Review Insomnia

REVIEW
Psychological And Behavioral Treatment Of Insomnia:Update Of The Recent Evidence (1998-2004)

1
Charles M. Morin, PhD, (Chair); 2Richard R. Bootzin, PhD; 3Daniel J. Buysse, MD; 4Jack D. Edinger, PhD; 5Colin A. Espie, PhD; 6Kenneth L. Lichstein, PhD
Universit Laval, Qubec, Canada; 2University of Arizona, Tucson, AZ; 3University of Pittsburgh School of Medicine, Pittsburgh, PA; 4VA and Duke University Medical Centers, Durham, NC; 5University of Glasgow, Glasgow, Scotland; 6University of Alabama, Tuscaloosa, AL
Background: Recognition that psychological and behavioral factors play an important role in insomnia has led to increased interest in therapies targeting these factors. A review paper published in 1999 summarized the evidence regarding the efcacy of psychological and behavioral treatments for persistent insomnia. The present review provides an update of the evidence published since the original paper. As with the original paper, this review was conducted by a task force commissioned by the American Academy of Sleep Medicine in order to update its practice parameters on psychological and behavioral therapies for insomnia. Methods: A systematic review was conducted on 37 treatment studies (N = 2246 subjects/patients) published between 1998 and 2004 inclusively and identied through PsycInfo and Medline searches. Each study was systematically reviewed with a standard coding sheet and the following information was extracted: Study design, sample (number of participants, age, gender), diagnosis, type of treatments and controls, primary and secondary outcome measures, and main ndings. Criteria for inclusion of a study were as follows: (a) the main sleep diagnosis was insomnia (primary or comorbid), (b) at least 1 treatment condition was psychological or behavioral in content, (c) the study design was a randomized controlled trial, a nonrandomized group design, a clinical case series or a single subject experimental design with a minimum of 10 subjects, and (d) the study included at least 1 of the following as dependent variables: sleep onset latency, number and/or duration of awakenings, total sleep time, sleep efciency, or sleep quality. Results: Psychological and behavioral therapies produced reliable changes in several sleep parameters of individuals with either primary insomnia
or insomnia associated with medical and psychiatric disorders. Nine studies documented the benets of insomnia treatment in older adults or for facilitating discontinuation of medication among chronic hypnotic users. Sleep improvements achieved with treatment were well sustained over time; however, with the exception of reduced psychological symptoms/ distress, there was limited evidence that improved sleep led to clinically meaningful changes in other indices of morbidity (e.g., daytime fatigue). Five treatments met criteria for empirically-supported psychological treatments for insomnia: Stimulus control therapy, relaxation, paradoxical intention, sleep restriction, and cognitive-behavior therapy. Discussion: These updated ndings provide additional evidence in support of the original reviews conclusions as to the efcacy and generalizability of psychological and behavioral therapies for persistent insomnia. Nonetheless, further research is needed to develop therapies that would optimize outcomes and reduce morbidity, as would studies of treatment mechanisms, mediators, and moderators of outcomes. Effectiveness studies are also needed to validate those therapies when implemented in clinical settings (primary care), by non-sleep specialists. There is also a need to disseminate more effectively the available evidence in support of psychological and behavioral interventions to health-care practitioners working on the front line. Keywords: Insomnia, treatment, behavioral, psychological, non pharmacological Citation: Morin CM; Bootzin RR; Buysse DJ et al. Psychological and behavioral treatment of insomnia: update of the recent evidence (19982004). SLEEP 2006;29(11):1398-1414.
1.0 INTRODUCTION INSOMNIA IS A PREVALENT COMPLAINT BOTH IN THE GENERAL POPULATION AND IN CLINICAL PRACTICE. IT MAY PRESENT AS THE PRIMARY COMPLAINT or in assoDisclosure Statement This was not an industry supported study. Dr. Morin has received research support from Sano-Aventis; has provided consulting services to Sepracor, Pzer, Neurocrine, Takeda, and Shire Biochem; and has participated in speaking engagements supported by Takeda, Sano-Aventis, and Merck. Dr. Buysse is a consultant for Actelion, Cephalon, Eli Lilly, GlaxoSmithKline, Merck, Neurocrine, Pzer, Respironics, Sano-Aventis, Servier, Sepracor, and Takeda. Dr. Edinger has received research support from Respironics; and has received fees for manuscript preparation from Sepracor. Dr. Lichstein is a consultant for Lilly and Takeda; has received research support from Respironics; and has participated in a speaking engagement supported by Sano-Aventis. Drs. Bootzin and Espie have indicated no nancial conicts of interest. Submitted for publication April 20, 2006 Accepted for publication April 30, 2006 Address correspondence to: Charles M. Morin, Ph.D., Universit Laval, cole de Psychologie, Pavillon F.A.S., Qubec, Qubec, Canada, G1K 7P4; Email: [email protected]
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ciation with another physical or mental-health problem. Prevalence estimates indicate that about one third of the adult population reports insomnia symptoms, 9%-12% experience additional daytime consequences, and approximately 6% meet formal criteria for an insomnia diagnosis.1 Insomnia is more common among women, middle-aged and older adults, shift workers, and patients with medical or psychiatric disorders. Persistent insomnia can produce an important burden for the individual and for society, as evidenced by reduced quality of life, impaired daytime functioning and increased absenteeism at work, and higher health-care costs. Persistent insomnia is also associated with increased risks of depression and chronic use of hypnotics.2-5 The diagnosis of insomnia is based on a subjective complaint of difficulties falling or staying asleep, or nonrestorative sleep, that is associated with marked distress or significant daytime impairments.6,7 Several indicators are useful to quantify the severity and clinical significance of insomnia. These markers may include the intensity (e.g., time to fall asleep, duration of awakenings, total sleep time), frequency, and duration of sleep difficulties. In the case of duration, a distinction is made between adjustment insomnia, a condition lasting a few days or weeks and often associated with stressful life events or changes in schedules and environment, and persistent insomnia, a condition lasting more than 1
Psychological And Behavioral Treatment Of InsomniaMorin et al
Table 1Psychological and Behavioral Treatments for Insomnia Therapy Stimulus control therapy Description A set of instructions designed to reassociate the bed/ bedroom with sleep and to re-establish a consistent sleep-wake schedule: (1) Go to bed only when sleepy; (2) get out of bed when unable to sleep; (3) use the bed/bedroom for sleep only (no reading, watching TV, etc); (4) arise at the same time every morning; (5) no napping. Sleep A method designed to curtail time in bed to the restriction actual amount of sleep time. For example, if a patient therapy reports sleeping an average of 6 hours per night, out of 8 hours spend in bed, the initial recommended sleep window (from lights out to nal arising time) would be restricted to 6 hours. Periodic adjustments to this sleep window are made contingent upon sleep efciency, until an optimal sleep duration is reached. Relaxation Clinical procedures aimed at reducing somatic training tension (e.g., progressive muscle relaxation, autogenic training) or intrusive thoughts at bedtime (e.g., imagery training, meditation) interfering with sleep. Cognitive Psychological methods aimed at challenging and therapy changing misconceptions about sleep and faulty beliefs about insomnia and its perceived daytime consequences. Other cognitive procedures may include paradoxical intention or methods aimed at reducing or preventing excessive monitoring of and worrying about insomnia and its correlates/consequences. Sleep hygiene General guidelines about health practices (e.g., diet, education exercise, substance use) and environmental factors (e.g., light, noise, temperature) that may promote or interfere with sleep. This may also include some basic information about normal sleep and changes in sleep patterns with aging. CognitiveA combination of any of the above behavioral (e.g., behavior stimulus control, sleep restriction, relaxation) and therapy cognitive procedures.
2.0 PURPOSE The objective of this paper is to provide an update of the evidence regarding the efficacy, effectiveness, durability, and generalizability of psychological and behavioral interventions for persistent insomnia. The evidence is reviewed for the treatment of both primary insomnia and insomnia associated with other medical, psychiatric, or substance abuse disorders. As with the initial review paper12 this updated review was commissioned by the Standards of Practice Committee of the American Academy of Sleep Medicine. 3.0 METHODS 3.1 Search Methods, Keywords, and Databases Treatment studies selected for review in this paper were identified through PsycInfo and Medline searches for research conducted from 1998 through 2004 inclusively. The following key words were used: nonpharmacologic, behavior therapy, cognitive therapy, psychotherapy, alternative medicine, stimulus control, progressive relaxation therapy or progressive muscle relaxation, paradoxical techniques or paradoxical intention, behavior modification, cognitive behavior therapy, psychological therapy, treatment, intervention, behavioral intervention, treatment, cognitive treatment, alternative treatment, therapy, biofeedback, sleep restriction, sleep deprivation, complementary therapies, mind-body and relaxation techniques, aromatherapy, biofeedback, hypnosis, imagery, or meditation, relaxation, relaxation techniques, yoga, massage. These terms were combined with sleep disorders or sleep initiation and maintenance disorders, or insomnia, or dyssomnia. The search was limited to humans, adults (18 and older), English or French language. 3.2 Selection Criteria of Treatment Studies The initial PsycInfo and Medline searches yielded a total of 312 titles of potential interest; an additional 34 titles were identified by members of the task force through their own reading of the literature, for a total of 346 titles of potential interest. Of these, 102 abstracts were read by the task force chair for initial screening and 53 articles were selected for full review by 2 independent members of the task force. Only peer-reviewed published articles were retained at this phase. Each rater used a standard extraction sheet to summarize information about the study including experimental design, sample (number of participants, age, gender), diagnosis, type of treatments and controls, primary and secondary outcome measures, and main findings. Data extraction was completed independently and discrepancies between 2 members of a pair of raters were resolved through discussion with the chair and other members of the task force. The criteria for inclusion of a study were: (a) the main sleep diagnosis was insomnia (primary or comorbid), (b) at least 1 treatment condition was psychological or behavioral in content, (c) the study design was a randomized controlled trial, a nonrandomized group design, a clinical case series or a single subject experimental design with a minimum of 10 subjects, (d) the dependent measure included 1 or more of the following variables (as measured by daily sleep diaries, polysomnography (PSG), or actigraphy): Sleep onset latency (SOL), number of awakenings (NA), time awake after sleep onset (WASO), total sleep time (TST), sleep efficiency (SE), or sleep quality
1399 Psychological And Behavioral Treatment Of InsomniaMorin et al
month and often several years. Insomnia complaints are typically associated with reports of daytime fatigue, problems with memory and concentration, and mood disturbances, impairments that may be the primary concerns prompting patients to seek treatment. Insomnia can be a symptom of several other conditions including medical, psychiatric, substance abuse or another sleep disorder; or, it can be a disorder in itself as in primary insomnia.6-8 There are several treatment options available for insomnia, including psychological/ behavioral approaches, various classes of medications, and a host of complementary and alternative therapies (e.g., herbal/dietary supplement, acupuncture). The present paper focuses on psychological and behavioral approaches to treating insomnia. These procedures have received increasing research attention in the past 2 decades, and were noted as effective therapies at a recent National Institutes of Health State-of-theScience Conference9on the manifestations and management of chronic insomnia. These methods include stimulus control therapy, sleep restriction, relaxation-based interventions, paradoxical intention, cognitive therapy, and combined cognitive-behavioral therapy. A brief summary of the nature of these interventions is presented in Table 1; more extensive descriptions are available in other sources.10,11
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(SQ). Studies using global measures of treatment outcome were included if those measures had been validated. Studies of circadian disorders (e.g., phase delay or phase advance syndromes) and those using other nonpharmacological therapies (e.g., light therapy, electro-sleep therapy) or complementary and alternative therapies (e.g., acupuncture) were excluded from this review. The majority of the initial 346 titles of potential interest were excluded either because they were not treatment studies for insomnia or because the main intervention was pharmacological. Of the 53 full articles reviewed and rated, 16 were rejected. The main reasons for article rejection were: no documentation of an insomnia diagnosis, sample size smaller than 10, results were secondary analyses of other databases (e.g., predictors of treatment response) and used global and non-validated measures of outcome. A list of excluded studies with reasons for exclusion is provided in an, Appendix A. The 37 studies that met inclusion criteria are listed in Table 2. For each study, we report the study design and the evidence level (using the Sackett System, 1993), the sample size (enrolled/completed), age, gender, insomnia diagnosis (primary or secondary), types of treatment and control conditions, therapy dosage, format, setting, therapist training, treatment duration and longest follow-up, primary and secondary outcome measures, and summary of main findings. Although some studies not meeting inclusion criteria are discussed in the text they are not included in the evidence table. Based on the Sackett sytem,13 the criteria for grading evidence level of each study were: Randomized well-designed trials with low alpha and beta error (Grade I), randomized trials with high alpha and beta error (Grade II), nonrandomized concurrently controlled studies (Grade III), nonrandomized historically controlled studies (Grade IV), case series (Grade V). 4.0 RESULTS 4.1 Descriptive Features of the Studies and Samples Table 2 summarizes the main features of the 37 studies selected for this review paper. The number of studies meeting Sackett System standards for grading evidence levels13 was as follows: 11 studies were graded I, 13 studies graded II, 2 studies graded III, 5 studies graded IV, and 6 studies graded V. A total of 2246 patients with insomnia were enrolled in the 37 studies and approximately 2029 of those completed treatment, for an attrition rate of less than 10% overall. With a few exceptions (studies of Veterans, substance abusers, internet-based treatment), there was a larger representation of women than men enrolled in most studies, with a typical ratio of 2:1, which is representative of insomnia prevalence estimates.1 Nine of the 37 studies focused specifically on older adults (average age > 60 years old). The main sleep diagnoses of patients enrolled in the studies were primary or psychophysiological insomnia (28 studies), insomnia associated with medical (4 studies) or psychiatric disorders (3 studies) or a mix of both conditions (6 studies), and hypnotic-dependent insomnia (5 studies). Eight studies examined treatment efficacy in patients with different subgroups of insomnia diagnoses, leading to a total number of studies greater than 37 studies. The majority of reviewed studies (n = 33) relied on prospective daily sleep diaries to document treatment outcome. Participants
were typically required to complete a daily diary for a minimum of a 1 or 2 week baseline period, for the duration of treatment, and for an additional 1 or 2 week period at post treatment and follow-ups. We retained 3 studies using the Pittsburgh Sleep Quality Index (PSQI) as the primary outcome.14-16 A few studies have also included polysomnography (n = 7)17-23and actigraphy (n = 6)18,19,24-27 to complement subjective reports from daily sleep diaries. Those studies are identified in Table 2 and in the appropriate subsections of the results. Primary dependent variables derived from these assessment methods were sleep onset latency (SOL), wake time after sleep onset (WASO), total sleep time (TST), sleep efficiency (SE), and sleep quality (SQ). Secondary outcomes included measures of insomnia severity (Insomnia Severity Index; ISI,28 sleep quality (PSQI),29 psychological symptoms (Beck Depression Inventory, BDI,30 State-Trait Anxiety Inventory STAI31, and fatigue (Multidimensional Fatigue Inventory, MFI32). The following sections summarize the evidence regarding the efficacy of treatment for primary insomnia, the generalizability of the evidence to different forms of insomnia (primary, secondary, hypnotic-dependent), insomnia in older adults, and the clinical significance and durability of sleep improvements over time. Comparative findings of single and multifaceted therapies and of different treatment implementation models are also summarized. 4.2 Treatment of Primary Insomnia Seventeen studies evaluated the effects of treatment for primary insomnia (see Table 2). Five of those studies were randomized clinical trials (RCT; with grade I,17,20,21,33,34 4 of which used CBT as the main intervention. In a comparative study of CBT (without relaxation), relaxation, and a psychological placebo (i.e., quasidesensitization) with a sample of 75 primary insomniacs,17 CBT produced greater improvements on the main diary and PSG-defined sleep measures (e.g., SE, WASO) relative to relaxation and control. More CBT patients (64%) achieved clinically significant outcomes compared to relaxation (12%) and placebo (8%). In an effectiveness trial33 conducted in primary care that evaluated CBT against a wait-list control group, active treatment was found superior to the control condition on most primary and secondary outcome measures. SOL was reduced from 61 to 28 min following active treatment compared to a change from 74 to 70 min for the control condition.a Smaller improvements were noted on WASO. There was no significant change on TST during treatment, but an increase of about one-half hour over baseline was obtained at follow up. Of those patients using hypnotic medications at baseline, 76% were medication-free at the end of treatment and 80% at the 12-month follow up. In a comparative study21 of CBT, medication (temazepam), and combined CBT plus medication, all 3 active treatments improved more than pill placebo on the main outcomes of WASO and SE, with a trend for the combined intervention to yield the greatest benefits. PSG data produced similar outcomes, although of smaller magnitude, but only the combined condition was significantly superior to placebo on the main outcome variables. According to PSG, more patients in the CBT (56%) and combined (68%) conditions achieved clinically significant changes (i.e., SE > 85%) relative to medication alone (47%) or placebo groups (22%). In another clinical trial of primary insomnia in older adults,20 sleep restriction and relaxation were more effective than placebo on sleep diary variables but not on PSG measures. Sleep restriction produced the best outcome
1400 Psychological And Behavioral Treatment Of InsomniaMorin et al
Unless otherwise stated, reported outcomes are based on daily sleep diaries.
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Davidson et al. (2001);42 8 wk; No FU
14/11; 91%; 54.7; Insomnia associated Non RCT; IV with a medical condition (cancer) Multi-component (SC, Rel, SHE) Sleep diaries; ISI, Hospital Anxiety and Depression Scale; QoL
Signicant improvements in SOL (42 to 6 min), NA (1.7 to 1.0), WASO (42 to 11 min), SE (73 to 89%), TST (376 to 411 min), sleep quality and impairments ratings. All patients (n = 9) with baseline SOL or WASO > 30 min and SE < 85% no longer met these criteria after treatment. Signicant improvements on QoL for role functioning and fatigue. No signicant improvement on SOL or WASO, but signicant reductions of ISI scores.
SLEEP, Vol. 29, No. 11, 2006 Multicomponent (SH+SC+SR+ Rel ) 10 wk; No FU Sleep diaries; ISI CBT; Rel; Placebo (psychological) 6 wk; 6 mo Sleep diaries; PSG; BDI, Insomnia Symptom Questionnaire, Selfefcacy Scale CBT produced greater improvements on most sleep measures, with higher PSG and diary SE (86% and 84% respectively) and lower diary WASO (28 min) than relaxation (PSG SE: 78%, diary SE: 78%; WASO: 44 min), and placebo ( PSG SE: 76%, diary SE: 76%, diary WASO: 47 min). More CBT patients (64%) achieved clinically signicant outcomes compared to relaxation (12%) and placebo (8%). Greater improvements of self-efcacy in CBT and larger reductions of depressive symptoms in relaxation relative to placebo. Multi-component (SC, SR, SHE); Control (SHE only) 2 wk; 3 mo Sleep diaries; Insomnia Symptoms QuestionnaireSelfefcacy Scale, DBAS Signicantly greater reductions in WASO (97 to 54 min) and SOL (39 to 31 min), and greater increases in SE (71 to 80%) and sleep quality in CBT patients relative to sleep hygiene education controls. These results were maintained at FU. Larger FU changes in CBT patients relative to controls on measures of restedness, insomnia symptoms, control over sleep and sleep-related cognitions. 6 wk; 12 mo SOL reduced from 61 to 28 min following CBT compared to 74 to 70 min for controls; results maintained at FU. Mean Sleep diaries; PSQI, BDI, reduction of WASO from 78 to 47 min at posttreatment and STAI, Penn State Worry partially maintained (53 min.) at FU. No change in TST during Questionnaire treatment, but increase of 30 min at FU. Of the 74 patients using medications, 56 had discontinued hypnotic usage at posttreatment and 50 were still medication free at FU. SR + SHE; SR (with optional nap) + SHE; SHE 4 wk; 3 mo Sleep diaries: Higher SE and reduced time in bed for the two sleep restriction conditions at posttreatment. Slower but comparable improvement for the sleep hygiene only condition at FU. Actigraphy: reductions of TST at posttreatment Sleep diaries; PSG; and return towards baseline at follow-up for the two sleep Actigraphy; MSLT, Stanford Sleepiness Scale restriction conditions. No group differences on any actigraphy measure. PSG (n=16) data not formally analyzed but descriptive data suggest similar pattern of results as those observed on actigraphy. CBT; Control (SHE); Sleep disordered breathing (SDB) treatment (Nasal CPAP or ENT nasal treatment) 6 mo; no FU PSG-dened SOL reduced by 12 min in CBT groups (with or w/o sleep-disordered breathing). WASO was reduced PSG; Actigraphy; Visual in all groups. TST signicantly increased in CBT group (without sleep-disordered breathing). No signicant change in Analogue Scales (sleep quality, daytime fatigue); actigraphy-dened measures of SOL and WASO, but all groups Epworth Sleepiness Scale improved quantity and quality of sleep at FU. No change on measure of sleepiness; fatigue ratings decreased for the sleep disordered breathing group.
Dopke et al. (2004);45
11/10; 60%; 45.6; NonRCT; IV Insomnia associated with psychological disorders
Edinger et al. (2001);17
RCT; I
75/70; 46.7%; 55.3; Persistent primary insomnia
Edinger & Sampson (2003);35
RCT; II
20/19;10%;51.0; Primary insomnia
1401
Espie et al. (2001);33
RCT; I
161/138; 68%; 51.4; Persistent sleep-onset CBT (with Rel); and/maintenance insomnia Wait list control (probable mix of primary and secondary insomnia)
Friedman et al. (2000);18
RCT; II
39/35; 69%; 64.2; Psychophysiologic (n =28), inadequate sleep hygiene (n=9), insufcient sleep (n= 2)
Guilleminault et al. (2002);19
RCT; II
130/126; 100%; 62.4; Chronic insomnia
Davidson et al. (2001);42 8 wk; No FU
14/11; 91%; 54.7; Insomnia associated Non RCT; IV with a medical condition (cancer) Multi-component (SC, Rel, SHE) Sleep diaries; ISI, Hospital Anxiety and Depression Scale; QoL
Signicant improvements in SOL (42 to 6 min), NA (1.7 to 1.0), WASO (42 to 11 min), SE (73 to 89%), TST (376 to 411 min), sleep quality and impairments ratings. All patients (n = 9) with baseline SOL or WASO > 30 min and SE < 85% no longer met these criteria after treatment. Signicant improvements on QoL for role functioning and fatigue. No signicant improvement on SOL or WASO, but signicant reductions of ISI scores.
SLEEP, Vol. 29, No. 11, 2006 Multicomponent (SH+SC+SR+ Rel ) 10 wk; No FU Sleep diaries; ISI CBT; Rel; Placebo (psychological) 6 wk; 6 mo Sleep diaries; PSG; BDI, Insomnia Symptom Questionnaire, Selfefcacy Scale CBT produced greater improvements on most sleep measures, with higher PSG and diary SE (86% and 84% respectively) and lower diary WASO (28 min) than relaxation (PSG SE: 78%, diary SE: 78%; WASO: 44 min), and placebo ( PSG SE: 76%, diary SE: 76%, diary WASO: 47 min). More CBT patients (64%) achieved clinically signicant outcomes compared to relaxation (12%) and placebo (8%). Greater improvements of self-efcacy in CBT and larger reductions of depressive symptoms in relaxation relative to placebo. Multi-component (SC, SR, SHE); Control (SHE only) 2 wk; 3 mo Sleep diaries; Insomnia Symptoms QuestionnaireSelfefcacy Scale, DBAS Signicantly greater reductions in WASO (97 to 54 min) and SOL (39 to 31 min), and greater increases in SE (71 to 80%) and sleep quality in CBT patients relative to sleep hygiene education controls. These results were maintained at FU. Larger FU changes in CBT patients relative to controls on measures of restedness, insomnia symptoms, control over sleep and sleep-related cognitions. 6 wk; 12 mo SOL reduced from 61 to 28 min following CBT compared to 74 to 70 min for controls; results maintained at FU. Mean Sleep diaries; PSQI, BDI, reduction of WASO from 78 to 47 min at posttreatment and STAI, Penn State Worry partially maintained (53 min.) at FU. No change in TST during Questionnaire treatment, but increase of 30 min at FU. Of the 74 patients using medications, 56 had discontinued hypnotic usage at posttreatment and 50 were still medication free at FU. SR + SHE; SR (with optional nap) + SHE; SHE 4 wk; 3 mo Sleep diaries: Higher SE and reduced time in bed for the two sleep restriction conditions at posttreatment. Slower but comparable improvement for the sleep hygiene only condition at FU. Actigraphy: reductions of TST at posttreatment Sleep diaries; PSG; and return towards baseline at follow-up for the two sleep Actigraphy; MSLT, Stanford Sleepiness Scale restriction conditions. No group differences on any actigraphy measure. PSG (n=16) data not formally analyzed but descriptive data suggest similar pattern of results as those observed on actigraphy. CBT; Control (SHE); Sleep disordered breathing (SDB) treatment (Nasal CPAP or ENT nasal treatment) 6 mo; no FU PSG-dened SOL reduced by 12 min in CBT groups (with or w/o sleep-disordered breathing). WASO was reduced PSG; Actigraphy; Visual in all groups. TST signicantly increased in CBT group (without sleep-disordered breathing). No signicant change in Analogue Scales (sleep quality, daytime fatigue); actigraphy-dened measures of SOL and WASO, but all groups Epworth Sleepiness Scale improved quantity and quality of sleep at FU. No change on measure of sleepiness; fatigue ratings decreased for the sleep disordered breathing group.
Dopke et al. (2004);45
11/10; 60%; 45.6; NonRCT; IV Insomnia associated with psychological disorders
Edinger et al. (2001);17
RCT; I
75/70; 46.7%; 55.3; Persistent primary insomnia
Edinger & Sampson (2003);35
RCT; II
20/19;10%;51.0; Primary insomnia
1402
Espie et al. (2001);33
RCT; I
161/138; 68%; 51.4; Persistent sleep-onset CBT (with Rel); and/maintenance insomnia Wait list control (probable mix of primary and secondary insomnia)
Friedman et al. (2000);18
RCT; II
39/35; 69%; 64.2; Psychophysiologic (n =28), inadequate sleep hygiene (n=9), insufcient sleep (n= 2)
Guilleminault et al. (2002);19
RCT; II
130/126; 100%; 62.4; Chronic insomnia
SLEEP, Vol. 29, No. 11, 2006 CBT (with Rel) 10 wk; 1 mo Sleep diaries CBT produced signicant improvements in most sleep parameters. For patients with sleep onset insomnia, SOL was reduced from 69.4 to 32.9 min and SE increased from 59.3% to 75.6%; for those with sleep-maintenance insomnia, WASO was decreased from 65 to 41.5 min, SE increased from 62.1% to 75.9%, and TST increased from 298 to 333 min. CBT (with Rel); SHE + zolpidem; CBT + zolpidem; Pill placebo 8 wk; 12 mo Sleep diaries; BDI, Prole of Moods State scale SE increased by 14% and SOL decreased by 34 min in CBT group. TST increased in all 4 groups, with largest gain (78 min) in the medication only group. No differences on mood measures. Gains maintained at 12-month FU for CBT and CBT + zolpidem conditions. No information for medication only groups. More CBT patients achieved clinically signicant changes on SOL and SE measures. Rel with medication withdrawal; Medication withdrawal alone; Rel alone; No treatment 6 wk; 2 mo Sleep diaries; Epworth Sleepiness Scale, BDI, STAI. Relaxation increased SE in both medicated (from 75.7% to 79.6%) and nonmedicated insomniacs (from 67.0% to 78.8%). Worsening of all other sleep measures during medication withdrawal; relaxation did not attenuate this effect. Only medicated participants receiving relaxation reported improved sleep quality. Relaxation associated with fewer withdrawal symptoms than no relaxation. Medicated participants (with or without relaxation) reduced medication use by 78% at FU. Signicant reductions of anxiety and depressive symptoms but no change in sleepiness. Multicomponent (SC, Rel, SHE); Wait list control 4 wk; 3 mo Sleep diaries; STAI, Geriatric Depression Scale, Insomnia Impact Scale No difference in outcome between insomnia secondary to medical or psychiatric disorders. Greater improvements for treated patients relative to controls with WASO reductions from 87min (baseline) to 61 min (posttreatment) to 56 min (follow-up) and SE increases from 67% (baseline) to 78% (posttreatment) to 78% (follow-up). SOL reduced and TST increased in both conditions at post-treatment. 57% of treated patients achieved clinical improvement in SE compared with 19% of control patients. None of the secondary measures were signicant. Rel; SR; Placebo (psychological) 6 wk; 12 mo Sleep diaries; PSG; Epworth Sleepiness Scale, DBAS; Insomnia Impact Scale, Fatigue Severity Scale Sleep Restriction and Relaxation more effective than Placebo on sleep continuity variables at post and FU. WASO reduced from 67 min (baseline) to 43 (post) to 38 (FU) in Sleep Restriction, compared to 67 min (baseline), 43 (post), and 52 (FU) for Relaxation. No signicant gains in daytime functioning. Sleep restriction produced best outcomes at FU. No signicant change on PSG measures. All groups (including placebo) improved on the secondary variables. Rel; Wait list control 3 wk; 5 wk Sleep diaries; DBAS, Fatigue Severity and; Epworth Sleepiness Scales, Penn State Worry Questionnaire Relaxation produced more improvement than no treatment on diary measures of WASO, SE, sleep quality, but not SOL. The magnitude of improvement was small. For example, WASO for treated insomniacs went from 22 min (baseline) to 13 min (posttreatment) and SE went from 84.8% (baseline) to 88.4% (posttreatment). No group differences for daytime measures.
Hryshko-Mullen (2000);40
Case replication series; V
42/42; 52%; 53.6; Primary insomnia
Jacobs et al. (2004);34
RCT; I
Lichstein et al. (1999);50
NonRCT; III
40/40; 58%; 52; Psychophysiologic insomnia and Hypnotic dependent insomnia
1403
RCT; I
49/44; 48%; 68.6; Insomnia secondary to medical/ psychiatric conditions
RCT; I
89/72; 74%; 68.03; Psychophysiological insomnia
Means et al. (2000);37
RCT; I
NS/57;68.5%; 21.2 Primary insomnia
SLEEP, Vol. 29, No. 11, 2006 Self-help CBT with telephone contact; Self-help CBT only; Wait list control 6 wk; 3 mo Sleep diaries; PSQI, ISI, DBAS, BAI The addition of telephone consultations to a self-help treatment slightly enhanced outcome on TWT (- 82 min vs. - 62 min) and SE (+ 15% vs. + 11%) at posttreatment, but both treated groups were comparable at follow-up and remained more improved than controls. 59% (17/29) of treated patients had SE > 80% at follow up. Improvements were also obtained on secondary measures of PSQI, ISI, DBAS and BDI. Hypnotic use decreased in all three groups. CBT (with Rel) and medication withdrawal; No treatment control 3 mo; 6 mo PSQI (TST, SOL,SE, global score), SF-36, use of hypnotic medication, treatment costs CBT; Med (temazepam); Combined CBT+Med; Placebo 8 wk; 24 mo Sleep diaries; PSG; ISI All three treatments improved signicantly more than placebo, with a trend for the combined condition to yield greatest benets. CBT reduced diary measures of WASO from 50 to 22 min, Med 55 to 29 min and combined 57 to 21 min compared with 62 to 52 min for placebo. SE increased by 17% (CBT), 11% (PCT), 21% (CBT+Med), and 4% (Placebo). PSG data showed that all three treated groups spent less time awake after sleep-onset than placebo, but only the combined approach was superior to placebo. CBT patients best sustained sleep improvements over time, whereas Medication a lone group did not, and the combined condition showed more variable longterm outcomes. CBT; Medication taper; Combined CBT + medication taper Sleep diaries; PSG; 10 wk; 12 mo ISI, BAI, BDI, benzodiazepine use. All three groups reduced both the quantity (90%) and frequency (80%) of benzodiazepine use, but more participants receiving the combined intervention were drug-free at post treatment. Modest changes in sleep during initial withdrawal but participants receiving CBT, alone or combined with medication taper, reported greater sleep improvements relative to patients receiving medication taper alone. Improvements reported on secondary variables (ISI, BAI BDI) in all three groups, with gains maintained through FU. Rel + SHE; SC + SHE; Wait list control 4 wk; 6 mo Sleep diaries; ISI, rating of daytime alertness, use of hypnotic medication, life satisfaction SHE+SC reduced SOL from 87 to 56 min and WASO from 55 to 42 min. SHE+Rel reduced SOL from 71 to 51 min and WASO from 47 to 33 min. No signicant group differences between treatments. Effect sizes were of medium size and greater for sleep than daytime measures. Treatment effects maintained in both treatment groups. Controls showed no improvement on any variable.
Mimeault & Morin (1999);38
RCT; I
Morgan et al. (2003);15
RCT; I
209/123; 67.5%; 65.5; chronic insomnia and chronic use of hypnotics
CBT patients showed signicant improvements in PSQI scores (global, sleep latency, sleep efciency) and reductions of hypnotic use at 3- and 6-month follow-ups. Greater percentages of the CBT group (39%) than controls (11%) achieved low hypnotic (< 50% of baseline) or no hypnotic use at 6-month follow-up. Lower SF-36 vitality scale at the three month follow-up in CBT than in control group. Greater costs for CBT initially but evidence of longer term cost offsets due to reduction of sleep medication usage.
1404
Morin et al. (1999);12
RCT; I
Morin et al. (2004);22
RCT; I
76/69; 50%; 62.5; Hypnotic-dependent insomnia
Pallesen et al. (2003);49
NonRCT; III
66/55; 84%; 69.8; Primary and secondary insomnia
SLEEP, Vol. 29, No. 11, 2006 CBT 4-9 wk; NS Sleep diaries 61% completing adequate treatment trial showed signicant improvement, with averaged SOL reduction of 48 min (65%; effect size = 1.25), WASO reduction of 61 min (48%; effect size = 1.42), and TST increase of 34 min (13%; effect size = .41). CBT 4-9 wk; NS Sleep diaries Subjects completing a minimum adequate trial reduced their SOL (55 to 21 min: effect size = .85), WASO (83 to 28 min: effect size = 1.14), number of awakenings (effect size = .54), and increased TST (291 to 341 min: effect size = .54). Outcomes did not vary relative to medical or psychiatric morbidity. CBT + placebo drug; CBT+ modanil 100 mg; Contact control + modanil 100 mg 8 wk; No FU Sleep diaries; Epworth Sleepiness Scale SC + med withdrawal; SC alone; Med withdrawal alone; Wait list control 4-6 wk; 2 mo Sleep diaries; Use of hypnotic medication, Epworth Sleepiness Scale, BDI, STAI Signicant improvements on most sleep parameters over time among stimulus control subjects but not in controls. Lower daytime sleepiness in treated subjects relative to controls at post-treatment and follow-up. No signicant differences in outcomes between medicated an unmedicated patients. BDI and STAI showed no signicant changes over time. Med (estazolam) + relaxation; Med (estazolam) + imagery; Med (estazolam) + SHE 4 wk; 6 mo Sleep diaries; BDI, Pre-Sleep Arousal Scale, Sleep Efcacy Scale, Sleep Hygiene Practice and Knowledge Scale, Taylor Manifest Anxiety Scale All three groups showed signicant increase of TST (Med + Rel = + 65 min; Med + Imagery = + 40 min; Med + SHE = + 34 min). Only the relaxation and imagery groups showed signicant pre to post changes in WASO (- 17 min and - 33 min, respectively) and SE (+ 9.7%, + 7.4%). Signicant improvements in all groups at FU relative to baseline sleep. Signicant improvements across groups for the Pre-Sleep Arousal Scale, Sleep Efcacy Scale, and BDI (but not anxiety) from baseline to 6-month follow-up, but no group differences. CBT (with Rel); Rel; Wait list control 8 wk; 4 mo Sleep diaries, Actigraphy; PSQI, DBAS, GDS, BAI, SF-36, McGill Pain Questionnaire, Life satisfaction
Perlis et al. (2000);47
85/47; 64%; 43; Mix of primary insomnia and insomnia associated with medical or psychiatric disorders
89/28; 64%; 46.5; Mix of primary and secondary insomnia
RCT; II
30/27; 70%; 41.3; Psychophysiologic insomnia
Average SOL reduction of 17 min and WASO of 28 min among CBT patients. Trends suggesting lower Epworth Sleepiness Scale scores and higher adherence to prescribed bedtime during CBT among participants receiving modanil.
Riedel et al. (1998);51
RCT; II
1405
45/41; 54%; 56.6; Hypnotic-dependent insomnia, primary insomnia
Rosen et al. (2000); 55
RCT; II
Rybarczyk et al. (2002); 27
RCT; II
51/38; 58%; 67.8; Insomnia secondary to medical illness
CBT more effective than control at posttreatment and FU on measures of SE, WASO, PSQI, and DBAS. Relaxation produced greater change in TST than CBT at posttreatment, greater change than control in TST and PSQI at posttreatment, and greater change than control in SE, WASO, and PSQI at FU. More CBT than control patients achieved clinically signicant improvement at posttreatment and FU, and a higher proportion of Relaxation than controls had clinically signicant improvement at posttreatment. No group differences on actigraphy, medication use, or secondary outcomes.
SLEEP, Vol. 29, No. 11, 2006 CBT + Progressive muscle relaxation; CBT + Autogenic training Standard treatment 3-4 wk; 6 mo PSQI, Cancer Quality of Life Questionnaire Internet CBT (with Rel); 5 wk; 9 mo Wait list control Greater improvements observed on TWT (- 55 min), TST (+ 34 min), and SE (+ 10%) in treated relatie to controls. Greater Sleep diaries; reductions of hypnotic use and improvements of DBAS scores DBAS, Medication Index in CBT relative to controls. Improvements noted on other sleep measures in both treated and control conditions. Attrition rate of 24%. CBT (with Rel) and medication withdrawal 6 wk; NS Sleep diaries; Global improvement Signicant improvements on SOL (79 vs. 45 min), WASO (137 vs. 74 min), SE (56 vs. 71%). Overall treatment effect rated as good in 49%, reasonable in 37%, no change in 14%; no difference between hypnotic users and non-users. 37% of hypnotic users discontinued medication and 39% reduced their use. No difference between responders and non-responders on baseline measures of sleep, depression, or anxiety. Anxiety Management Training; Rel 9 wk; No FU Self-reported SOL signicantly decreased and sleep satisfaction improved signicantly. SOL measured by PSG; behavioral device improved signicantly for both treatments STAI, BDI, MMPI, Sleep (68 and 81 min at baseline vs. 43 and 46 min. at posttreatment). onset monitor, sleep No signicant effects for PSG measures of sleep continuity. satisfaction Secondary measures of depression and anxiety improved with treatment. CBT (with Rel) combined with hypnotic withdrawal and stress management 7 wk; No FU Sleep diaries;PSQI, DBAS, ISI, BDI Signicant improvements for SOL (46 vs. 26 min), TST (5.3 vs. 6.2 hrs.), SE (80 vs. 86%), but not for WASO. Signicant effect also found for PSQI, ISI, and DBAS. Better treatment compliance associated with better outcomes on DBAS, ISI, and PSQI but not with SOL, TST, SE. Rel; SR + SC; Med (urazepam); SHE 4 wk; No FU Sleep diaries Rel treatment had greater effect on sleep onset than SR/SC and SHE, whereas SR/SC had greater effect than Rel on sleep maintenance variables (WASO, NA). Medication produced largest changes in all sleep measures. CBT: Cognitivebehavior therapy; Rel: Relaxation; SR: Sleep restriction; SC: Stimulus control; SHE: sleep hygiene education; Med: Medication; PSG: Polysomnography; PSQI: Pittsurgh Sleep Quality Index; ISI: Insomnia Severity Index; DBAS: Dysfunctional SOL: Sleep onset latency; WASO: Wake time after sleep onset; Belief and Attitudes TST: Total sleep time; SE: Sleep efciency about Sleep Scale; BDI: Beck Depression Inventory; BAI: Beck Anxiety Inventory; STAI: State-Trait Anxiety Inventory
Simeit et al. (2004); 16
NS/229; 75%; 58; NonRCT; IV Insomnia secondary to cancer
Signicant improvement from baseline to FU on SOL, TST, SE for all groups; no group differences. On sleep quality, daytime energy, daytime dysfunction and most other quality of life measures, improvement occurred in all groups. Sleep medication use decreased among participants receiving CBT only.
Strom et al. (2004); 39
RCT; II
Verbeek et al. (1999); 48
127/86; 65%; 46; 54 psychophysiologic, 5 hypnotic dependent, 14 secondary (9 affective, 4 neurological, 1 medical)
Viens et al. (2003); 23
RCT; II
23/20; 70%; 36.0; Sleep onset insomnia
1406
Vincent & Hameed (2003);41
50; 66%; 51.4; Primary insomnia
Waters et al. (2003);52
RCT; II
Abbreviations
RCT: Randomized controlled trial
on sleep efficiency but there was no evidence of improvements on secondary measures of daytime functioning. In a study that focused specifically on sleep onset insomnia,34 CBT (with relaxation) decreased SOL by a mean of 34 min with a corresponding 14% increase of SE. Sleep improvements, which had limited impact on secondary mood measures, were well maintained at follow up. Several additional studies, including both controlled and uncontrolled studies, have documented treatment efficacy for insomnia in the context of primary care settings,14,35,36 in comparisons of different interventions23,37 or treatment implementation models,38,39 or as part of case series.40,41 Some of these studies will be discussed in later sections of this paper. 4.3 Treatment of Insomnia Associated with other Medical or Psychiatric Disorders Twelve investigations have evaluated the efficacy of psychological and behavioral treatments for insomnia associated with another medical or psychiatric disorder. These studies have focused, for example, on patients with chronic pain,25 cancer,16,42 alcohol dependence 26and older adults with various medical illnesses.27,43 Only 4 of those 12 studies were RCT (Grade I or II)25-27,43 and the remaining were nonrandomized studies or clinical replication series. In a study of 60 patients with insomnia associated with chronic pain,25 CBT was significantly more effective than control on measures of SOL, WASO, and SE, but not on number of awakenings and TST. SOL was reduced from 55 min to 28 min and SE increased from 72% to 85%. Nocturnal motor activity (as measured by actigraphy) was reduced in the treated group but not in the control group; there were no group differences on pain ratings, depressive symptoms, or medication use. In a study of 51 older adults with insomnia associated with medical illness,27 CBT and relaxation conditions were more effective than control on diary measures of WASO and SE, as well as on a measure of overall sleep quality (PSQI); the relaxation group had a greater increase in TST than CBT and controls. A higher proportion of treated patients relative to controls achieved clinically significant improvements. There were no differential group effects on actigraphy, medication use, or other secondary measures of anxiety, depression, and quality of life. In a study of 49 older adults with insomnia associated with medical and psychiatric conditions,43a combined intervention of stimulus control, relaxation, and education reduced WASO 25 min and increased SE 11% at post treatment. Fifty-seven percent (57%) of treated patients achieved clinically significant improvements on SE relative to 19% of control patients; there was no significant change on secondary measures of anxiety, depression, and impact of insomnia. Outcomes were similar for individuals with insomnia associated with a medical condition and those with insomnia related to a psychiatric disorder. A controlled study conducted with recovered alcoholics26 showed modest but significant improvements of SOL (- 18 min) and SE (+10%) among insomnia-treated patients. At the 6 month follow-up, 15% of treated participants had relapses with alcohol and this proportion was not different between treated and control patients. Several additional studies (clinical replication series or uncontrolled group studies) have also provided evidence showing that patients with medical and psychiatric disorders could also benefit from sleep/insomnia specific interventions. Two investigations
SLEEP, Vol. 29, No. 11, 2006 1407
with cancer patients16,42 showed that CBT was associated with improvements of sleep and of daytime functioning (e.g., fatigue, energy). One case series study of 67 patients with psychiatric disorders and insomnia44 reported significant improvements of sleep, mood, fatigue, and reduced use of sleep medication, while a smaller study45 found no change on specific sleep parameters (SOL and WASO) but reported significant reductions of global insomnia severity as measured by the ISI. Additional evidence supporting the efficacy of CBT was reported in 3 clinical replications series 46-48 conducted with heterogeneous samples of patients presenting to sleep disorders clinics with a variety of primary and secondary insomnia diagnoses. Although conclusions drawn from these uncontrolled studies should be treated with caution because of the studies high attrition rate, the evidence suggests that among those who received an adequate treatment exposure (average of 6 - 8 therapy sessions) outcomes were comparable to those patients with primary insomnia enrolled in controlled clinical trials. Furthermore, treatment response appeared comparable between patients with medical or psychiatric comorbidity and those with primary insomnia in one study. Baseline anxiety, depression, and insomnia severity did not differ among treatment responders and nonresponders.48 4.4 Treatment of Insomnia in Older Adults Nearly 25% (9 studies out of 37) of reviewed studies were conducted with older adults (average age > 60 years old). This is in sharp contrast to our previous review 12 that included only a handful of studies with older subjects. Three studies focused on older adults with primary insomnia,18,20,21 2 on insomnia associated with medical or psychiatric illnesses,27,43 1 included a mix of patients with primary and comorbid insomnia,49 2 evaluated the impact of psychological and behavioral interventions specifically in older adults who were chronic users of hypnotic medications,15,22 and 1 study19 examined the moderating role of upper airway resistance syndrome in the treatment of postmenopausal insomnia. With the exception of the study conducted by Pallesen et al,49 all these investigations were RCT. In a study of 89 older adults with primary insomnia,20 sleep restriction and relaxation were both more effective than a psychological placebo for reducing WASO; changes were identical (67 min to 43 min) for the 2 treatment groups at the end of the 6-week treatment phase, but sleep restriction produced the best outcome at the 1-year follow up. No significant changes were obtained on PSG measures. All 3 conditions, including placebo control, showed improvements on secondary measures of fatigue and a measure of insomnia impact. In another placebo-controlled study,21 76 older adults treated with CBT, medication (temazepam), or combined CBT + medication improved more than those receiving placebo on the main outcome measures of WASO and SE. PSG comparisons yielded improvements in the same direction, albeit of smaller magnitude, than those reported on sleep diaries. A greater proportion of patients treated with CBT, alone or combined with medication, achieved clinically significant improvements (i.e., SE > 85%) compared to those receiving medication alone or placebo. In a comparison of sleep restriction, with and without an optional daytime nap, to sleep education alone,18 both sleep restriction conditions produced greater SE increase, with reduced time spent in bed, relative to the control condition. There was no sigPsychological And Behavioral Treatment Of InsomniaMorin et al
nificant group difference on actigraphy or PSG measures; TST was reduced for the sleep restriction conditions at post treatment and returned towards baseline values at the 3-month follow-up. There was a mild increase of physiological sleepiness (as measured by the MSLT) but no change on subjective sleepiness. In another investigation,49 a combination of sleep education plus stimulus control was as effective as sleep education plus relaxation, and more effective than a wait-list control, in older adults with mixed primary and secondary insomnia; there were modest improvements of daytime measures for both active conditions. Two additional studies (reviewed in section 4.3) provided evidence that older adults with insomnia and comorbid medical disorders also benefitted from sleep-specific interventions.20,27 4.5 Treatment of Insomnia Among Chronic Hypnotic Users Four investigations examined the efficacy of psychological and behavioral interventions for insomnia in the context of chronic hypnotic usage, including 2 that were conducted with older adults.15,22 In a study of 209 chronic hypnotic users,15 CBT (with an optional medication taper) was associated with improved PSQI scores and reductions of hypnotic use at 3- and 6-month follow ups. A greater percentage of patients treated with CBT for insomnia (39%) relative to no treatment controls (11%) achieved at least a 50% reduction of hypnotic use relative to baseline at the 6-month follow up. A cost-offset analysis revealed that while CBT added to the initial treatment cost, there was a significant cost offset at follow up resulting from a reduction of sleep medication usage. In another study comparing a supervised medication withdrawal program, alone and combined with CBT for insomnia, to CBT alone,22 all 3 interventions produced significant reductions in both the quantity (90%) and the frequency (80%) of benzodiazepine use, and more patients in the combined approach (85%) were medication free at post-treatment than for those receiving the taper schedule alone (48%) or CBT alone (54%). There were modest changes in sleep patterns during the initial 10-week withdrawal phase, but CBT-treated patients reported greater sleep improvements relative to those receiving the medication withdrawal alone. Several improvements were also reported on secondary measures of insomnia severity (ISI), anxiety (BAI) and depressive (BDI) symptoms. Two additional studies have examined the impact of chronic hypnotic use on outcome with middle-aged adults. One study50 found a significant worsening of sleep parameters during medication withdrawal and the addition of relaxation therapy did not attenuate this effect. In a similar study using stimulus control as the main behavioral intervention,51 stimulus control produced significant improvements on most sleep parameters relative to no additional treatment. There was no difference in sleep outcomes between medicated and nonmedicated patients. 4.6 Validation and Comparative Efficacy of Single and Multifaceted Therapies Although there are several distinct psychological and behavioral therapies for insomnia, there was a clear trend/preference for investigators to combine 2 or more of these methods when treating insomnia. The most common combination involves an educational (sleep hygiene), behavioral (stimulus control, sleep restriction, relaxation), and a cognitive therapy component, usually referred to as cognitive-behavior therapy. Indeed, 21 studSLEEP, Vol. 29, No. 11, 2006 1408
ies have evaluated the efficacy of CBT, either with (12 studies) or without relaxation (9 studies), and 5 more studies have used a similar multi-component interventions but without cognitive therapy (see Table 2). There has been no complete dismantling of CBT to isolate the relative efficacy of each component within the same study. However, comparisons of some components revealed that CBT was superior to relaxation alone in 1 study of primary insomnia17 and sleep restriction was superior to relaxation at follow-up in another study with older adults.20 In another study,52 relaxation was more effective for sleep initiation problems relative to sleep hygiene education alone and a combination of stimulus control plus sleep restriction, whereas the latter combination had greater effects on sleep maintenance variables. Twelve studies have isolated in a controlled trial at least 1 therapy component such as relaxation, sleep restriction, stimulus control, or paradoxical intention. All 6 studies contrasting relaxation-based interventions (either progressive muscle relaxation or similar procedures) to a control condition, have reported that this single therapy was more effective than wait-list,27 placebo,17,20 no treatment,37,50 and minimal sleep hygiene education control.52 Two studies showed that sleep restriction was superior to either placebo20 or sleep hygiene education alone,18 1 study found that stimulus control was more effective than a wait-list control,51 and 1 additional investigation reported that paradoxical intention was superior to a wait-list control for sleep onset insomnia.24 In spite of the inclusion of a cognitive therapy component in numerous studies, no study has yet evaluated its unique contribution to outcomes. As in the earlier review paper,12 criteria developed by the American Psychological Association53 for defining empirically-validated psychological treatments, were used to determine whether additional evidence was available for each psychological and behavioral interventions (See Table 3). Based on the criteria outlined in our previous review,12 stimulus control therapy, relaxation training, and paradoxical intention met criteria for wellestablished psychological treatment for insomnia. With the additional evidence from the present review (indicated by studies in boldface in Table 3), sleep restriction18,20 and CBT17,21 would also meet criteria for well-established treatments. Furthermore, additional studies strengthened the level of evidence supporting stimulus control,51 relaxation,17,20,27,37 and paradoxical intention.24 4.7 Comparisons of Psychological/Behavioral Therapies and Medication Five controlled studies conducted with primary/psychophysiological insomnia patients have evaluated the impact of psychological/behavioral interventions in comparison to or as an adjunct to hypnotic medications. Two studies evaluated the efficacy of CBT, singly and combined with medication,21,34 1 used a medication alone condition as a comparator to psychological treatments,52 and 2 examined the incremental benefits of adding 1 treatment to the other.54,55 In a placebo-controlled comparison of CBT and medication (temazepam) singly and combined21 (study described in Sections 4.2 and 4.4), all 3 active treatments were more effective than placebo on sleep continuity variables, with a trend for the combined approach to yield better outcomes. These results were corroborated with PSG measures, although the magnitudes of sleep improvePsychological And Behavioral Treatment Of InsomniaMorin et al
Table 3Key Studies Supporting Efcacy Of Psychological And Behavioral Treatments Of Insomnia Study reference Evidence Espie et al. (1989)69 SC > Pla & Rel Lacks et al. (1983)70 SC > Pla Lacks et al. (1983)71 SC > Pla Morin & Azrin (1987;1988)72,73 SC > IT Turner & Asher (1979)74 SC > Pla Riedel et al. (1998)51 SC > WL Relaxation* Edinger et al. (2001)17a Rel > Pla Lichstein et al. ((2001)20b Rel > Pla Lick & Hefer (1977)75 Rel > Pla Nicassio et al. (1982)76 Rel > No treatment Turner & Asher (1979)74 Rel > Pla Woolfolk & McNulty (1983)77 Rel > WL Means et al. (2000)37 Rel > No treatment Rybarczyk et al. (2002)27c Rel > WL Paradoxical Espie et al. (1989)69 PI > Pla Intention* Turner & Ascher (1979)74 PI > Pla Broomeld et al. (2003)24 PI > WL Sleep restriction* Friedman et al. (1991)78 SR > Pla Friedman et al. (2000)18 SR + SHE > SHE Lichstein et al. (2001)20 b SR > Pla EMG Nicassio et al. (1982)76 BF > No treatment biofeedback Sanavio et al. (1990)79 BF > WL VanderPlate & Eno (1983)80 BF > WL Freedman & Papsdorf (1976)81 BF > Pla CBT* Edinger et al. (2001)17a CBT > Rel > Pla Mimeault & Morin (1999)38 CBT > WL Morin et al. (1993)82 CBT > WL Morin et al. (1999)21 CBT > Pla Morin et al. (2004)22 CBT > Medication taper Perlis et al. (2004)54 CBT > Contact control CBT (with Rel)* Currie et al. (2000)25 CBT > WL Currie et al. (2004)26 CBT > WL Espie et al. (2001)33 CBT > WL Jacobs et al. (2004)34 CBT > Pla Morgan et al. (2003)15 CBT > No treatment Rybarczyk et al. (2002)27c CBT > WL MultiEdinger & Sampson (2003)35 MC > SHE component Lichstein et al. (2000)43 MC > WL Waters et al. (2003)52 MC > SHE Note: Citations in boldface are for studies published between 1998 and 2004; all other studies were published prior to this period. BF = EMG Biofeedback; CBT = Cognitive Behavior Therapy; IT = Imagery Training; PI = Paradoxical Intention; Pla = Placebo; Rel = Relaxation; SC = Stimulus Control; SR = Sleep Restriction; SHE = Sleep Hygiene Education; WL = Wait-List Control; MC=Multicomponent. a,b,c These studies provided evidence supporting more than 1 treatment. *Well established treatments according to APA criteria for empirically supported treatments. Criteria for well-established treatments require at least 2 between-group design studies demonstrating efcacy in 1 or more of the following ways: I. superior to pill or psychological placebo or to another treatment; or equivalent to an already established treatment in a study with adequate statistical power; II. a large series of single case design experiments (n > 9) demonstrating efcacy as in I; III. the studies must be conducted with treatment manuals; IV. the characteristics of the sample must be well-described; V. the effects must have been demonstrated by at least 2 different investigators or investigatory teams. Probably efcacious treatments according to APA criteria for empirically supported treatments. Criteria for probably efcacious treatments are: I. 2 studies showing the treatment is more effective than a waiting-list control group, or II. 1 or more studies meeting the wellestablished treatment criteria I, III, and IV, but not V, or III. a small series of single case design studies (n > 3) otherwise meeting wellestablished treatment criteria II, III, and IV. SLEEP, Vol. 29, No. 11, 2006 1409 Treatment Stimulus control*
ments were smaller on PSG than on diary measures. Long-term follow-up data showed that subjects treated with CBT sustained their clinical gains over time, whereas those treated with medication alone did not. The combined approach showed some loss of therapeutic benefits over the follow-up periods, although there was more variability across subjects in that condition. In a similar study design with 63 young and middle-aged adults with sleep onset insomnia34 (study described in Section 4.2), CBT was shown more effective than medication (zolpidem) and placebo on measures of SOL and SE. All 4 conditions, including placebo, increased their TST, with medication yielding the largest increase in TST (69 min), though this finding was not significantly different from the other groups. There was no significant difference between CBT alone and CBT combined with medication. Sleep changes were well maintained at the 12-month follow up for patients treated with CBT, singly or combined with medication, but no follow up data was available for those treated with medication alone. Data obtained from a Nightcap device showed sleep changes in the same direction as those from diaries, except that no improvement was obtained on any of the measures for the placebo condition. An investigation of 41 patients treated with estazolam examined the added benefits of muscle relaxation, imagery training, and sleep hygiene education to medication.55 There was no group difference on any outcome. Significant improvements from baseline to post treatment were obtained on WASO and SE for the relaxation (-17 min and + 9.7% respectively) and imagery training groups (- 33 min and + 7.4%). TST was increased by 34 min (education), 40 min (imagery), and 65 min (muscle relaxation) for the same period but there was no significant group difference. SOL was not changed in any of the groups. Significant changes were obtained from baseline to follow up in all 3 groups on sleep measures and on secondary measures of arousal, self-efficacy, and depressive (but not anxiety) symptoms. Another study of 30 patients54 examined the added benefits of modafinil when combined with CBT in the management of primary insomnia. Although there was no significant gain from modafinil in terms of sleep continuity parameters, there were trends suggesting that the addition of modafinil to CBT reduced daytime sleepiness and enhanced compliance with prescribed bedtime. Finally, data from 53 patients with primary insomnia52 showed that while relaxation was more effective for sleep onset problems and a combination of stimulus control plus sleep restriction had more benefits for sleep maintenance variables, medication (flurazepam) produced the largest improvements on all sleep variables during the initial 2-week intervention. 4.8 Treatment Implementation Methods: Individual, Group, and Self-Help Treatment was implemented on an individual basis in 22 studies (54%), in a group format in 11 studies (29.7%), and a few additional studies relied on self-help materials with or without additional telephone consultations. An average of 5.7 consultation visits was conducted over a mean treatment period of 6.5 weeks. 1 study directly compared the relative efficacy of CBT implemented in group or individual sessions, or through self-help written materials combined with brief telephone consultations.56 All 3 groups produced significant improvements of sleep and secondary measures and there was no between group difference on any
measure. A similar study of insomnia in recovered alcoholics also found equivalent outcome between individual CBT and self-help CBT plus telephone consultation.26 In contrast, 1 study38 found that the addition of telephone consultation to self-help written material enhanced outcomes at post treatment, but those initial gains tended to disappear at follow up. An internet-based intervention produced greater improvement in several sleep parameters relative to controls,39 but the attrition rate (24%) was higher than in studies using face-to-face consultation visits. While the majority of reviewed studies have used psychologists or psychology trainees as therapist (with treatment manual), 2 studies examined treatment efficacy as implemented by primary care physicians36 or by nurse practitioners33 who had also been trained before the studies; treatment benefits were generally equivalent to those obtained with therapists who had mental-health training. 4.9 Durability of Sleep Improvements Twenty-six of the 37 reviewed studies reported follow up data of at least 1 month duration after completing treatment (mean duration = 7.7 months; range 1-36 months). The remaining 11 studies reported no follow-up data. As was the case in the initial review, a very robust finding across studies is that treatmentproduced changes in sleep parameters are well maintained at short (1-3 month), intermediate (6-month), and long-term (> 12 months) follow-ups. One interesting finding from studies using sleep restriction is that total sleep time may be reduced during the initial intervention, but it is significantly increased at follow up evaluation.20 Despite fairly robust long-term outcomes, follow-up data must be interpreted cautiously as there are relatively few studies reporting long-term (> 1 year) follow-ups (see Table 2) and, among those that do, attrition rates increase substantially over time. 5.0 CONCLUSIONS This updated review of treatment studies conducted between 1998 and 2004 provides additional evidence that psychological and behavioral interventions represent an effective treatment option for the management of persistent insomnia. In addition to studies further documenting treatment efficacy for primary insomnia, recent studies indicate that treatment is also effective for insomnia associated with some medical conditions and, to a lesser extent, with psychiatric conditions. Treatment benefits are well sustained over time. There is still limited evidence of clinically meaningful changes beyond reductions of insomnia symptoms (i.e., improved daytime functioning, quality of life). These findings are consistent with our previous systematic review12 as well as with other meta-analyses of the efficacy of psychological and behavioral interventions for insomnia.57-59 For instance, of the 17 most recent treatment studies of primary insomnia, 5 were randomized controlled trials,17,20,21,33,34 and all 5 yielded additional evidence of significant sleep improvements with psychological and behavioral interventions. Although most of this additional evidence is based on daily sleep diaries, 3 of the 5 key studies included PSG measures and 2 of them reported outcomes that paralleled findings from diary measures. Actigraphy, on the other hand, was not very sensitive for detecting changes in sleep/wake variables in the few studies using this device. The treatment of comorbid insomnia has received limited attention until recently, perhaps owing to the traditional notion that
SLEEP, Vol. 29, No. 11, 2006 1410
it would not respond to treatment unless the associated condition was treated first. The present review, as well as recent findings,6062 challenge this traditional notion and indicate that insomnia-specific treatment is of benefit even among those whose insomnia is associated with comorbid conditions such as cancer, pain, alcohol abuse, and some psychiatric conditions. Nonetheless, there is a need for additional prospective and randomized controlled studies of comorbid insomnia contrasting outcomes when sleep is or is not directly targeted in treatment. The treatment of insomnia in older adults is another area previously neglected and for which there was limited evidence to guide practitioners. Nearly 25% of the studies reviewed in this paper focused on older adults. The findings from those studies indicate that older adults with primary insomnia respond to treatment as well as younger and middle-aged adults, although the presence of comorbid medical or psychiatric condition may moderate outcomes.27,43 A recent meta-analysis 63also confirmed that treatment effect sizes are comparable for middle-aged and older adults. There is additional evidence that psychological treatment can facilitate hypnotic discontinuation in older adults who are chronic users of hypnotics.15,22 This is an important finding as older adults are more likely to be long-term hypnotic users which, in some cases, may perpetuate sleep disturbances. Thus, although heterogeneity in diagnosis makes it more difficult to compare studies,64 such heterogeneity of insomnia samples also enhances generalizability of outcomes. This review highlights an emerging trend among investigators for combining multiple treatments, which contrasts with the earlier review describing numerous studies comparing treatment efficacy among 2 or more single therapies. Indeed, 26 of the 37 reviewed studies evaluated the efficacy a multi component approaches, including 21 studies using multicomponent therapy, with or without relaxation, and 5 more combining behavioral interventions (e.g., stimulus control and sleep restriction) but without cognitive therapy. Although the reason for this shift in paradigm is not entirely clear, the use of multi-component approaches is more likely, at least on a clinical basis, to address the different facets/perpetuating factors of insomnia.11 Whether CBT produces outcome that is superior to single therapies remains largely unexplored. The few comparative studies available show that outcome is superior for CBT, stimulus control, and for sleep restriction relative to relaxation alone,17,20,27,49 however, there has been no complete dismantling of CBT to isolate the relative efficacy of each component. Furthermore, although some findings65 suggest that change in beliefs and attitudes is an important mediator of long-term outcomes, there has been no direct controlled evaluation to isolate the relative contribution of cognitive therapy. Our previous review had identified 3 treatments as well-validated and 2 more as probably efficacious according to criteria set by the American Psychological Association.53 This updated review provides further evidence supporting stimulus control, relaxation, paradoxical intention as well validated therapies, and new evidence to upgrade sleep restriction and CBT from probably efficacious to well-established treatments. Although there is evidence supporting the efficacy of psychological and behavioral treatment for insomnia, there is still little information about the specificity of this treatment modality and the active therapeutic mechanisms responsible for sleep improvePsychological And Behavioral Treatment Of InsomniaMorin et al
ments. With a few notable exceptions using attention-placebo conditions,17,20 most CBT trials have used wait-list control groups, precluding the unequivocal attribution of treatment effects to any specific ingredient of psychological and behavioral treatment. The lack of a pill-placebo control equivalent in psychological outcome research makes it difficult to determine what percentage of the variance in outcomes is due to specific therapeutic ingredients (i.e., restriction of time in bed, cognitive restructuring), the measurement process (i.e., self-monitoring), or to non-specific factors (e.g., therapist attention, patients expectations). An important limitation noted in the previous review that is still evident in recent studies is the limited evidence documenting the clinical significance of outcomes beyond insomnia symptom reductions (i.e., reduced morbidity, improved quality of life). There is a need for broadening the scope of outcome measures66 and for standardizing assessment methodology in insomnia research,64,67 Furthermore, even for patients meeting criteria for what might be considered a clinically meaningful change, many such treatment responders reach a plateau and continue showing residual sleep disturbances after treatment and may remain at risk for relapse. There is a need to develop and validate more potent interventions that would increase the rate of patients reaching full remission.9 Ongoing studies are currently examining optimal treatment dosage, treatment combination involving medication, and maintenance therapies. A related issue is that most of the outcome evidence currently available is about improving sleep initiatiation and sleep continuity parameters, with essentially no information about the impact of treatment on more qualitative aspects of sleep, i.e., non-restorative sleep. Although this qualitative feature is part of the standard insomnia definition, no study has of yet examined the impact of psychological treatment on this variable. Proper implementation of psychological and behavioral therapies usually requires more time than prescribing a hypnotic medication, which may represent an important barrier to using such interventions in clinical practice. Nonetheless, several studies have documented the benefits of cost-effective implementation models using nurse practitioners, group therapy, or self-help materials to complement therapist-guided intervention. Whereas such implementation models are likely to make treatment more readily available, adequate therapist training remains an important consideration in using CBT effectively to optimize outcome. Additional studies examining the relative cost-effectiveness of different insomnia interventions would be warranted68 In summary, this updated review provides additional evidence supporting the use of psychological and behavioral interventions for primary insomnia, for insomnia associated with medical or psychiatric conditions, and for insomnia in older adults. Additional research is still needed to develop and validate treatment algorithms that would optimize outcomes and reduce morbidity; clinical research that would examine treatment mechanisms, mediators and moderators of outcomes is also warranted; and, additional effectiveness trials are particularly needed to document outcomes in unselected patients seeking treatment in various clinical settings (e.g., primary care). Finally, an important challenge for the future will be to disseminate more efficiently the available evidence to health-care providers and translate that evidence into meaningful clinical guidelines in order to ensure a more widespread use of validated therapies.
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preliminary evaluation. Psychiatr Rehabil J 2004;27:235-42 46. Perlis ML, Sharpe M, Smith MT, Greenblatt D, Giles D. Behavioral treatment of insomnia: treatment outcome and the relevance of medical and psychiatric morbidity. J Behav Med 2001;24:281-96 47. Perlis M, Aloia M, Millikan A, Boehmler J, Smith M, Greenblatt D, Giles D. Behavioral treatment of insomnia: a clinical case series study. J Behav Med 2000;23:149-61 48. Verbeek I, Schreuder K, Declerck G. Evaluation of short-term nonpharmacological treatment of insomnia in a clinical setting. J Psychosom Res 1999;47:369-83 49. Pallesen S, Nordhus IH, Kvale G, Nielsen GH, Havik OE, Johnsen BH, Skjotskift S. Behavioral treatment of insomnia in older adults: an open clinical trial comparing two interventions. Behav Res Ther 2003;41:31-48 50. Lichstein KL, Peterson BA, Riedel BN, Means MK, Epperson MT, Aguillard RN. Relaxation to assist sleep medication withdrawal. Behav Modif 1999;23:379-402 51. Riedel B, Lichstein KL, Peterson BA, Means MK, Epperson MT, Aguillarel RN. A comparison of the efficacy of stimulus control for medicated and nonmedicated insomniacs. Behav Modif 1998;22:328 52. Waters WF, Hurry MJ, Binks PG, et al. Behavioral and hypnotic treatments for insomnia subtypes. Behav Sleep Med 2003;1:81101 53. Chambless DL, Hollon SD. Defining empirically supported therapies. J Consult Clin Psychol 1998;66:7-18 54. Perlis ML, Smith MT, Orff H, Enright T, Nowakowski S, Jungquist C, Plotkin K. The effects of modafinil and cognitive behavior therapy on sleep continuity in patients with primary insomnia. Sleep 2004;15:715-25 55. Rosen RC, Lewin DS, Goldberg L, Woolfolk RL. Psychophysiological insomnia: combined effects of pharmacotherapy and relaxation-based treatments. Sleep Med 2000;1:279-88 56. Bastien CH, Morin CM, Ouellet MC, Blais FC, Bouchard S. Cognitive-behavioral therapy for insomnia: comparison of individual therapy, group therapy, and telephone consultations. J Consult Clin Psychol 2004;72:653-59 57. Smith MT, Perlis ML, Park A, Smith MS, Pennington J, Giles D, Buysse D. Comparative meta-analysis of pharmacotherapy and behavior therapy for persistent insomnia. Am J Psychiatry 2002;159:511 58. Murtagh DR, Greenwood KM. Identifying effective psychological treatments for insomnia: a meta-analysis. J Consult Clin Psychol 1995;63:79-89 59. Morin CM, Culbert JP, Schwartz SM. Nonpharmacological interventions for insomnia: a meta-analysis of treatment efficacy. Am J Psychiatry 1994;151:1172-80 60. Rybarczyk B, Stepanski E, Fogg L, Lopez M, Barry P, Davis A. A placebo-controlled test of cognitive-behavioral therapy for comorbid insomnia in older adults. J Consult Clin Psychol 2005;73:116474 61. Savard J, Simard S, Ivers H, Morin CM. Randomized study on the efficacy of cognitive-behavioral therapy for insomnia secondary to breast cancer, part I: Sleep and psychological effects. J Clin Oncol 2005;23:6083-96. 62. Smith MT, Huang MI, Manber R. Cognitive behavior therapy for chronic insomnia occurring within the context of medical and psychiatric disorders. Clin Psychol Rev 2005;25:559-92 63. Irwin MR, Cole JC, Nicassio PM. Comparative meta-analysis of behavioral interventions for insomnia and their efficacy in middleaged adults and in older adults 55+ years of age. Health Psychol 2006;25:3-14 64. Martin JL, Ancoli-Israel S. Assessment and diagnosis of insomnia in non-pharmacological intervention studies. Sleep Med Rev 2002;6:379-406 65. Morin CM, Blais F, Savard J. Are changes in beliefs and attitudes about sleep related to sleep improvements in the treatment of inPsychological And Behavioral Treatment Of InsomniaMorin et al
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somnia? Behav Res Ther 2002;40:741-52 66. Morin CM. Measuring outcome in randomized clinical trials of insomnia therapies. Sleep Med Rev 2003;7:263-79 67. Buysse DJ, Ancoli-Israel S, Edinger JD, Lichstein KL, Morin CM. Recommendations for a standard research assessment of insomnia. Sleep. Sleep 2006 29:1155-73. 68. Martin SA, Aikens JE, Chervin RD. Toward cost-effectiveness analysis in the diagnosis and treatment of insomnia. Sleep Med Rev 2004;8:63-72 69. Espie CA, Lindsay WR, Brooks DN, Hood EM, Turvey T. A controlled comparative investigation of psychological treatments for chronic sleep-onset insomnia. Behav Res Ther 1989;27:79-88 70. Lacks P, Bertelson AD, Sugerman J, Kunkel J. The treatment of sleep-maintenance insomnia with stimulus-control techniques. Behav Res Ther 1983;21:291-95 71. Lacks P, Bertelson AD, Gans L, Kunkel J. The effectiveness of three behavioral treatments for different degrees of sleep onset insomnia. Behav Ther 1983;14:593-605 72. Morin CM, Azrin NH. Stimulus control and imagery training in treating sleep-maintenance insomnia. J Consult Clin Psychol 1987;55:260-62 73. Morin CM, Azrin NH. Behavioral and cognitive treatments of geriatric insomnia. J Consult Clin Psychol 1988;56:748-753 74. Turner RM, Ascher LM. Controlled comparison of progressive relaxation, stimulus control, and paradoxical intention therapies for insomnia. J Consult Clin Psychol 1979;47:500-08 75. Lick JR, Heffler D. Relaxation training and attention placebo in the treatment of severe insomnia. J Consult Clin Psychol 1977;45:153161 76. Nicassio PM, Boylan MB, McCabe TG. Progressive relaxation, EMG biofeedback and biofeedback placebo in the treatment of sleep-onset insomnia. Br J Med Psychol 1982;55:159-66 77. Woolfolk RL, McNulty TF. Relaxation treatment for insomnia: a component analysis. J Consult Clin Psychol 1983;51:495-503 78. Friedman L, Bliwise DL, Yesavage JA, Salom S. A preliminary study comparing sleep restriction and relaxation treatments for insomnia in older adults. J Gerontol 1991;46:1-8 79. Sanavio E, Vidotto G, Bettinardi O, Roletto T, Zorzi M. Behavior therapy for DIMS: Comparison of three treatment procedures with follow-up. Behav Psychother 1990;18:151-67 80. VanderPlate C, Eno EN. Electromyograph biofeedback and sleep onset insomnia: Comparison of treatment and placebo. Behav Eng 1983;8:146-53 81. Freedman R, Papsdorf JD. Biofeedback and progressive relaxation treatment of sleep-onset insomnia: a controlled, all-night investigation. Biofeedback Self Regul 1976;1:253-71 82. Morin CM, Kowatch R, Barry T, Walton E. Cognitive-behavior therapy for late-life insomnia. J Consult Clin Psychol 1993;61:13746
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Appendix A. Studies reviewed but excluded A. Baillargeon L, Landreville P, Verreault R, Beauchemin JP, Grgoire JP, Morin CM. Discontinuation of benzodiazepines among older insomniac adults treated through cognitive-behavioral therapy combined with gradual tapering: a randomized trial. CMAJ 2003;169:1015-20. [no sleep data] B. Espie CA, Inglis SJ, Harvey L. Predicting clinically significant response to cognitive behavior therapy for chronic insomnia in general medical practice: analyses of outcome data at 12 months posttreatment. J Consul Clin Psychol 2001;69:58-66. [secondary analysis of another paper included in the review] C. Greeff AP, Conradie WS. Use of progressive relaxation training for chronic alcoholics with insomnia. Psychol Rep 1998;82:407-12. [only outcome measure, sleep quality, obtained from a single 10-point rating scale] D. Gunning M, Espie CA. Psychological treatment of reported sleep disorder in adults with intellectual disability using a multiple baseline design. J Intellect Disabil Res 2003;47:191-202. [sample size smaller than 10] E. Hajak G, Bandelow B, Zulley J, Pittrow D. As needed pharmacotherapy combined with stimulus control treatment in chronic insomnia--Assessment of a novel intervention strategy in a primary care setting. Ann Clin Psychiatry 2002;14:1-7. [main intervention was pharmacological, with optional use of stimulus control procedures] F. Harvey AG, Farrell C. The efficacy of a Pennebaker-like writing intervention for poor sleepers. Behav Sleep Med 2003;1:115-24. [not a clinical treatment study; no insomnia diagnosis] G. Harvey AG, Payne S. The management of unwanted pre-sleep thoughts in insomnia: distraction with imagery versus general distraction. Behav Res Ther 2002;40:267-77. [not a clinical treatment study] H. Krakow B, Johnston L, Melendrez D et al. An open-label trial of evidence-based cognitive behavior therapy for nightmares and insomnia in crime victims with PTSD. Am J Psychiatry 2001;158:2043-7. [primary diagnosis of post traumatic stress disorder with primary outcome measures of nightmare frequency; no insomnia diagnosis] I. Krakow B, Melendrez D, Lee SA, Warner TD, Clark JO, Sklar D. l. Refractory insomnia and sleep-disordered breathing, a pilot study. Sleep Breath 2004;8:15-29. [main sleep diagnosis was sleep-related breathing disorder, not insomnia] J. Lundh LG, Hindmarsh H. Can meta-cognitive observation be used in the treatment of insomnia? A pilot study of a cognitive-emotional self-observation task. Behav Cogni Psychoth 2002;30:233-36. [no insomnia diagnosis] K. Morawetz D. Depression and insomnia: Which comes first? Australian Journal of Counseling Psychology 2001;3:19-24. [no insomnia diagnosis; did not use sleep diaries or other recognized measures to evaluate outcome] L. Morgan K, Thompson J, Dixon S, Tomeny M, Mathers N. Predicting longer-term outcomes following psychological treatment for hypnotic-dependent chronic insomnia. J Psychosom Res 2003;54:21-9. [secondary analysis of another paper included in the review] M. Quesnel C, Savard J, Simard S, Ivers H, Morin CM. Efficacy of cognitive-behavioral therapy for insomnia in women treated for non-metastatic breast cancer. J Consul Clin Psychol 2003;71:189-200. [final sample size smaller than 10] N. Riedel BW, Lichstein KL. Strategies for evaluating adherence to sleep restriction treatment for insomnia. Behav Res Ther 2001;39:201-12. [secondary analysis of another paper included in the review] O. Tang NK, Harvey AG. Correcting distorted perception of sleep in insomnia: a novel behavioural experiment? Behav Res Ther 2004;42:27-39. [not a clinical treatment study] P. Verbeek I, Declerck G, Neven AK, Coenen A. Sleep information by telephone: Callers indicate positive effects on sleep problems. Sleep and Hypnosis 2002 ;4:47-51. [not a clinical treatment study; no diagnosis of insomnia]
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REVIEW

Psychological And Behavioral Treatment Of Insomnia:Update Of The Recent Evidence (1998-2004)

SLEEP, Vol. 29, No. 11, 2006

Davidson et al. (2001);42 8 wk; No FU

Dopke et al. (2004);45

11/10; 60%; 45.6; NonRCT; IV Insomnia associated with psychological disorders

Edinger et al. (2001);17

75/70; 46.7%; 55.3; Persistent primary insomnia

Edinger & Sampson (2003);35

20/19;10%;51.0; Primary insomnia

Espie et al. (2001);33

Friedman et al. (2000);18

Psychological And Behavioral Treatment Of InsomniaMorin et al

Guilleminault et al. (2002);19

130/126; 100%; 62.4; Chronic insomnia

Davidson et al. (2001);42 8 wk; No FU

Dopke et al. (2004);45

11/10; 60%; 45.6; NonRCT; IV Insomnia associated with psychological disorders

Edinger et al. (2001);17

75/70; 46.7%; 55.3; Persistent primary insomnia

Edinger & Sampson (2003);35

20/19;10%;51.0; Primary insomnia

Espie et al. (2001);33

Friedman et al. (2000);18

Psychological And Behavioral Treatment Of InsomniaMorin et al

Guilleminault et al. (2002);19

130/126; 100%; 62.4; Chronic insomnia

Case replication series; V

42/42; 52%; 53.6; Primary insomnia

Jacobs et al. (2004);34

63/54; 70%; 47.1; Primary insomnia

Lichstein et al. (1999);50

40/40; 58%; 52; Psychophysiologic insomnia and Hypnotic dependent insomnia

Lichstein et al. (2000);43

49/44; 48%; 68.6; Insomnia secondary to medical/ psychiatric conditions

Lichstein et al. (2001);20

89/72; 74%; 68.03; Psychophysiological insomnia

Psychological And Behavioral Treatment Of InsomniaMorin et al

Means et al. (2000);37

NS/57;68.5%; 21.2 Primary insomnia

Mimeault & Morin (1999);38

58/54; 59%; 50.8; Primary insomnia

Morgan et al. (2003);15

209/123; 67.5%; 65.5; chronic insomnia and chronic use of hypnotics

Morin et al. (1999);12

78/72; 65%; 65.0; Primary insomnia

Morin et al. (2004);22

76/69; 50%; 62.5; Hypnotic-dependent insomnia

Psychological And Behavioral Treatment Of InsomniaMorin et al

Pallesen et al. (2003);49

66/55; 84%; 69.8; Primary and secondary insomnia

Perlis et al. (2000);47

Case replication series; V

Perlis et al. (2001);46

Case replication series; V

89/28; 64%; 46.5; Mix of primary and secondary insomnia

Perlis et al. (2004);54

30/27; 70%; 41.3; Psychophysiologic insomnia

Riedel et al. (1998);51