katheen Stinsond, David M. Clarkd a
Department of Psychology, Sleep and Psychological Disorders Lab, University of California, 3210 Tolman Hall #1650, Berkeley, CA 94720-1650, USA b Department of Psychiatry, University of Oxford, Oxford, UK c The Marian Centre, Perth, Australia d Institute of Psychiatry, London, UK Received 11 December 2006; received in revised form 11 April 2007; accepted 12 April 2007
Abstract We describe the development of a cognitive therapy intervention for chronic insomnia. The therapy is based on a cognitive model which suggests that the processes that maintain insomnia include: (1) worry and rumination, (2) attentional bias and monitoring for sleep-related threat, (3) unhelpful beliefs about sleep, (4) misperception of sleep and daytime deficits and (5) the use of safety behaviors that maintain unhelpful beliefs. The aim of cognitive therapy for insomnia is to reverse all five maintaining processes during both the night and the day. In an open trial 19 patients meeting diagnostic criteria for primary insomnia were treated with cognitive therapy for insomnia. Assessments were completed pretreatment, posttreatment and at 3-, 6- and 12-month followup. The significant improvement in both nighttime and daytime impairment evident at the posttreatment assessment was retained up to the 12 month followup. Published by Elsevier Ltd. Keywords: Insomnia; Sleep; Cognitive therapy; Cognitive behavioral treatment
Introduction Cognitive behavior therapy for insomnia (CBT-I) Insomnia is a chronic difficulty getting to sleep, maintaining sleep, waking too early or waking in the morning without feeling restored, along with daytime impairment (e.g., Edinger et al., 2004). Cognitive behavior therapy for insomnia (CBT-I) is a multi-component treatment comprised of: stimulus control, sleep restriction, sleep hygiene, paradoxical intention, relaxation and cognitive restructuring of unhelpful beliefs about sleep. The formal cognitive therapy component of CBT-I, often administered in one session, involves altering faulty beliefs about sleep by education (e.g., Edinger, Wohlgemuth, Radtke, Marsh, & Quillian, 2001).
Corresponding author. Tel.: +1 510 642 7138; fax: +1 510 642 5293.
E-mail address: [email protected] (A.G. Harvey). 0005-7967/$ - see front matter Published by Elsevier Ltd. doi:10.1016/j.brat.2007.04.007
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There is no doubt that CBT-I is effective (Morin et al., 2006). However, there is room for improvement: (1) there are subset of patients who do not improve (19–26%) and (2) the average overall improvement of 50–60% (Morin, Culbert, & Schwartz, 1994) suggests that a minority of patients become good sleepers. Cognitive therapy for insomnia The aim of this paper is to describe the development and initial evaluation of a new treatment approach that was derived from a cognitive model of insomnia (Harvey, 2002). The model draws heavily from, and owes much to, theorizing relating to a range of psychological disorders as well as to theories of insomnia. Predictions from the model have begun to accrue empirical support (Harvey, 2005). There are two reasons for developing a cognitive therapy treatment in an attempt to maximize treatment outcome. First, cognitive therapy for insomnia has not yet received sufficient evaluation (Morin et al., 2006). Second, treatments that devote considerable therapy time to the reversing cognitive maintaining processes have been associated with strong outcomes (e.g., Beck, 2005). What does cognitive therapy for insomnia involve? For a detailed description see Harvey (2005) and Ree and Harvey (2004a). In brief, and following cognitive therapy interventions developed for other disorders, the treatment is delivered in three phases and relies heavily on the core cognitive therapy skills of Socratic questioning and guided discovery. In Phase 1, case formulation involves deriving an individualized version of the cognitive model; one for a typical recent night of insomnia and one for a typical recent day of insomnia (see Fig. 1 for one example). In Phase 2, the maintaining processes are reversed. Several of the procedures used are described below. Intervention to reduce worry and rumination: The patient is taught to identify and evaluate their sleep-related worrisome thoughts, such as ‘if I can’t get to sleep soon, tomorrow will be a disaster’ (following Beck, 1995). The strategies often used by patients to manage worry (e.g., thought suppression) are assessed and, if unhelpful strategies are identified, they are altered. If the patient holds positive beliefs about worry (e.g., worrying while trying to get to sleep helps me get things sorted out in my mind), guided discovery and individualized experiments are used to examine and test their validity. Intervention to reduce attentional bias and monitoring for sleep-related threat: The types of monitoring in which the patient engages are identified (e.g., monitoring the clock, monitoring for signs of fatigue and concentration lapses during the day) and homework assignments used to identify the associated meaning and delineate consequences (typically monitoring exacerbates insomnia). Interventions to reduce or cease
Fig. 1. Case formulation: example individualized version of the cognitive model for a typical recent night (on the left) and a typical recent day (on the right).
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Table 1 Examples of individualized interventions administered in cognitive therapy for insomnia Attentional bias and monitoring A patient who habitually internally focused on her body sensations (to check for feelings of energy/fatigue which she would then use to guide whether or not she should reduce her activity or take a nap) took a walk and contrasted how energetic/fatigued she felt: after 5 min of directing her attention internally (asking and answering questions like ‘how do my legs feel’, ‘are my shoulders sore’) after 5 min of directing her attention externally (asking and answering questions like ‘are there flowers out’, ‘are there people about’) She found that internally attending was associated with more fatigue and less energy and externally attending lifted her energy and reduced her fatigue Unhelpful beliefs about sleep Over two days a patient tested his beliefs that: (a) he had to plan his day carefully in order to conserve his energy and (b) that energy progressively drains away throughout the day and that the only way to generate energy is to sleep or rest. On the first day he spent one 3 h block conserving energy (e.g., avoiding socializing with colleagues, setting work tasks at a slow pace, attempting only mundane tasks) and then a 3 h block ‘using’ energy (e.g., taking a 10 min walk, returning all phone calls, arranging to have a coffee with a colleague, going to the water cooler to get a drink). The following day he did this in the reverse order. Contrary to his beliefs, his mood and energy were improved by ‘‘using’’ energy. As a result of this experiment, ‘‘using’’ energy became synonymous with ‘‘generating’’ energy and this became one strategy for managing daytime tiredness Misperception For those insomnia patients who tend to overestimate how long it takes them to get to sleep and underestimate how long they have slept in total, a comparison of their sleep diary data and actigraphy data can help reduce misperception of sleep and anxiety about sleep (see Tang & Harvey, 2006 for details) Safety behaviors A patient who cancelled important appointments at work (the safety behavior) every time he experienced a night of insomnia contrasted how he felt after canceling appointments for two days with how he felt if he attended the appointments for two days. He discovered that he felt worse on the two days he cancelled appointments because he got behind in his work and this made him feel anxious, which exacerbated his insomnia. In contrast, attending the appointments helped lift his energy levels and disconfirmed his belief that ‘‘if I feel tired at work the best and only way to cope is to cancel my appointments’’ See Ree and Harvey (2004a) for further details and more examples.
monitoring by actively directing attention to the broadest range of stimuli and away from sleep-related threat are then implemented. See Table 1 for example. Intervention to reduce unhelpful beliefs about sleep: As unhelpful beliefs about sleep are identified over the course of therapy individualized experiments are devised to test their validity and utility (see Table 1 for example) and to test out the validity of new beliefs. Intervention to reduce misperception: Opportunities that arise naturally over the course of therapy and individualized experiments allow the following themes to be introduced and elaborated upon: (a) that there is a distinction between how much sleep we feel we get and how much we actually get, (b) that sleep is difficult to perceive because sleep onset is defined by the absence of memories and (c) that nighttime sleep is not the only influence on daytime functioning (other influences include poor diet, not enough exercise). See Table 1 for example. Intervention to reduce use of safety behaviors: A safety behavior is an overt or covert action that is adopted to avoid feared outcomes. The problem is that they: (1) prevent the person experiencing disconfirmation of their unrealistic beliefs and (2) may make the feared outcome more likely to occur (Salkovskis, 1991). Guided discovery is used to identify the advantages and disadvantages of using safety behaviors and individualized experiments are then devised to observe the consequences of dropping or reversing the safety behavior. See Table 1 for example. In the third and final phase the goal is to consolidate treatment gains, set goals to ensure continued progress and make plans for preventing relapse. Novel features of cognitive therapy for insomnia relative to CBT-I: (1) The focus of session time and homework assignments is divided equally between nighttime symptoms and processes and daytime symptoms and processes. In contrast, in CBT-I the focus is typically on nighttime
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symptoms and processes. We suggest that focusing on the daytime is justified by the evidence that aspects of the daytime impairment suffered by patients with insomnia may be independent of nighttime sleep (e.g., Neitzert Semler & Harvey, 2005) and the absence of evidence that a treatment that addresses sleep always addresses all of the daytime consequences of insomnia (Means, Lichstein, Epperson, & Johnson, 2000). (2) Cognitive therapy for insomnia makes heavy use of individually formulated experiments which are ‘‘planned experiential activities, based on experimentation or observation, which are undertaken by patients in or between ,y, therapy sessions’’ to test potentially unhelpful beliefs, establish new beliefs and identify and devise ways to change maintaining processes (Bennett-Levy et al., 2004, p. 8). (3) The only common treatment component is one that targets unhelpful beliefs. However, the method is different; cognitive therapy emphasizes individually formulated experiments to test beliefs (one or more are conducted in most treatment sessions) whereas the cognitive therapy session in CBT-I emphasizes verbal techniques, especially education. (4) The focus in cognitive therapy is on reversing the five cognitive processes suggested to maintain insomnia.
Method Participants The sample was recruited from local psychiatrists, general practitioners, and psychologists and advertisements in the local press. The inclusion criteria were: (1) age between 18 and 65, (2) meeting criteria for primary insomnia (American Psychiatric Association, 2000) and experience of insomnia for at least 1 year and, based on Lichstein, Durrence, Taylor, Bush, and Riedel (2003) quantitative criteria, we also required that the self-reported sleep onset latency (SOL) and/or wake after sleep onset (WASO) be longer than 31 min and/ or total sleep time (TST) be under 6.5 h for more than three nights out of every seven as assessed on 2 weeks of sleep diary. The exclusion criteria were: (1) evidence that the insomnia could be accounted for by another sleep disorder (such as sleep apnoea, operationalized as an apnea–hypopnea index of 410, or periodic limb movement disorder, operationalized as a myoclonic index with arousal 410) or psychiatric disorder, (2) evidence of a medical/physical condition that could account for the poor sleep (e.g., chronic pain), (3) lack of willingness or ability to cease taking medications that have a proven impact on sleep (including hypnotics, antidepressants, beta blockers) and (4) insufficient proficiency in English. An initial phone screen was completed for 207 calls. Of these, 167 did not meet entry criteria and 40 attended the pretreatment clinical assessment. Reasons for exclusion were: outside age range (n ¼ 24), insomnia not the main problem (n ¼ 43), use of medications that affect sleep (n ¼ 25), English not the primary language (n ¼ 3), and participation declined (n ¼ 72; e.g., lived too far away to attend weekly). After the pretreatment clinical assessment, there were 21 further exclusions: declined participation due to time commitment required (n ¼ 3), use of medications that interfere with sleep (n ¼ 7) and insomnia not the most disabling/distressing problem (n ¼ 11). Note that as insomnia is commonly comorbid with a range of psychological disorders, individuals with comorbid problems were not automatically excluded because: (1) the occurrence of a comorbid psychological problem does not necessarily mean the insomnia is ‘secondary’ and (2) selecting just ‘pure’ cases would reduce representativeness. Instead, participants were assessed for primary insomnia using Section C of the insomnia diagnostic interview (IDI) which assesses whether the insomnia or the comorbid disorder is currently the most distressing and disabling problem (based on di Nardo, Moras, Barlow, Rapee, & Brown, 1993). Nineteen consecutive patients (10 women and 9 men) met the study inclusion criteria as determined by the IDI and the Structured Clinical Interview for DSM-IV (SCID-I; First, Spitzer, & Gibbon, 1996). Characteristics of the sample are shown in Table 2. The distribution of the insomnia subtypes were: n ¼ 4 onset (SOL criteria X3 times a week), n ¼ 10 maintenance (WASO criteria X3 times a week), n ¼ 1 mixed (if neither SOL or WASO criteria were X3 times a week, but when SOL and WASO criteria are combined they occurred X3 times a week) and n ¼ 4 combined (both SOL and WASO criteria were met X3 times a week) (Taylor, Lichstein, Durrence, Reidel, & Bush, 2005).
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Table 2 Description of the samples: n (%) or means (standard deviations) Variable Sex Female Male Age (in years) Mean (SD) Range Insomnia duration (in years) Mean (SD) Range Marital status Single Married Cohabiting Divorced Education: exams passed University A levels (17+years) GCSE (15+years) None Current employment Unemployed/on disability Part-time Full-time Student Retired Homemaker Ethnicity Caucasian Not caucasian
n ¼ 19
10 9 48.5 (9.9) 23–61 22.89 (14.28) 2–45 years 5 12 0 2 6 10 3 0 3 9 6 2 0 0 18 1
One or more lifetime psychiatric disorders were present in 68% of the patients (n ¼ 13; 9 unipolar depression, 3 dysthymia, 4 generalized anxiety disorder, 2 panic disorder with agoraphobia, 1 obsessive compulsive disorder) and 16% had a current diagnosis (n ¼ 3; all generalized anxiety disorder). Measures Diagnostic measures The Structured Clinical Interview for DSM-IV (SCID-I) was administered to assess for comorbid axis 1 disorder (Spitzer, Williams, Gibbon, & First, 1996). A structured clinical interview, the IDI, was administered to identify the presence of insomnia. The IDI assesses each of the DSM-IV-TR criteria. The IDI was selected because at the time the study began there was no validated diagnostic interview for insomnia. Preliminary unpublished psychometric data on a sample of 55 individuals with insomnia showed the IDI had high internal consistency (a ¼ 0.87), sensitivity (92%), and specificity (89%). The test–retest reliability has been evaluated on 62 individuals with a re-administration interval of 1–2 weeks. The results indicated strong test–retest reliability (r ¼ 0.90) and good diagnostic agreement for the presence (90%) and absence (92%) of insomnia. Primary outcome measure The Insomnia Severity Index (ISI; Bastien, Vallieres, & Morin, 2001) was selected as the primary outcome measure because the intervention focused equally on the night and the day. Hence, a primary outcome that indexed both outcomes was required. The ISI has established psychometric properties (Bastien et al., 2001).
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Secondary outcome measures Two secondary measures were taken at all assessment points: As a measure of nighttime impairment, a sleep diary was completed immediately on waking over 14 consecutive nights. Participants were asked to record how long it took them to fall asleep (SOL), the amount of time they were awake during the night (WASO), and the amount of sleep obtained in total (TST). As a measure of daytime impairment, the Work and Social Adjustment Scale (WSAS; Mundt, Marks, Shear, & Greist, 2002) assessed functioning across work, home management, social leisure activities, private leisure activities and relationships with others. The psychometric properties are adequate. Process measures Five process measures were administered to assess the extent of change on four of the five specific cognitive processes the treatment was designed to reverse. The Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS; Morin, 1993) measured change to unhelpful beliefs about sleep. Sleep-related worry and rumination was measured with the Anxiety and Preoccupation about Sleep Questionnaire (APSQ; Tang & Harvey, 2004). The APSQ has high internal consistency (a ¼ 0.92). The cognitive subscale of the Pre-Sleep Arousal Scale (PSAS-C; Nicassio, Mendlowitz, Fussell, & Petras, 1985) was also included as a measure of change in worry and rumination about sleep. The cognitive subscale has exhibited adequate reliability and validity (Nicassio et al., 1985). The Sleep Associated Monitoring Index (SAMI; Semler & Harvey, 2004) was included as a measure of monitoring for sleep-related threat. The psychometric properties are adequate (Neitzert Semler & Harvey, 2004). The Sleep Related Behaviors Questionnaire (SRBQ; Ree & Harvey, 2004b) was included as a measure of the use of safety behaviors. Preliminary psychometric properties have been reported (Ree & Harvey, 2004b). Treatment credibility The Credibility/Expectancy Questionnaire (CEQ; Devilly & Borkovec, 2000) measures treatment expectancy and rationale credibility and has established psychometric properties. Measures of anxiety and depression The Beck Depression Inventory (BDI; Beck, Ward, Mock, & Erbaugh, 1961) and Beck Anxiety Inventory (Beck, Epstein, Brown, & Steer, 1988) were used as measures of depression and anxiety, respectively. Polysomnography (PSG) screen A pretreatment PSG night was undertaken as a screen for comorbid sleep disorders. PSG recording channels included four electroencephalogram (EEG) channels (C3/A2, C4/A1, O1/A2, O2/A1), two electrooculogram (EOG) channels from the outer canthus of each eye referred to the mastoid, a submentalis (surface) electromyogram (EMG) and two electrocardiogram (EKG) channels. Additional channels were included to screen for comorbid sleep disorders: two bilateral anterior tibialis EMG channels, airflow (nasal cannular linked to pressure transducer), thoracic and abdominal displacement (respiratory inductive plethysmography), finger pulse oximeter, snoring sensor and position sensor. PSGs were staged in 30 s epochs using the Embla diagnostic software, Somnologica Studio (Medcare, Reykjavik, Iceland). This software provides measures for all aspects of sleep architecture according to standard criteria (Rechtschaffen & Kales, 1968) and the analysis of respiratory events, periodic limb movements and EKG. Therapists and adherence checks The therapists who delivered the treatment were qualified clinical psychologists (M.R. and A.H.) with specific training and experience in CBT. The therapists met weekly to review each case and develop/hone the treatment procedures. To enhance protocol compliance, a treatment manual was prepared and therapists attended a weekly supervision session in which all cases were discussed. All therapy sessions were video recorded and a random sample were evaluated by an independent rater for adherence to the manual.
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Procedure After a telephone screen, an initial detailed pretreatment clinical assessment comprised of: (1) written informed consent, (2) the administration of the IDI and SCID and the BDI, BAI, ISI, WSAS, DBAS, APSQ, PSAS-C, SAMI, and SRBQ, (3) one night of PSG to screen for other sleep disorders and (4) 2 weeks of daily sleep diary. One goal was to establish the ‘dose’ necessary for achieving optimal improvement. The number of therapy sessions ranged from 6 to 22 (average 14). Session length was determined by two factors: (a) participants without comorbidity completed the treatment protocol in 6–8 sessions, those with comorbidity completed the treatment protocol in 8–17 sessions, and (b) as the therapists gained experience they delivered the treatment more efficiently; the first three patients completed the treatment in an average of 17 sessions and the last two patients completed the treatment in six sessions. No patient dropped out during the treatment or followup. As an index of treatment acceptability, at the end of the case formulation phase of treatment (i.e., at the end of either session 1 or 2) the CEQ was administered. As part of the posttreatment assessment the CEQ was readministered along with two additional questions (from Edinger et al., 2001) to measure therapist warmth and competence (1 ‘not at all’ to 9 ‘very much). The posttreatment assessment and 3- , 6- and 12-month followup was completed by an independent assessor (K.S. or A.S.). Participants were offered an honorarium for the completion of the posttreatment and followup assessments (but not for the pretreatment assessment or attending therapy sessions). All assessment sessions were video recorded and a random sample evaluated for treatment adherence by an independent rater (K.S.). Data analysis Changes to each measure across time (pretreatment, posttreatment, 3-, 6-, 12-month followup) were assessed with repeated measures analysis of variance. Significance was followed with scheffe tests. Treatment effect sizes were calculated using Cohen’s d statistic (Cohen, 1988): d ¼ MinitialMpost/SDpooled, where SDpooled ¼ O[ ](SD2initial+SD2post)/2 (Cohen, 1988). Results Purity checks Treatment A random sample (15%) of videotaped treatment sessions were evaluated by an independent rater using integrity checklists to index the occurrence of cognitive therapy-specific components (e.g., exploration and testing of negative thoughts about sleep and tiredness) and CBT-I-specific components (e.g., stimulus control or sleep restriction procedures) (Edinger et al., 2001). On average, 21.19 (5.55) cognitive therapy components and 0.22 (0.51) CBT-I components were present in each session. Hence, the sample of rated sessions were 98.97% pure. Assessment A random sample of 15% of the videos of the assessment sessions were coded by an independent rater. Interrater reliabilities were very good (insomnia diagnosis k ¼ 1.00; SCID diagnoses k ¼ 0.80). Outcome measures Diagnostic outcome measures At the pretreatment assessment, 100% of the participants met DSM-IV-TR diagnostic criteria for primary insomnia. At the posttreatment, 3-, 6- and 12-month followup no participant (0%) met criteria (assessed with the IDI).
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The three patients who met criteria for GAD at pretreatment did not meet criteria at the posttreatment, 3-, 6- or 12-month followup. There were no reoccurrences or new occurrences of axis 1 disorders at postreatment, 3-, 6- or 12-month followup (assessed with the SCID). Primary outcome measures As evident in Table 3, compared to pretreatment there was a significant reduction in scores on the ISI total at posttreatment (d ¼ 5.17), which was retained up to the 12 month followup. Secondary outcomes measures Compared to pretreatment, there was an improvement in daytime functioning on the WSAS at posttreatment (d ¼ 2.20), which was retained for 12 months. There was also a decrease in SOL and WASO at the posttreatment assessment which was retained to 12 months and an increase in TST at posttreatment which was retained to 12 months (SOL d ¼ 0.48; WASO d ¼ 0.45; TST d ¼ 0.64) (see Table 3). Process measures Compared to pretreatment there were reductions in the extent to which participants held unhelpful beliefs about sleep (d ¼ 2.46), experienced sleep-related worry and rumination (d ¼ 2.66, 1.75), engaged in Table 3 Means and standard deviations (in parentheses) for main outcome measures Posttreatment
Primary outcome measure ISI total
23.92 (2.67)
10.53 (2.50)
11.98 (3.28)
12.29 (3.98)
11.66 (2.88)
89.99**
Secondary outcome measures Daytime WSAS
18.11 (6.33)
4.37 (6.17)
4.79 (5.85)
3.53 (3.96)
3.42 (5.62)
39.16**
14.18 (14.32) 24.51 (26.58) 414.39 (60.42)
12.78 (12.99) 25.56 (27.18) 417.46 (63.41)
16.03 (19.15) 26.78 (28.23) 415.10 (71.05)
18.21(20.60) 29.64 (31.36) 415.62 (72.77)
15.15** 7.20** 17.38**
Nighttime (sleep diary for 2 weeks in minutes) Sleep onset latency 29.59 (42.66) Wake after sleep onset 38.95 (36.39) Total sleep time 368.44 (81.13) Process measures Unhelpful beliefs (DBAS) Worry (APSQ) Worry (PSAS-C) Monitoring (SAMI) Safety behaviors (SRBQ) Measures of depression and anxiety BDI BAI Credibility/expectancy questionnaire Logic Utility Confidence in recommending Feeling it will help Therapist warmth Therapist competence Improvement thought would occur Improvement felt would occur
45.01 59.39 22.84 74.74 52.87
(9.60) (17.56) (8.17) (14.05) (13.32)
7.63 (5.11) 4.21 (3.37) 7.78 6.94 7.33 6.69
(1.11) (1.43) (1.68) (1.58)
63.33 (17.82) 60.83 (19.12)
18.63 21.28 11.74 47.13 25.10
(11.71) (10.13) (3.71) (12.18) (12.85)
1.84 (2.41) 2.32 (2.47) 8.58 8.05 8.37 7.97 8.56 8.89 80.00 78.94
3 months followup
20.54 21.78 13.21 48.63 25.79
(9.30) (10.70) (4.81) (12.83) (13.51)
3.26 (3.14) 3.00 (3.23)
6 months followup
18.86 20.28 12.65 43.32 22.98
(11.78) (10.97) (4.46) (13.68) (12.60)
2.84 (2.61) 2.74 (2.99)
12 months followup
F (4,15)
Pretreatment
19.17 18.22 12.89 46.11 21.18
(11.40) (7.02) (4.08) (11.35) (16.40)
3.00 (3.21) 2.21 (2.55)
46.39** 45.90** 24.70** 31.20** 28.16** 16.41** 12.24*
(0.61) (0.78) (0.90) (0.72) (0.78) (0.32) (11.43) (12.76)
Note: BDI, Beck Depression Inventory; BAI, Beck Anxiety Inventory; ISI, Insomnia Severity Index; WSAS, Work and Social Adjustment; DBAS, Dysfunctional Beliefs and Attitudes about Sleep; APSQ, Anxiety and Preoccupation about Sleep; PSAS-C, Cognitive, Pre-Sleep Arousal; SAMI, Sleep Associated Monitoring; SRBQ, Sleep Related Behaviors Questionnaire. *po0.05; **po0.001.
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monitoring for sleep-related threat (d ¼ 2.10), and made use of safety behaviors (d ¼ 2.12) at posttreatment. These changes were retained to 12 months (see Table 3). Measures of anxiety and depression Compared to pretreatment there was a reduction in scores on the BDI (d ¼ 1.45) and BAI (d ¼ 0.64) at posttreatment, which was retained up to the 12-month followup. The effect sizes for pre to posttreatment change were on the BDI and on the BAI (see Table 3). Treatment credibility Possible scores on this measure ranged from 0% to 100%. As evident in Table 3, cognitive therapy was rated as an acceptable treatment. Discussion Diagnostic and primary outcome measures The results of this open trial of a theoretically derived treatment for insomnia were encouraging. Prior to treatment all participants met DSM-IV-TR criteria for primary insomnia. At posttreatment and 3-, 6- and 12month followup no participant met criteria for primary insomnia. Moreover, on the ISI there was a significant reduction from pre to post treatment, an improvement that was retained to the 12-month followup. These findings are consistent with the hypothesis that one pathway to reduce insomnia is to reverse cognitive maintaining processes (Harvey, 2002). Secondary outcome measures Effects on daytime measures The intervention administered was novel in that half of session time and homework was allocated to reversing daytime symptoms and processes. There was a significant reduction in daytime impairment (measured by the WSAS) from pre to posttreatment, which was retained up to 12-month followup. Hence, cognitive therapy holds promise as an intervention for improving daytime functioning in insomnia. Effects on nighttime measures There was significant improvement on the three sleep diary measures (SOL, WASO, TST) from pre to posttreatment and these were retained to 12-month followup. Process measures Process measures were administered to assess the extent to which there was change on the specific cognitive processes that the treatment aimed to reverse; namely, unhelpful beliefs about sleep, worry and rumination about sleep, monitoring for sleep-related threat, and the use of safety behaviors. Significant reductions were observed across all process measures posttreatment and these were retained to 12 months. Hence, four of the processes that cognitive therapy for insomnia set out to reverse do indeed appear to have reversed. Limitations These results must be interpreted within the confines of several limitations. First, there was no control group. Thus, we cannot rule out that the improvement was due to the passage of time or to non-specific therapy effects (e.g., expectation of therapeutic benefit). As such, the conclusions drawn are preliminary and await replication in a randomized controlled trial. Second, the sample was small and although it included a range of ages, generalizability to individuals from a range of ethnic groups and those with less education is unknown. Another reason to check on generalizability is the relatively low yield of participants from the initial
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phone calls (n ¼ 207). Third, multiple comparisons may have inflated type 2 errors. Hence, placing more confidence in results significant at the po0.001 level is advised. Finally, due to differences in baseline variables, outcome measures and populations, it is not possible to compare the results presented here with the results of studies that have tested CBT-I. When comparing the two, consideration should be given to reducing potential confounds by: (a) balancing the measures of the day and the night such that they both include global measures and daily measures and (b) equating familiarity with and habituation to the sleep diary across the two treatments. Treatment credibility, dose, and comorbidity Cognitive therapy for insomnia appears to be an acceptable treatment. There were no dropouts and the ratings on the CEQ indicated the treatment was regarded as logical and credible. As discussed in Procedure Section, one goal was to establish the ‘dose’ of cognitive therapy required. The number of sessions ranged from 6 to 22 (average 14). Session length was determined by comorbidity and most importantly, therapist experience with the treatment (the first three patients completed the treatment in an average of 17 sessions and the last two patients completed the treatment in six sessions). We envisage that the maximum dose of future treatment outcome studies should be 10 sessions. Given that cognitive therapy for insomnia reverses maintaining mechanisms known to be common across the psychiatric disorders most often comorbid with insomnia it is notable that the intervention contributed to the alleviation of anxiety and depression symptoms and GAD in three patients. These findings raise the possibility that targeting cognitive processes shared between insomnia and the commonly comorbid disorders might improve both the insomnia and the symptoms associated with the comorbid disorder. Conclusions In summary, cognitive therapy for insomnia awaits evaluation in a controlled trial. The preliminary results presented suggest it is: (a) acceptable to patients with insomnia: (b) improves sleep and (c) improves daytime functioning. Overall, the results were strongest on measures of daytime functioning and moderate for measures derived from the sleep diary. Acknowledgment This research was supported by a grant from the Wellcome Trust (Grant reference number—065913).
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Edinger, J. D., Bonnet, M. H., Bootzin, R. R., Doghramji, K., Dorsey, C. M., Espie, C. A., et al. (2004). Derivation of research diagnostic criteria for insomnia: Report of an American academy of sleep medicine work group. Sleep, 27, 1567–1596. Edinger, J. D., Wohlgemuth, W. K., Radtke, R. A., Marsh, G. R., & Quillian, R. E. (2001). Cognitive behavioral therapy for treatment of chronic primary insomnia: A randomized controlled trial. Journal of the American Medical Association, 285, 1856–1864. First, M., Spitzer, R., & Gibbon, M. (1996). Structured clinical interview for DSM-IX axis i disorders. New York: Biomedics Research Department, New York State Psychiatric Institute. Harvey, A. G. (2002). A cognitive model of insomnia. Behaviour Research and Therapy, 40, 869–894. Harvey, A. G. (2005). A cognitive theory of and therapy for chronic insomnia. Journal of Cognitive Psychotherapy. An International Quarterly, 19, 41–60. Lichstein, K. L., Durrence, H. H., Taylor, D. J., Bush, A. J., & Riedel, B. W. (2003). Quantitative criteria for insomnia. Behaviour Research and Therapy, 41, 427–445. Means, M. K., Lichstein, K. L., Epperson, M. T., & Johnson, C. T. (2000). Relaxation therapy for insomnia: Nighttime and daytime effects. Behaviour Research and Therapy, 38, 665–678. Morin, C. M. (1993). Insomnia: Psychological assessment and management. New York: Guilford Press. Morin, C. M., Bootzin, R. R., Buysse, D. J., Edinger, J. D., Espie, C. A., & Lichstein, K. L. (2006). Psychological and behavioral treatment of insomnia: An update of recent evidence (1998–2004). Sleep, 29, 1396–1406. Morin, C. M., Culbert, J. P., & Schwartz, S. M. (1994). Nonpharmacological interventions for insomnia: A meta-analysis of treatment efficacy. American Journal of Psychiatry, 151, 1172–1180. Mundt, J. C., Marks, I. M., Shear, M. K., & Greist, J. H. (2002). The work and social adjustment scale: A simple measure of impairment in functioning. British Journal of Psychiatry, 180, 461–464. Neitzert Semler, C., & Harvey, A. G. (2004). Monitoring for sleep-related threat: A pilot study of the sleep associated monitoring index (SAMI). Psychosomatic Medicine, 66, 242–250. Neitzert Semler, C., & Harvey, A. G. (2005). Misperception of sleep can adversely affect daytime functioning in insomnia. Behaviour Research and Therapy, 43, 843–856. Nicassio, P. M., Mendlowitz, D. R., Fussell, J. J., & Petras, L. (1985). The phenomenology of the pre-sleep state: The development of the pre-sleep arousal scale. Behaviour Research and Therapy, 23, 263–271. Rechtschaffen, A., & Kales, A. (1968). A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects. Bethesda, MD: US Department of Health Education and Welfare. Ree, M., & Harvey, A. G. (2004a). Insomnia. In J. Bennett-Levy, G. Butler, M. Fennell, A. Hackman, M. Mueller, & D. Westbrook (Eds.), Oxford guide to behavioural experiments in cognitive therapy (pp. 287–305). Oxford: Oxford University Press. Ree, M., & Harvey, A. G. (2004b). Investigating safety behaviours in insomnia: The development of the sleep-related behaviours questionnaire (SRBQ). Behaviour Change, 21, 26–36. Salkovskis, P. M. (1991). The importance of behaviour in the maintenance of anxiety and panic: A cognitive account. Behavioural Psychotherapy, 19, 6–19. Semler, C. N., & Harvey, A. G. (2004). Monitoring of sleep-related threat in primary insomnia: Development and validation of the sleep associated monitoring inventory (SAMI). Psychosomatic Medicine, 66, 242–250. Spitzer, R. L., Williams, J. B. W., Gibbon, M., & First, M. (1996). Structured clinical interview for DSM-IV (SCID). Washington, DC: American Psychiatric Association. Tang, N. K., & Harvey, A. G. (2004). Correcting distorted perception of sleep in insomnia: A novel behavioural experiment? Behaviour Research and Therapy, 42, 27–39. Tang, N. K. Y., & Harvey, A. G. (2006). Altering misperception of sleep in insomnia: Behavioural experiments versus verbal explanation. Journal of Consulting and Clinical Psychology, 74, 767–776. Taylor, D. J., Lichstein, K. L., Durrence, H., Reidel, B. W., & Bush, A. J. (2005). Epidemiology of insomnia, depression, and anxiety. Sleep, 28, 1457–1464.
Behaviour Research and Therapy 45 (2007) 2491–2501 www.elsevier.com/locate/brat
Shorter communication
An open trial of cognitive therapy for chronic insomnia Allison G. Harveya,, Ann L. Sharpleyb, Melissa J. Reec, Katheen Stinsond, David M. Clarkd a
Department of Psychology, Sleep and Psychological Disorders Lab, University of California, 3210 Tolman Hall #1650, Berkeley, CA 94720-1650, USA b Department of Psychiatry, University of Oxford, Oxford, UK c The Marian Centre, Perth, Australia d Institute of Psychiatry, London, UK Received 11 December 2006; received in revised form 11 April 2007; accepted 12 April 2007
Abstract We describe the development of a cognitive therapy intervention for chronic insomnia. The therapy is based on a cognitive model which suggests that the processes that maintain insomnia include: (1) worry and rumination, (2) attentional bias and monitoring for sleep-related threat, (3) unhelpful beliefs about sleep, (4) misperception of sleep and daytime deficits and (5) the use of safety behaviors that maintain unhelpful beliefs. The aim of cognitive therapy for insomnia is to reverse all five maintaining processes during both the night and the day. In an open trial 19 patients meeting diagnostic criteria for primary insomnia were treated with cognitive therapy for insomnia. Assessments were completed pretreatment, posttreatment and at 3-, 6- and 12-month followup. The significant improvement in both nighttime and daytime impairment evident at the posttreatment assessment was retained up to the 12 month followup. Published by Elsevier Ltd. Keywords: Insomnia; Sleep; Cognitive therapy; Cognitive behavioral treatment
Introduction Cognitive behavior therapy for insomnia (CBT-I) Insomnia is a chronic difficulty getting to sleep, maintaining sleep, waking too early or waking in the morning without feeling restored, along with daytime impairment (e.g., Edinger et al., 2004). Cognitive behavior therapy for insomnia (CBT-I) is a multi-component treatment comprised of: stimulus control, sleep restriction, sleep hygiene, paradoxical intention, relaxation and cognitive restructuring of unhelpful beliefs about sleep. The formal cognitive therapy component of CBT-I, often administered in one session, involves altering faulty beliefs about sleep by education (e.g., Edinger, Wohlgemuth, Radtke, Marsh, & Quillian, 2001).
Corresponding author. Tel.: +1 510 642 7138; fax: +1 510 642 5293.
E-mail address: [email protected] (A.G. Harvey). 0005-7967/$ - see front matter Published by Elsevier Ltd. doi:10.1016/j.brat.2007.04.007
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There is no doubt that CBT-I is effective (Morin et al., 2006). However, there is room for improvement: (1) there are subset of patients who do not improve (19–26%) and (2) the average overall improvement of 50–60% (Morin, Culbert, & Schwartz, 1994) suggests that a minority of patients become good sleepers. Cognitive therapy for insomnia The aim of this paper is to describe the development and initial evaluation of a new treatment approach that was derived from a cognitive model of insomnia (Harvey, 2002). The model draws heavily from, and owes much to, theorizing relating to a range of psychological disorders as well as to theories of insomnia. Predictions from the model have begun to accrue empirical support (Harvey, 2005). There are two reasons for developing a cognitive therapy treatment in an attempt to maximize treatment outcome. First, cognitive therapy for insomnia has not yet received sufficient evaluation (Morin et al., 2006). Second, treatments that devote considerable therapy time to the reversing cognitive maintaining processes have been associated with strong outcomes (e.g., Beck, 2005). What does cognitive therapy for insomnia involve? For a detailed description see Harvey (2005) and Ree and Harvey (2004a). In brief, and following cognitive therapy interventions developed for other disorders, the treatment is delivered in three phases and relies heavily on the core cognitive therapy skills of Socratic questioning and guided discovery. In Phase 1, case formulation involves deriving an individualized version of the cognitive model; one for a typical recent night of insomnia and one for a typical recent day of insomnia (see Fig. 1 for one example). In Phase 2, the maintaining processes are reversed. Several of the procedures used are described below. Intervention to reduce worry and rumination: The patient is taught to identify and evaluate their sleep-related worrisome thoughts, such as ‘if I can’t get to sleep soon, tomorrow will be a disaster’ (following Beck, 1995). The strategies often used by patients to manage worry (e.g., thought suppression) are assessed and, if unhelpful strategies are identified, they are altered. If the patient holds positive beliefs about worry (e.g., worrying while trying to get to sleep helps me get things sorted out in my mind), guided discovery and individualized experiments are used to examine and test their validity. Intervention to reduce attentional bias and monitoring for sleep-related threat: The types of monitoring in which the patient engages are identified (e.g., monitoring the clock, monitoring for signs of fatigue and concentration lapses during the day) and homework assignments used to identify the associated meaning and delineate consequences (typically monitoring exacerbates insomnia). Interventions to reduce or cease
Fig. 1. Case formulation: example individualized version of the cognitive model for a typical recent night (on the left) and a typical recent day (on the right).
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Table 1 Examples of individualized interventions administered in cognitive therapy for insomnia Attentional bias and monitoring A patient who habitually internally focused on her body sensations (to check for feelings of energy/fatigue which she would then use to guide whether or not she should reduce her activity or take a nap) took a walk and contrasted how energetic/fatigued she felt: after 5 min of directing her attention internally (asking and answering questions like ‘how do my legs feel’, ‘are my shoulders sore’) after 5 min of directing her attention externally (asking and answering questions like ‘are there flowers out’, ‘are there people about’) She found that internally attending was associated with more fatigue and less energy and externally attending lifted her energy and reduced her fatigue Unhelpful beliefs about sleep Over two days a patient tested his beliefs that: (a) he had to plan his day carefully in order to conserve his energy and (b) that energy progressively drains away throughout the day and that the only way to generate energy is to sleep or rest. On the first day he spent one 3 h block conserving energy (e.g., avoiding socializing with colleagues, setting work tasks at a slow pace, attempting only mundane tasks) and then a 3 h block ‘using’ energy (e.g., taking a 10 min walk, returning all phone calls, arranging to have a coffee with a colleague, going to the water cooler to get a drink). The following day he did this in the reverse order. Contrary to his beliefs, his mood and energy were improved by ‘‘using’’ energy. As a result of this experiment, ‘‘using’’ energy became synonymous with ‘‘generating’’ energy and this became one strategy for managing daytime tiredness Misperception For those insomnia patients who tend to overestimate how long it takes them to get to sleep and underestimate how long they have slept in total, a comparison of their sleep diary data and actigraphy data can help reduce misperception of sleep and anxiety about sleep (see Tang & Harvey, 2006 for details) Safety behaviors A patient who cancelled important appointments at work (the safety behavior) every time he experienced a night of insomnia contrasted how he felt after canceling appointments for two days with how he felt if he attended the appointments for two days. He discovered that he felt worse on the two days he cancelled appointments because he got behind in his work and this made him feel anxious, which exacerbated his insomnia. In contrast, attending the appointments helped lift his energy levels and disconfirmed his belief that ‘‘if I feel tired at work the best and only way to cope is to cancel my appointments’’ See Ree and Harvey (2004a) for further details and more examples.
monitoring by actively directing attention to the broadest range of stimuli and away from sleep-related threat are then implemented. See Table 1 for example. Intervention to reduce unhelpful beliefs about sleep: As unhelpful beliefs about sleep are identified over the course of therapy individualized experiments are devised to test their validity and utility (see Table 1 for example) and to test out the validity of new beliefs. Intervention to reduce misperception: Opportunities that arise naturally over the course of therapy and individualized experiments allow the following themes to be introduced and elaborated upon: (a) that there is a distinction between how much sleep we feel we get and how much we actually get, (b) that sleep is difficult to perceive because sleep onset is defined by the absence of memories and (c) that nighttime sleep is not the only influence on daytime functioning (other influences include poor diet, not enough exercise). See Table 1 for example. Intervention to reduce use of safety behaviors: A safety behavior is an overt or covert action that is adopted to avoid feared outcomes. The problem is that they: (1) prevent the person experiencing disconfirmation of their unrealistic beliefs and (2) may make the feared outcome more likely to occur (Salkovskis, 1991). Guided discovery is used to identify the advantages and disadvantages of using safety behaviors and individualized experiments are then devised to observe the consequences of dropping or reversing the safety behavior. See Table 1 for example. In the third and final phase the goal is to consolidate treatment gains, set goals to ensure continued progress and make plans for preventing relapse. Novel features of cognitive therapy for insomnia relative to CBT-I: (1) The focus of session time and homework assignments is divided equally between nighttime symptoms and processes and daytime symptoms and processes. In contrast, in CBT-I the focus is typically on nighttime
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symptoms and processes. We suggest that focusing on the daytime is justified by the evidence that aspects of the daytime impairment suffered by patients with insomnia may be independent of nighttime sleep (e.g., Neitzert Semler & Harvey, 2005) and the absence of evidence that a treatment that addresses sleep always addresses all of the daytime consequences of insomnia (Means, Lichstein, Epperson, & Johnson, 2000). (2) Cognitive therapy for insomnia makes heavy use of individually formulated experiments which are ‘‘planned experiential activities, based on experimentation or observation, which are undertaken by patients in or between ,y, therapy sessions’’ to test potentially unhelpful beliefs, establish new beliefs and identify and devise ways to change maintaining processes (Bennett-Levy et al., 2004, p. 8). (3) The only common treatment component is one that targets unhelpful beliefs. However, the method is different; cognitive therapy emphasizes individually formulated experiments to test beliefs (one or more are conducted in most treatment sessions) whereas the cognitive therapy session in CBT-I emphasizes verbal techniques, especially education. (4) The focus in cognitive therapy is on reversing the five cognitive processes suggested to maintain insomnia.
Method Participants The sample was recruited from local psychiatrists, general practitioners, and psychologists and advertisements in the local press. The inclusion criteria were: (1) age between 18 and 65, (2) meeting criteria for primary insomnia (American Psychiatric Association, 2000) and experience of insomnia for at least 1 year and, based on Lichstein, Durrence, Taylor, Bush, and Riedel (2003) quantitative criteria, we also required that the self-reported sleep onset latency (SOL) and/or wake after sleep onset (WASO) be longer than 31 min and/ or total sleep time (TST) be under 6.5 h for more than three nights out of every seven as assessed on 2 weeks of sleep diary. The exclusion criteria were: (1) evidence that the insomnia could be accounted for by another sleep disorder (such as sleep apnoea, operationalized as an apnea–hypopnea index of 410, or periodic limb movement disorder, operationalized as a myoclonic index with arousal 410) or psychiatric disorder, (2) evidence of a medical/physical condition that could account for the poor sleep (e.g., chronic pain), (3) lack of willingness or ability to cease taking medications that have a proven impact on sleep (including hypnotics, antidepressants, beta blockers) and (4) insufficient proficiency in English. An initial phone screen was completed for 207 calls. Of these, 167 did not meet entry criteria and 40 attended the pretreatment clinical assessment. Reasons for exclusion were: outside age range (n ¼ 24), insomnia not the main problem (n ¼ 43), use of medications that affect sleep (n ¼ 25), English not the primary language (n ¼ 3), and participation declined (n ¼ 72; e.g., lived too far away to attend weekly). After the pretreatment clinical assessment, there were 21 further exclusions: declined participation due to time commitment required (n ¼ 3), use of medications that interfere with sleep (n ¼ 7) and insomnia not the most disabling/distressing problem (n ¼ 11). Note that as insomnia is commonly comorbid with a range of psychological disorders, individuals with comorbid problems were not automatically excluded because: (1) the occurrence of a comorbid psychological problem does not necessarily mean the insomnia is ‘secondary’ and (2) selecting just ‘pure’ cases would reduce representativeness. Instead, participants were assessed for primary insomnia using Section C of the insomnia diagnostic interview (IDI) which assesses whether the insomnia or the comorbid disorder is currently the most distressing and disabling problem (based on di Nardo, Moras, Barlow, Rapee, & Brown, 1993). Nineteen consecutive patients (10 women and 9 men) met the study inclusion criteria as determined by the IDI and the Structured Clinical Interview for DSM-IV (SCID-I; First, Spitzer, & Gibbon, 1996). Characteristics of the sample are shown in Table 2. The distribution of the insomnia subtypes were: n ¼ 4 onset (SOL criteria X3 times a week), n ¼ 10 maintenance (WASO criteria X3 times a week), n ¼ 1 mixed (if neither SOL or WASO criteria were X3 times a week, but when SOL and WASO criteria are combined they occurred X3 times a week) and n ¼ 4 combined (both SOL and WASO criteria were met X3 times a week) (Taylor, Lichstein, Durrence, Reidel, & Bush, 2005).
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Table 2 Description of the samples: n (%) or means (standard deviations) Variable Sex Female Male Age (in years) Mean (SD) Range Insomnia duration (in years) Mean (SD) Range Marital status Single Married Cohabiting Divorced Education: exams passed University A levels (17+years) GCSE (15+years) None Current employment Unemployed/on disability Part-time Full-time Student Retired Homemaker Ethnicity Caucasian Not caucasian
n ¼ 19
10 9 48.5 (9.9) 23–61 22.89 (14.28) 2–45 years 5 12 0 2 6 10 3 0 3 9 6 2 0 0 18 1
One or more lifetime psychiatric disorders were present in 68% of the patients (n ¼ 13; 9 unipolar depression, 3 dysthymia, 4 generalized anxiety disorder, 2 panic disorder with agoraphobia, 1 obsessive compulsive disorder) and 16% had a current diagnosis (n ¼ 3; all generalized anxiety disorder). Measures Diagnostic measures The Structured Clinical Interview for DSM-IV (SCID-I) was administered to assess for comorbid axis 1 disorder (Spitzer, Williams, Gibbon, & First, 1996). A structured clinical interview, the IDI, was administered to identify the presence of insomnia. The IDI assesses each of the DSM-IV-TR criteria. The IDI was selected because at the time the study began there was no validated diagnostic interview for insomnia. Preliminary unpublished psychometric data on a sample of 55 individuals with insomnia showed the IDI had high internal consistency (a ¼ 0.87), sensitivity (92%), and specificity (89%). The test–retest reliability has been evaluated on 62 individuals with a re-administration interval of 1–2 weeks. The results indicated strong test–retest reliability (r ¼ 0.90) and good diagnostic agreement for the presence (90%) and absence (92%) of insomnia. Primary outcome measure The Insomnia Severity Index (ISI; Bastien, Vallieres, & Morin, 2001) was selected as the primary outcome measure because the intervention focused equally on the night and the day. Hence, a primary outcome that indexed both outcomes was required. The ISI has established psychometric properties (Bastien et al., 2001).
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Secondary outcome measures Two secondary measures were taken at all assessment points: As a measure of nighttime impairment, a sleep diary was completed immediately on waking over 14 consecutive nights. Participants were asked to record how long it took them to fall asleep (SOL), the amount of time they were awake during the night (WASO), and the amount of sleep obtained in total (TST). As a measure of daytime impairment, the Work and Social Adjustment Scale (WSAS; Mundt, Marks, Shear, & Greist, 2002) assessed functioning across work, home management, social leisure activities, private leisure activities and relationships with others. The psychometric properties are adequate. Process measures Five process measures were administered to assess the extent of change on four of the five specific cognitive processes the treatment was designed to reverse. The Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS; Morin, 1993) measured change to unhelpful beliefs about sleep. Sleep-related worry and rumination was measured with the Anxiety and Preoccupation about Sleep Questionnaire (APSQ; Tang & Harvey, 2004). The APSQ has high internal consistency (a ¼ 0.92). The cognitive subscale of the Pre-Sleep Arousal Scale (PSAS-C; Nicassio, Mendlowitz, Fussell, & Petras, 1985) was also included as a measure of change in worry and rumination about sleep. The cognitive subscale has exhibited adequate reliability and validity (Nicassio et al., 1985). The Sleep Associated Monitoring Index (SAMI; Semler & Harvey, 2004) was included as a measure of monitoring for sleep-related threat. The psychometric properties are adequate (Neitzert Semler & Harvey, 2004). The Sleep Related Behaviors Questionnaire (SRBQ; Ree & Harvey, 2004b) was included as a measure of the use of safety behaviors. Preliminary psychometric properties have been reported (Ree & Harvey, 2004b). Treatment credibility The Credibility/Expectancy Questionnaire (CEQ; Devilly & Borkovec, 2000) measures treatment expectancy and rationale credibility and has established psychometric properties. Measures of anxiety and depression The Beck Depression Inventory (BDI; Beck, Ward, Mock, & Erbaugh, 1961) and Beck Anxiety Inventory (Beck, Epstein, Brown, & Steer, 1988) were used as measures of depression and anxiety, respectively. Polysomnography (PSG) screen A pretreatment PSG night was undertaken as a screen for comorbid sleep disorders. PSG recording channels included four electroencephalogram (EEG) channels (C3/A2, C4/A1, O1/A2, O2/A1), two electrooculogram (EOG) channels from the outer canthus of each eye referred to the mastoid, a submentalis (surface) electromyogram (EMG) and two electrocardiogram (EKG) channels. Additional channels were included to screen for comorbid sleep disorders: two bilateral anterior tibialis EMG channels, airflow (nasal cannular linked to pressure transducer), thoracic and abdominal displacement (respiratory inductive plethysmography), finger pulse oximeter, snoring sensor and position sensor. PSGs were staged in 30 s epochs using the Embla diagnostic software, Somnologica Studio (Medcare, Reykjavik, Iceland). This software provides measures for all aspects of sleep architecture according to standard criteria (Rechtschaffen & Kales, 1968) and the analysis of respiratory events, periodic limb movements and EKG. Therapists and adherence checks The therapists who delivered the treatment were qualified clinical psychologists (M.R. and A.H.) with specific training and experience in CBT. The therapists met weekly to review each case and develop/hone the treatment procedures. To enhance protocol compliance, a treatment manual was prepared and therapists attended a weekly supervision session in which all cases were discussed. All therapy sessions were video recorded and a random sample were evaluated by an independent rater for adherence to the manual.
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Procedure After a telephone screen, an initial detailed pretreatment clinical assessment comprised of: (1) written informed consent, (2) the administration of the IDI and SCID and the BDI, BAI, ISI, WSAS, DBAS, APSQ, PSAS-C, SAMI, and SRBQ, (3) one night of PSG to screen for other sleep disorders and (4) 2 weeks of daily sleep diary. One goal was to establish the ‘dose’ necessary for achieving optimal improvement. The number of therapy sessions ranged from 6 to 22 (average 14). Session length was determined by two factors: (a) participants without comorbidity completed the treatment protocol in 6–8 sessions, those with comorbidity completed the treatment protocol in 8–17 sessions, and (b) as the therapists gained experience they delivered the treatment more efficiently; the first three patients completed the treatment in an average of 17 sessions and the last two patients completed the treatment in six sessions. No patient dropped out during the treatment or followup. As an index of treatment acceptability, at the end of the case formulation phase of treatment (i.e., at the end of either session 1 or 2) the CEQ was administered. As part of the posttreatment assessment the CEQ was readministered along with two additional questions (from Edinger et al., 2001) to measure therapist warmth and competence (1 ‘not at all’ to 9 ‘very much). The posttreatment assessment and 3- , 6- and 12-month followup was completed by an independent assessor (K.S. or A.S.). Participants were offered an honorarium for the completion of the posttreatment and followup assessments (but not for the pretreatment assessment or attending therapy sessions). All assessment sessions were video recorded and a random sample evaluated for treatment adherence by an independent rater (K.S.). Data analysis Changes to each measure across time (pretreatment, posttreatment, 3-, 6-, 12-month followup) were assessed with repeated measures analysis of variance. Significance was followed with scheffe tests. Treatment effect sizes were calculated using Cohen’s d statistic (Cohen, 1988): d ¼ MinitialMpost/SDpooled, where SDpooled ¼ O[ ](SD2initial+SD2post)/2 (Cohen, 1988). Results Purity checks Treatment A random sample (15%) of videotaped treatment sessions were evaluated by an independent rater using integrity checklists to index the occurrence of cognitive therapy-specific components (e.g., exploration and testing of negative thoughts about sleep and tiredness) and CBT-I-specific components (e.g., stimulus control or sleep restriction procedures) (Edinger et al., 2001). On average, 21.19 (5.55) cognitive therapy components and 0.22 (0.51) CBT-I components were present in each session. Hence, the sample of rated sessions were 98.97% pure. Assessment A random sample of 15% of the videos of the assessment sessions were coded by an independent rater. Interrater reliabilities were very good (insomnia diagnosis k ¼ 1.00; SCID diagnoses k ¼ 0.80). Outcome measures Diagnostic outcome measures At the pretreatment assessment, 100% of the participants met DSM-IV-TR diagnostic criteria for primary insomnia. At the posttreatment, 3-, 6- and 12-month followup no participant (0%) met criteria (assessed with the IDI).
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The three patients who met criteria for GAD at pretreatment did not meet criteria at the posttreatment, 3-, 6- or 12-month followup. There were no reoccurrences or new occurrences of axis 1 disorders at postreatment, 3-, 6- or 12-month followup (assessed with the SCID). Primary outcome measures As evident in Table 3, compared to pretreatment there was a significant reduction in scores on the ISI total at posttreatment (d ¼ 5.17), which was retained up to the 12 month followup. Secondary outcomes measures Compared to pretreatment, there was an improvement in daytime functioning on the WSAS at posttreatment (d ¼ 2.20), which was retained for 12 months. There was also a decrease in SOL and WASO at the posttreatment assessment which was retained to 12 months and an increase in TST at posttreatment which was retained to 12 months (SOL d ¼ 0.48; WASO d ¼ 0.45; TST d ¼ 0.64) (see Table 3). Process measures Compared to pretreatment there were reductions in the extent to which participants held unhelpful beliefs about sleep (d ¼ 2.46), experienced sleep-related worry and rumination (d ¼ 2.66, 1.75), engaged in Table 3 Means and standard deviations (in parentheses) for main outcome measures Posttreatment
Primary outcome measure ISI total
23.92 (2.67)
10.53 (2.50)
11.98 (3.28)
12.29 (3.98)
11.66 (2.88)
89.99**
Secondary outcome measures Daytime WSAS
18.11 (6.33)
4.37 (6.17)
4.79 (5.85)
3.53 (3.96)
3.42 (5.62)
39.16**
14.18 (14.32) 24.51 (26.58) 414.39 (60.42)
12.78 (12.99) 25.56 (27.18) 417.46 (63.41)
16.03 (19.15) 26.78 (28.23) 415.10 (71.05)
18.21(20.60) 29.64 (31.36) 415.62 (72.77)
15.15** 7.20** 17.38**
Nighttime (sleep diary for 2 weeks in minutes) Sleep onset latency 29.59 (42.66) Wake after sleep onset 38.95 (36.39) Total sleep time 368.44 (81.13) Process measures Unhelpful beliefs (DBAS) Worry (APSQ) Worry (PSAS-C) Monitoring (SAMI) Safety behaviors (SRBQ) Measures of depression and anxiety BDI BAI Credibility/expectancy questionnaire Logic Utility Confidence in recommending Feeling it will help Therapist warmth Therapist competence Improvement thought would occur Improvement felt would occur
45.01 59.39 22.84 74.74 52.87
(9.60) (17.56) (8.17) (14.05) (13.32)
7.63 (5.11) 4.21 (3.37) 7.78 6.94 7.33 6.69
(1.11) (1.43) (1.68) (1.58)
63.33 (17.82) 60.83 (19.12)
18.63 21.28 11.74 47.13 25.10
(11.71) (10.13) (3.71) (12.18) (12.85)
1.84 (2.41) 2.32 (2.47) 8.58 8.05 8.37 7.97 8.56 8.89 80.00 78.94
3 months followup
20.54 21.78 13.21 48.63 25.79
(9.30) (10.70) (4.81) (12.83) (13.51)
3.26 (3.14) 3.00 (3.23)
6 months followup
18.86 20.28 12.65 43.32 22.98
(11.78) (10.97) (4.46) (13.68) (12.60)
2.84 (2.61) 2.74 (2.99)
12 months followup
F (4,15)
Pretreatment
19.17 18.22 12.89 46.11 21.18
(11.40) (7.02) (4.08) (11.35) (16.40)
3.00 (3.21) 2.21 (2.55)
46.39** 45.90** 24.70** 31.20** 28.16** 16.41** 12.24*
(0.61) (0.78) (0.90) (0.72) (0.78) (0.32) (11.43) (12.76)
Note: BDI, Beck Depression Inventory; BAI, Beck Anxiety Inventory; ISI, Insomnia Severity Index; WSAS, Work and Social Adjustment; DBAS, Dysfunctional Beliefs and Attitudes about Sleep; APSQ, Anxiety and Preoccupation about Sleep; PSAS-C, Cognitive, Pre-Sleep Arousal; SAMI, Sleep Associated Monitoring; SRBQ, Sleep Related Behaviors Questionnaire. *po0.05; **po0.001.
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monitoring for sleep-related threat (d ¼ 2.10), and made use of safety behaviors (d ¼ 2.12) at posttreatment. These changes were retained to 12 months (see Table 3). Measures of anxiety and depression Compared to pretreatment there was a reduction in scores on the BDI (d ¼ 1.45) and BAI (d ¼ 0.64) at posttreatment, which was retained up to the 12-month followup. The effect sizes for pre to posttreatment change were on the BDI and on the BAI (see Table 3). Treatment credibility Possible scores on this measure ranged from 0% to 100%. As evident in Table 3, cognitive therapy was rated as an acceptable treatment. Discussion Diagnostic and primary outcome measures The results of this open trial of a theoretically derived treatment for insomnia were encouraging. Prior to treatment all participants met DSM-IV-TR criteria for primary insomnia. At posttreatment and 3-, 6- and 12month followup no participant met criteria for primary insomnia. Moreover, on the ISI there was a significant reduction from pre to post treatment, an improvement that was retained to the 12-month followup. These findings are consistent with the hypothesis that one pathway to reduce insomnia is to reverse cognitive maintaining processes (Harvey, 2002). Secondary outcome measures Effects on daytime measures The intervention administered was novel in that half of session time and homework was allocated to reversing daytime symptoms and processes. There was a significant reduction in daytime impairment (measured by the WSAS) from pre to posttreatment, which was retained up to 12-month followup. Hence, cognitive therapy holds promise as an intervention for improving daytime functioning in insomnia. Effects on nighttime measures There was significant improvement on the three sleep diary measures (SOL, WASO, TST) from pre to posttreatment and these were retained to 12-month followup. Process measures Process measures were administered to assess the extent to which there was change on the specific cognitive processes that the treatment aimed to reverse; namely, unhelpful beliefs about sleep, worry and rumination about sleep, monitoring for sleep-related threat, and the use of safety behaviors. Significant reductions were observed across all process measures posttreatment and these were retained to 12 months. Hence, four of the processes that cognitive therapy for insomnia set out to reverse do indeed appear to have reversed. Limitations These results must be interpreted within the confines of several limitations. First, there was no control group. Thus, we cannot rule out that the improvement was due to the passage of time or to non-specific therapy effects (e.g., expectation of therapeutic benefit). As such, the conclusions drawn are preliminary and await replication in a randomized controlled trial. Second, the sample was small and although it included a range of ages, generalizability to individuals from a range of ethnic groups and those with less education is unknown. Another reason to check on generalizability is the relatively low yield of participants from the initial
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phone calls (n ¼ 207). Third, multiple comparisons may have inflated type 2 errors. Hence, placing more confidence in results significant at the po0.001 level is advised. Finally, due to differences in baseline variables, outcome measures and populations, it is not possible to compare the results presented here with the results of studies that have tested CBT-I. When comparing the two, consideration should be given to reducing potential confounds by: (a) balancing the measures of the day and the night such that they both include global measures and daily measures and (b) equating familiarity with and habituation to the sleep diary across the two treatments. Treatment credibility, dose, and comorbidity Cognitive therapy for insomnia appears to be an acceptable treatment. There were no dropouts and the ratings on the CEQ indicated the treatment was regarded as logical and credible. As discussed in Procedure Section, one goal was to establish the ‘dose’ of cognitive therapy required. The number of sessions ranged from 6 to 22 (average 14). Session length was determined by comorbidity and most importantly, therapist experience with the treatment (the first three patients completed the treatment in an average of 17 sessions and the last two patients completed the treatment in six sessions). We envisage that the maximum dose of future treatment outcome studies should be 10 sessions. Given that cognitive therapy for insomnia reverses maintaining mechanisms known to be common across the psychiatric disorders most often comorbid with insomnia it is notable that the intervention contributed to the alleviation of anxiety and depression symptoms and GAD in three patients. These findings raise the possibility that targeting cognitive processes shared between insomnia and the commonly comorbid disorders might improve both the insomnia and the symptoms associated with the comorbid disorder. Conclusions In summary, cognitive therapy for insomnia awaits evaluation in a controlled trial. The preliminary results presented suggest it is: (a) acceptable to patients with insomnia: (b) improves sleep and (c) improves daytime functioning. Overall, the results were strongest on measures of daytime functioning and moderate for measures derived from the sleep diary. Acknowledgment This research was supported by a grant from the Wellcome Trust (Grant reference number—065913).
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