Behaviour Research and Therapy 41 (2003) 3148 www.elsevier.

com/locate/brat

Behavioral treatment of insomnia in older adults: an open clinical trial comparing two interventions
S. Pallesen
a

a,*

, I.H. Nordhus a, G. Kvale a, G.H. Nielsen a, O.E. Havik a, B.H. Johnsen a, S. Skjtskift b

Department of Clinical Psychology, University of Bergen, Christiesgt. 12, 5015 Bergen, Norway b Bjrgvin Marriage Guidance Ofce, vregt. 25, 5003 Bergen, Norway Accepted 25 October 2001

Abstract Fifty-ve insomniacs, 60 years or above, participated in a behavioral treatment program, comparing two interventions (sleep hygiene+stimulus control vs sleep hygiene+relaxation tape). Half of the subjects were randomized to a waiting-list condition prior to treatment. No signicant changes were observed during the waiting-list period. During the treatment period however, the subjects improved on several sleep parameters, and treatment gains were maintained at a 6-month follow-up. The effects of treatment were greater for nocturnal measures (e.g. sleep onset latency and total sleep time) as compared to daytime measures (e.g. life satisfaction, daytime alertness) and not-targeted behavior (medication use). There were no differences in treatment effects for the two interventions. 2003 Elsevier Science Ltd. All rights reserved.
Keywords: Insomnia; Older adults; Behavioral treatment; Sleep hygiene; Relaxation; Stimulus control

1. Introduction Insomnia is characterized by reduced quality, duration, or efciency of sleep (Morin et al., 1999b). Depending on the time of night the sleep disruption occurs, insomnia is usually subdivided into sleep onset insomnia (difculty falling asleep), maintenance insomnia (difculty getting back to sleep during the night), and early morning awakening (inability to return to sleep, even for a short while, after waking up during the night or early in the morning; Lacks & Morin, 1992).

This study was supported by a grant from the Norwegian Council of Mental Health. * Corresponding author. Tel.: +47-55-58-88-42; fax: +47-55-58-98-77. E-mail address: staale.pallesen@psych.uib.no (S. Pallesen).

0005-7967/03/$ - see front matter 2003 Elsevier Science Ltd. All rights reserved. PII: S 0 0 0 5 - 7 9 6 7 ( 0 1 ) 0 0 1 2 2 - X

32

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

Another subdivision, related to insomnia etiology, is between secondary and primary insomnia. Secondary insomnia is caused by medical, psychiatric or substance factors (Espie, 1991), in contrast to primary insomnia, which denotes insomnia without medical, psychiatric or substance etiology (Hauri, 2000). The latter is also a current diagnostic label used in DSM-IV (American Psychiatric Association, 1994). A third subdivision of insomnia emphasizes its duration: transient insomnia lasts only several days, short term insomnia up to three weeks, and long-term or chronic insomnia more than three weeks (National Institutes of Health, 1984). Epidemiological studies have demonstrated that the prevalence of insomnia increases with advancing age (Pallesen et al., 2001b). The elderly as a group may, therefore, be in particularly high need of adequate treatment for this condition. Until now, the most common treatment modality for insomnia has been the use of hypnotics (Bliwise, 1991). This approach has general disadvantages among which are tolerance development (Lader, 1991), worsening of sleep contingent upon medication withdrawal, i.e. rebound insomnia (Kales, Soldatos, Bixler, & Kales, 1983), and reduction of deep sleep related to long-term use (Schneider-Helmert, 1988). Toxic effects caused by a generally high level of medication use and altered drug metabolism (Salzman, 1982), cognitive and psychomotor retardation associated with falls, fractures and car accidents (Grad, 1995), and memory impairment (Roehrs, Merlotti, Zorick, & Roth, 1994) are side-effects reported for the pharmacological approach of insomnia in the elderly. Such side-effects are particularly marked for benzodiazepines, but also the new non-benzodiazepine hypnotics (e.g. zolpidem and zopiclone), seem to have several unwanted effects (Aragona, 2000; Noble, Langtry, & Lamb, 1998), and use of these drugs for more than four weeks are not recommended (Hajak, 1999; Holm & Goa, 2000). For chronic insomnia in elderly subjects, behavioral treatment as an alternative to the pharmacological approaches should be explored. Several different behavioral interventions have been developed: sleep hygiene consists of basic advises on how to improve sleep (Hauri, 1991; Zarcone, 2000), whereas relaxation techniques are aimed at reducing cognitive, somatic and emotional arousal counteracting sleep (Morin, 1993). Cognitive therapy focuses on identifying and altering sleep-incompatible thoughts about sleep and sleep loss (Morin, 1993), while stimulus control consists of behavioral prescriptions with the intention to strengthen the bed and bedroom as discriminative stimuli for sleep, and to weaken them as stimuli for sleep-incompatible activities (Bootzin & Nicassio, 1978). Sleep restriction is a procedure where the allowed time for staying in bed is set equal to total sleep time, gradually increasing allowed time spent in bed as sleep efciency [(time asleep/time in bed) 100] stays above 8085% (Spielman, Saskin, & Thorpy, 1987). Multicomponent intervention comprises the combination of all these interventions. Normally, these interventions are of short duration, about one session per week for 48 weeks, and they are also suitable as group interventions (Morin, 1993; for review see Pallesen, Nordhus, Havik, & Nielsen, 2001a). Meta-analyses show that these interventions, in general, produce signicant and long lasting sleep improvements in insomniacs (Morin, Culbert, & Schwartz, 1994; Murtagh & Greenwood, 1995). A recent meta-analysis, exclusively focusing on the elderly, concludes that behavioral interventions yield signicant and long-lasting gains also for this age group (Pallesen, Nordhus, & Kvale, 1998). However, the meta-analysis included only 13 studies and subsequently only four studies focusing on behavioral treatment of insomnia in the elderly have been published (Friedman et al., 2000; Lichstein, Riedel, Wilson, Lester, & Aguillard, 2001; Lichstein, Wilson and Johnson,

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

33

2000; Morin, Colecchi, Stone, Sood, & Brink, 1999). This indicates that treatment studies on the elderly still are rather sparse. The majority of former studies have excluded patients with secondary insomnia (Pallesen et al., 1998), which is a major weakness, considering that insomnia is highly related to psychiatric and somatic diseases (Soldatos, 1994; Wooten, 1994). Patients using hypnotics are also often excluded from treatment studies with elderly insomniacs (e.g. Morin, Kowatch, Barry, & Walton, 1993), in spite of ndings that use of hypnotics is more prevalent among the elderly compared to younger subjects (Pallesen et al., 2001b). Due to this, several authors have lately exhorted researchers to consider studies emphasizing effectiveness along the efcacy-effectiveness continuum in research on cognitive-behavioral interventions for insomnia (Espie, Inglis, & Harvey, 2001). Additionally, few studies have investigated the effects of insomnia treatment on general life satisfaction, despite the fact that insomniacs show impairment across multiple quality of life domains (Zammit, Weiner, Damato, Sillup, & McMillan, 1999). Against this background, we, therefore, decided to conduct an effectiveness treatment study for elderly insomniacs, including not only patients with primary insomnia, but also patients with secondary insomnia, and patients using hypnotics as well. The study addressed the following questions: (1) Do patients undergoing behavioral treatment improve compared to a waiting-list condition? (2) Will potential treatment gains be maintained six months after treatment termination? (3) Will there be any difference in terms of treatment effect between two treatment approaches (sleep hygiene+relaxation vs. sleep hygiene+stimulus control)? (4) Do variables such as type of insomnia (primary vs. secondary), medication use and compliance inuence stability and treatment effects? (5) Does insomnia treatment have impact on general life satisfaction for insomniacs?

2. Methods 2.1. Subjects Participants, 60 years or older, were recruited through newspaper advertisements to participate in a treatment study focusing on non-pharmacological interventions for insomnia. Before inclusion in the study the patients met with the therapist (rst author) and were given oral and written information about the study. Subjects who at this stage wanted to participate, signed an informed consent and were scheduled for a medical examination by a physician, who also tested them with the Mini Mental State (MMS; Folstein, Folstein, & McHugh, 1975), a screening instrument for dementia with a score range from 0 to 30. A low score indicates cognitive impairment, and patients with MMS-score below 25 were excluded from the study. Subjects whose primary goal was to stop taking hypnotics were also excluded, but were offered guidance on how to reduce their use of medication. The subjects included were then interviewed by a psychologist according to The Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I; First, Spitzer, Gibbon, & Williams, 1995), and also completed an insomnia interview developed by Morin (1993). Subjects without sleeping difculties were excluded from the study at this stage. In order to strengthen the external validity of the study, subjects with affective and anxiety disorders based on the Structural Clinical Interview for DSM-IV (First et al., 1995) and patients who used hyp-

34

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

notics were not excluded. Neither were subjects with restless legs excluded, based on the assumption that they might prot from behavioral interventions (Hening et al., 1999). From a sample of 132 eligible subjects, 35 did not want to participate after receiving information about the study. The main reason given by these subjects was that they felt the program was too demanding in terms of assessment and self-monitoring. Additionally, two were excluded because they did not have any sleeping difculties, one was excluded due to suspected dementia, and 28 subjects were excluded as their primary goal was to stop taking hypnotics. Thus, 66 subjects were nally included. Due to attrition of 11 subjects during treatment, a total of 55 completed the study. The 55 subjects of the nal sample completing treatment, comprising of nine males and 46 females, had a mean age of 69.8 (SD=6.53, range=6084). On average, the subjects reported having suffered from insomnia for 21.7 years (SD=16.2, range=1.068.5 years), which means that all of them suffered from chronic insomnia. Forty-ve subjects had primary insomnia according to the Diagnostic and Statistical Manual-IV (American Psychiatric Association, 1994), while 10 had insomnia secondary to somatic, psychiatric, or substance factors. Of the latter, two met the diagnostic criteria for restless legs, one a severe rheumatic disorder, one bronchial asthma, three generalized anxiety disorder, one generalized anxiety disorder, social phobia and dysthymia, one dysthymia, and one suffered from major depression. Based on sleep diaries kept by the subjects, all fullled at least one of the following three criteria: (1) mean sleep onset latency exceeding 30 min and sleep efciency lower than 80% (sleep onset insomnia); (2) mean wake time after sleep onset exceeding 30 min and sleep efciency lower than 80% (maintenance insomnia); (3) mean nal awakening time 30 min earlier than preferred, total sleep time less than 390 min and sleep efciency lower than 80% (early morning awakening). Before treatment, 47 subjects fullled the criteria for sleep onset insomnia, 34 for maintenance insomnia and seven for early morning awakening, which means that several subjects fullled the criteria for more than one insomnia subtype. Twenty-eight patients had sleep onset and maintenance insomnia, four had sleep onset insomnia and early morning awakening, three had all three types of insomnia, while one had maintenance insomnia and early morning awakening. 2.2. Measures 2.2.1. Sleep diary Diaries were kept by each subject. These comprised of daily morning estimates of the previous nights sleep and behavior and functioning during the previous day. The following sleep parameters were included in the sleep diary: (1) time entering and leaving bed; (2) latency to sleep; (3) number and duration of awakenings during the night; (4) time of nal awakening; (5) rating of daytime sleepiness; (6) napping; and (7) medication/alcohol usage. These are standard observations recommended to be included in a sleep diary (Lichstein & Riedel, 1994). Based on the sleep diaries, the following sleep parameters were derived: (1) sleep onset latency (SOL); (2) total duration of wake time after sleep onset (WASO); (3) total sleep time (TST); (4) sleep efciency [(total time in bedtime awake)/total time in bed 100]; (5) daytime sleepiness; and (6) percentages of days with hypnotic use.

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

35

2.2.2. Sleep Impairment Index The Sleep Impairment Index (SII) comprises seven items that yields a quantitative index of insomnia severity. Each item is rated on a 5-point scale, giving a composite score between 7 and 35, with higher scores indicating more severe insomnia (Morin, 1993). In clinical use the SII has demonstrated adequate psychometric properties (Morin & Azrin, 1988). The Chronbachs alpha for SlI in this study was 0.72. 2.2.3. Life satisfaction The life satisfaction measure included nine of the 10 items of the WHO (Ten) Well-Being Index, and tapping both negative and positive aspects of well-being. One item from the original scale was excluded as it pertained to sleep problems, yielding a composite score ranging from 0 to 27. The WHO (Ten) has demonstrated satisfactorily psychometric properties with respect to internal and external validity (Bech, Gudex, & Johansen, 1996). The Chronbachs alpha for the nine items from WHO (Ten) in this study was 0.87. 2.2.4. Intervention log This instrument was constructed by the authors. The patients should give daily estimates, on a scale ranging from one to three, of their degree of compliance with the single treatment constituents, where three represented complete compliance. For the subjects in the sleep hygiene+stimulus control condition the intervention log comprised 10 items, whereas the intervention log for the sleep hygiene+relaxation condition comprised eight items. A sum score was made by adding the various estimates for each day, dividing by number of estimates and days. Thus, a composite score ranging from one to three was obtained, reecting the degree of compliance with the treatment prescriptions. 2.3. Design and procedure After completing the SII and the life satisfaction measure, as well as 14 days of sleep diary registration, subjects were randomized to either immediate treatment (n=29) or to a waiting-list condition (n=26). For the subjects in the immediate treatment condition these registrations were used as pretreatment measures, and the subjects were then randomized to one of two conditions: sleep hygiene+relaxation tape condition (n=14) or sleep hygiene+stimulus control condition (n=15). The subjects met with the therapist on an individual basis once a week, for about 30 min for four consecutive weeks. Immediately following treatment, the subjects again completed the SII and the life satisfaction measure. They also kept a sleep diary for another 14 days following treatment, which constituted posttreatment data. The subjects in the waiting-list condition completed the same registrations following a four week waiting-list period. These data constituted pretreatment registrations for these wait-list subjects, and they were then randomized to either the sleep hygiene+relaxation tape condition (n=12) or to the sleep hygiene+stimulus control condition (n=14). Thereafter, subjects in these groups followed the same treatment and posttreatment registration procedure as the subjects in the immediate treatment groups. Thus, 26 subjects went through the sleep hygiene+relaxation treat-

36

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

ment condition, whereas 29 subjects completed the sleep hygiene+stimulus control. During treatment the patients made daily estimates of compliance by the intervention log. Subjects were again contacted six months after treatment, and asked to keep a sleep diary for 14 days and to complete the SII and the life satisfaction measure for follow-up registrations. At this point in time, eight of the 55 patients were not able to, or did not want to, participate in the follow-up assessment. The eight subjects were all women, with mean age of 66.5 (SD=6.0). Of these, two had secondary insomnia, one was suffering from bronchial asthma, the other had generalized anxiety disorder, while the remaining six had primary insomnia. Among the eight who did not participate at follow-up, six had been treated with sleep hygiene+stimulus control, while two had been treated with sleep hygiene+relaxation tape. Thus, 47 (85.5%) of the patients who completed treatment, also completed the 6-month follow-up registrations. There were no differences between the subjects in the immediate treatment groups and subjects on the waiting-list condition in terms of gender distribution (c2=0.84, df=1, p0.36), number of patients with primary and secondary insomnia (c2=0.79, df=1, p0.37) and age (F(1,53)=0.41, p0.52). Nor were there any differences between the two intervention groups (sleep hygiene+relaxation tape vs. sleep hygiene+stimulus control) in terms of gender distribution (c2=1.62, df=1, p0.20), number of patients with primary and secondary insomnia (c2=0.26, df=1, p0.61) and age (F(1,53)=1.18, p0.28). 2.4. Treatment 2.4.1. Sleep hygiene The sleep hygiene intervention was based on nine pieces of advice on sleep improvement, based on standard sleep treatment (Hauri, 1991; Zarcone, 2000). The advices were given as both oral and written instructions: (1) do not drink caffeine-containing beverages after lunch; (2) do not smoke after dinner; (3) do not consume alcohol after dinner; (4) eat a light meal 12 h before bedtime; (5) exercise in the afternoon, albeit not later than 4 h before bedtime; (6) avoid noise in the bedroom and keep the bedroom as dark as possible during the night. Keep the temperature in the bedroom stable (not too cold and not too hot); (7) expose yourself daily to outdoor light for at least 30 min in the morning; (8) avoid daytime naps; and (9) get out of bed the same time every morning. 2.4.2. The relaxation tape This tape was based on oral instructions developed by Holte (1992). The same version of the tape was handed out to the subjects, and they were instructed to listen to the tape and to follow the instructions whenever they had difculties sleeping. The taped instructions were based on the Holte Sleeping Technique (Holte, 1989). The technique has three components: (1) progressive relaxation (the subjects are instructed to relax according to a quick version of a structured progressive relaxation procedure, starting with the feet and ending up with, and particularly concentrating on the facial muscles); (2) passive focal attention (the subjects are instructed to listen to the sound of their own expiration); and (3) active expiration (the subjects are instructed to breath rhythmically and to amplify the sound of their expiration, so much that they clearly hear its sound). Active expiration is presumed to act as a potential sleep releasing stimuli (Holte, 1989).

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

37

2.4.3. The stimulus control procedure This procedure (Bootzin & Nicassio, 1978) contained the following six prescriptions: (1) lie down intending to go to sleep only when drowsiness is experienced; (2) do not use your bed for anything except sleep (e.g. not to read, eat, watch television etc.), although sexual activity is an exception to this rule; (3) if you nd yourself unable to fall asleep, get up and go to another room, staying up for as long as you wish, and return to the bedroom to sleep when you feel sleepy; (4) if you still cannot sleep, repeat step three for as many times as necessary during the night; (5) get up at the same time every morning, irrespective of amount of sleep obtained; (6) do not nap during the day. 2.5. Statistical analysis procedure A 22 (TimeIntervention) ANOVA analysis with repeated measurement was used in order to investigate whether there were any differences between the two interventions in terms of treatment effects and a 22 (TimeImmediate/Delayed Treatment) ANOVA analysis with repeated measurement was used to investigate whether the Immediate treatment group changed signicantly from the Delayed treatment group. For the other analyses, one-way ANOVA with repeated measurement were conducted. In addition to signicant testing of changes during waiting-list or course of treatment, effect sizes were calculated in order to examine the magnitude of the these changes (Wilkinson & the Task Force on Statistical Inference, 1999) and to compare the results with the ndings from the meta-analysis with elderly subjects (Pallesen et al., 1998). The effect sizes (ES) were based on the posttreatment or follow-up scores minus the scores at pretreatment, divided by the pooled standard deviation. Thus, an ES of 1.0 would imply that the mean level of insomnia symptomatology at posttreatment or follow-up was one standard deviation lower than the pretreatment score. In some cases the sign of the effect size was reversed in order to ensure that a positive effect size always indicated a reduction in insomnia symptomatology with time, whereas negative effect sizes always indicated a worsening of insomnia symptomatology with time. 2.6. Clinical signicant improvement Consensus criteria were used for evaluation of clinical signicant improvement in the treatment of insomnia (Lacks & Morin, 1992; Morin et al., 1999b). For sleep onset insomnia, clinically signicant improvement was obtained if the following criteria was met at posttreatment or 6month follow-up: (1) mean sleep onset latency was 30 min or below; (2) reduction of sleep onset latency of 50% or more, or both of these. For maintenance insomnia at least one of the following criteria for clinically signicant improvement had to be fullled: (1) mean wake time after sleep onset latency was 30 min or below; (2) reduction of WASO of 50% or more, or both of these. For early morning awakening clinically improvement was considered obtained if at least one of the following two criteria was fullled: (1) total sleep time was 390 min or above; or (2) sleep efciency 80% or above. 2.7. Additional analyses Based on the research literature, the following characteristics were selected as potential prognostic factors: type of insomnia, medication use and compliance. The prognostic factors were all

38

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

dichotomized (primary vs. secondary insomnia, with or without medication and compliance below or over mean), and associations with outcome were investigated by chi-square analyses. In these analyses the dependent variable constituted the fulllment of both criteria for clinical signicant improvement. As only seven subjects suffered from early morning awakening, chi-square analyses for this variable was not conducted. 2.8. Stability As studies have indicated that symptom change is common among insomniacs (Hohagen et al., 1994), we investigated whether instability was related to factors as type of intervention, hypnotic use, type of insomnia and compliance. Instability was dened as obtaining clinically signicant improvement only at posttreatment or 6-months follow up. Stability was dened as clinically signicant improvement at both posttreatment and follow-up.

3. Results 3.1. Effects at posttreatment Table 1 displays the sleep diary data for the subjects on the waiting-list. During the waitinglist period, there were no changes on any of the sleep parameters for those groups of subjets: sleep onset latency (F(1,25)=0.44, p0.51), WASO (F(1,25)=2.22, p0.14), total sleep time (F(1,25)=1.05, p0.31), daytime alertness (F(1,25)=0.01, p0.93), sleep efciency (F(1,25)=1.15, p0.29), SlI (F(1,24)=1.49, p0.23), and percent of days with hypnotic use (F(1,25)=0.00, p0.95). Nor was there signicant change on the life satisfaction measure (F(1,21)=1.34, p0.26). Analyzing the changes from pre- to posttreatment for all subjects (Table 1) revealed signicant main effects for Time for all included parameters: sleep onset latency (F(1,53)=27.51, p0.001), WASO (F(1,53)=6.87, p0.02), total sleep time (F(1,53)=15,40, p0.001), daytime alertness (F(1,53)=14.21, p0.001), sleep efciency (F(1,52)=41.64, p0.001), SII (F(1,52)=25.61, p0.001), percentage of days with hypnotic use (F(1,53)=4.28, p0.05) and life satisfaction (F(1,51)=8.12, p0.007). There was a signicant interaction effect for the TimeImmediate/Delayed Treatment on three of eight outcome variables: sleep onset latency (F(1,53)=12.9, p0.002), total sleep time (F(1,53)=7.43, p0.01), and sleep efcacy (F(1,52)=19.0, p0.001), and a near signicant effect for SII (F(1,52)=3.45, p0.07), all in favor of the immediate treatment condition. There were no statistical signicant differences in terms of treatment effect from pre- to posttreatment between the two interventions, sleep hygiene+stimulus control vs. sleep hygiene+relaxation tape (TimeIntervention), but for sleep efciency (F(1,52)=3.14, p0.09) and life satisfaction (F(1,51)=3.44, p0.08) the differences approached signicance, in both cases in favor of sleep hygiene+stimulus control.

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148 Table 1 Group means, standard deviations and effect sizes for changes during waiting-list and treatment Waitlist Sleep onset latency (min) (n=26) Wake time after sleep onset (min) (n=26) Total sleep time (min) (n=26) Daytime alertness (15) (n=26) Sleep efciency [(total sleep time/time in bed) 100] (n=26) Sleep Impairment Index (735) (n=25) Percentage of days with hypnotic use (n=26) Life satisfaction (027) (n=22) Treatment Before waiting-list X (SD) 72.59 (54.48) 52.60 (36.92) 325.7 (71.32) 3.02 (0.71) 61.76 (12.90) 24.04 (4.09) 28.35 (39.48) 16.82 (5.35) (SD) Pretreatment X After waiting-list X (SD) 76.24 (50.54) 47.83 (33.17) 332.9 (63.6) 3.02 (0.62) 63.18 (12.01) 23.32 (3.60) 28.27 (39.10) 17.59 (4.53) (SD) Posttreatment X Effect size 0.07 0.14 0.11 0.00 0.11 0.19 0.00 0.16 Effect size

39

Sleep onset latency (min) Sleep hygiene+stimulus control (n=29) 86.91 (77.04) Sleep hygiene+relaxation tape (n=26) 71.17 (41.36) Wake time after sleep onset (min) Sleep hygiene+stimulus control (n=29) 55.45 (41.77) Sleep hygiene+relaxation tape (n=26) 46.57 (33.58) Total sleep time (min) Sleep hygiene+stimulus control (n=29) 336.7 (75.63) Sleep hygiene+relaxation tape (n=26) 346.8 (49.27) Daytime alertness (15) Sleep hygiene+stimulus control (n=29) 2.78 (0.58) Sleep hygiene+relaxation tape (n=26) 3.26 (0.71) Sleep efciency [(total sleep time/time in bed) 100] Sleep hygiene+stimulus control (n=29) 60.79 (13.99) Sleep hygiene+relaxation tape (n=25) 63.60 (8.66) Sleep Impairment Index (735) Sleep hygiene+stimulus control (n=28) 23.64 (4.29) Sleep hygiene+relaxation tape (n=26) 22.50 (3.70) Percentage of days with hypnotic use Sleep hygiene+stimulus control (n=29) 32.36 (38.43) Sleep hygiene+relaxation tape (n=26) 16.07 (32.07) Life satisfaction (027) Sleep hygiene+stimulus control (n=27) 15.96 (4.19) Sleep hygiene+relaxation tape (n=26) 19.38 (3.48)

55.80 (47.26) 50.70 (29.35) 42.13 (31.65) 33.48 (25.21) 366.6 (78.24) 372.7 (54.92) 3.05 (0.71) 3.52 (0.71) 72.60 (12.45) 70.31 (8.34) 21.07 (5.20) 19.23 (5.01) 28.60 (38.82) 14.12 (32.13) 17.78 (3.72) 19.77 (4.49)

0.49 0.57 0.36 0.44 0.39 0.50 0.42 0.37 0.89 0.79 0.54 0.74 0.10 0.06 0.46 0.10

3.1.1. Clinical signicance The results are displayed in Table 2. Totally, 12.5% of the subjects with sleep onset insomnia improved according to both criteria (mean sleep onset latency equal to or below 30 min and at least 50% reduction of target symptom) during treatment, whereas 0% improved during waitinglist. Among the subjects with sleep maintenance insomnia, 20% obtained clinically signicant improvements during treatment while 0% improved during waiting-list. None of the seven subjects with early morning awakening improved during treatment or wait-list. In terms of clinically sig-

40

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

Table 2 Clinically signicant improvement of sleep onset insomnia and maintenance insomnia Variable At least 50% reduction of Treatment outcome target symptom (%) value30 min (%) At least 50% reduction of target symptom and treatment outcome value30 min (%)

Clinically signicant improvement during wait-list period (% of subjects with symptom before wait-list) according to three criteria Sleep onset insomnia 4.4 8.7 0.0 Maintenance insomnia 6.3 18.8 0.0 Clinically signicant improvement at posttreatment (% of subjects with symptom at pretreatment) according to three criteria Sleep onset insomnia 25.0 22.9 12.5 Maintenance insomnia 25.7 34.3 20.0 Clinically signicant improvement at 6 month follow-up (% of subjects with symptom at pretreatment) according to three criteria Sleep onset insomnia 34.1 31.7 26.8 Maintenance insomnia 41.9 29.0 25.8

nicant improvement on at least sleep onset insomnia or sleep maintenance insomnia results showed that eight of 29 subjects (27.6%) with sleep hygiene+stimulus control improved, while three of 26 subjects (11.5%) with sleep hygiene+relaxation improved (c2=2.21, df=1, p0.13). Furthermore, two of 23 subjects (8.7%) with compliance below mean improved compared to eight of 29 subjects (27.6%) above mean (c2=2.95, df=1, p0.08), ve of 25 subjects (20%) using hypnotics improved against six of 30 subjects (20%) not using hypnotics (c2=0.01, df=1, p0.99), and one of 10 subjects (10%) with secondary opposed to 10 of 45 subjects (22.2%) with primary insomnia improved (c2=0.76, df=1, p0.38). Two subjects got clinically worse from pre- to posttreatment on WASO (see Table 4). 3.2. Effects at 6-month follow-up 3.2.1. Statistical analyses The results are displayed in Table 3. Statistically signicant main effects for Time (changes from pretreatment to 6-month follow-up) were obtained for the following sleep parameters: sleep onset latency (F(1,45)=15.50, p0.001), WASO (F(1,45)=12.00, p0.001), total sleep time (F(1,45)=13.88, p0.001), daytime alertness (F(1,45)=4.67, p0.04), sleep efciency (F(1,45)=34.31, p0.001), and SII (F(1,45)=15.83, p0.001). The reduction in percent of nights with hypnotic use from pretreatment to 6-month follow-up was almost signicant (F(1,45)=3.22, p0.08). For life satisfaction the main effect of Time was non-signicant (F(1,44)=1.05, p0.30). There were no differences in the changes made from pretreatment to 6-month follow-up between the two interventions (TimeIntervention) on any of the parameters: sleep onset latency (F(1,45)=0.67, p0.41), WASO (F(1,45)=1.54, p0.22), total sleep time (F(1,45)=0.18, p0.67), daytime alertness (F(1,45)=0.37, p0.54), sleep efciency (F(1,45)=0.77, p0.38), SII

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148 Table 3 Group means and standard deviations at pretreatment, posttreatment and 6-month follow-up Pretreatment X (SD) Sleep onset latency (min) Sleep hygiene+stimulus control 83.12 (77.90) (n=23) Sleep hygiene+relaxation tape 72.02 (42.90) (n=24) Wake time after sleep onset (min) Sleep hygiene+stimulus control 55.71 (44.52) (n=23) Sleep hygiene+relaxation tape 48.89 (33.79) (n=24) Total sleep time (min) Sleep hygiene+stimulus control 345.7 (66.89) (n=23) Sleep hygiene+relaxation tape 341.8 (47.88) (n=24) Daytime alertness (15) Sleep hygiene+stimulus control 2.79 (0.60) (n=23) Sleep hygiene+relaxation tape 3.27 (0.74) (n=24) Sleep efciency [(total sleep time/time in bed) 100] Sleep hygiene+stimulus control 62.05 (12.21) (n=23) Sleep hygiene+relaxation tape 62.77 (8.46) (n=23) Sleep Impairment Index (735) Sleep hygiene+stimulus control 23.13 (4.56) (n=23) Sleep hygiene+relaxation tape 22.54 (3.56) (n=24) Percent of nights with hypnotic use Sleep hygiene+stimulus control 27.08 (36.26) (n=23) Sleep hygiene+relaxation tape 15.82 (32.94) (n=24) Life satisfaction (027) Sleep hygiene+stimulus control 16.68 (4.04) (n=22) Sleep hygiene+relaxation tape 19.54 (3.43) (n=24)
a

41

Posttreatment X (SD) 51.60 (48.57) 49.73 (29.20)

Follow up X (SD) 51.01 (39.01) 50.99 (35.92)

Effect sizea 0.52 0.53

43.13 (34.39) 35.00 (25.66)

36.66 (30.28) 39.89 (29.25)

0.50 0.27

377.6 (79.15) 370.3 (51.47)

374.0 (68.44) 377.4 (54.80)

0.42 0.69

3.09 (0.76) 3.52 (0.72)

3.07 (0.85) 3.42 (0.77)

0.38 0.20

74.34 (12.35) 70.17 (7.41)

72.83 (10.55) 70.74 (7.53)

0.94 1.00

20.13 (4.90) 19.17 (4.91)

20.00 (4.21) 19.54 (4.84)

0.71 0.71

22.82 (35.28) 15.30 (33.22)

19.55 (30.63) 14.15 (31.56)

0.22 0.05

18.55 (3.54) 19.92 (4.30)

17.64 (4.53) 19.63 (5.58)

0.22 0.02

The effect sizes are based on the difference between pretreatment and 6-month follow-up.

42

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

(F(1,45)=0.01, p0.93), percent of nights with hypnotic use (F(1,45)=1.31, p0.25), and life satisfaction (F(1,44)=.74, p0.39). From posttreatment to 6-month follow-up the main effects of Time were all non-signicant: sleep onset latency (F(1,45)=0.01, p0.93), WASO (F(1,45)=0.05, p0.81), total sleep time (F(1,45)=0.06, p0.80), daytime alertness (F(1,45)=0.53, p0.47), sleep efciency (F(1,44)=0.18, p0.67), SII (F(1,45)=0.05, p0.82), percent of nights with hypnotic use (F(1,45)=0.83, p0.36) and life satisfaction (F(1,45)=1.27, p0.27). There were no differences between the two interventions from posttreatment to 6-month followup (TimeIntervention) on any of the outcome variables: sleep onset latency (F(1,45)=0.05, p0.83), WASO (F(1,45)=2.79, p0.10), total sleep time (F(1,45)=0.63, p0.43), daytime alertness (F(1,45)=0.25, p0.62), sleep efciency (F(1,44)=0.87, p0.36), SII (F(1,45)=0.21, p0.65), percentage of nights with hypnotic use (F(1,45)=0.19, p0.66) and life satisfaction (F(1,45)=0.34, p0.56). 3.2.2. Clinical signicance Detailed results are displayed in Table 2. In all, 26.8% of the subjects with sleep onset insomnia improved from pretreatment to 6-month follow up. For maintenance insomnia 25.8% of the subjects obtained clinically signicant improvement at 6-months follow up. Of the seven subjects with early morning awakening none gained clinically signicant improvement at 6-months followup. In terms of clinically signicant improvement on at least sleep onset insomnia or sleep maintenance insomnia results showed that 10 of 23 subjects (43.4%) with sleep hygiene+stimulus control improved, while eight of 24 subjects (33.3%) with sleep hygiene+relaxation improved (c2=0.51, df=1, p0.47). Furthermore, eight of 24 subjects (33.3%) with compliance below mean improved compared to nine of 21 subjects (42.9%) above mean (c2=0.43, df=1, p0.51), six of 19 subjects (31.6%) using hypnotics improved against 12 of 28 subjects (42.9%) not using hypnotics (c2=0.60, df=1, p0.43), and two of eight subjects (25.0%) with secondary opposed to 16 of 39 subjects (41.0%) with primary insomnia improved (c2=0.72, df=1, p0.39). One subject got clinically worse on WASO from pretreatment to 6-months follow-up (see Table 4).
Table 4 Clinically signicant worsening of sleep onset insomnia and maintenance insomnia after treatment initation Variable At least 100% increase target behavior (%) Treatment outcome value30 min (%) At least 100% increase of target behavior and treatment outcome value30 min (%)

Clinically signicant worsening at posttreatment (% of subjects with no symptom at pretreatment who developed symptoms during treatment) according to three criteria Sleep onset insomnia 0.0 0.0 0.0 Maintenance insomnia 25.0 30.0 10.0 Clinically signicant worsening at 6 months follow up (% of subjects with no symptom at pretreatment who developed symptoms during treatment) according to three criteria Sleep onset insomnia 0.0 14.3 0.0 Maintenance insomnia 31.3 18.8 6.3

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

43

3.3. Stability Instability was detected in four and stability was detected in seven subjects in the sleep hygiene+stimulus control condition whereas the corresponding gures for sleep hygiene+relaxation were seven and two (c2=3.43 df=1, p0.07). None of the prognostic factors showed statistical signicant associations with stability. Compliance showed a trend toward signicant association with stability, as four subjects with compliance above mean showed instability, while six showed stability, whereas for subjects below mean in compliance seven showed instability and two stability (c2=2.77, df=1, p0.10). 4. Discussion The results indicate that the insomnia problems in the present sample did not improve during the waiting-list period, a nding in line with other studies employing waiting-list or placebo control conditions (Morin et al., 1993, 1999a). Following treatment, improvement was observed on several outcome measures. The improvement was more consistent when analyzing the overall changes from pre- to posttreatment, than comparing the changes from pre- to posttreatment for the immediate treatment group to the changes during waiting-list for the delayed treatment group. In terms of effect sizes the changes from pre- to posttreatment were 0.49 and 0.57 for sleep onset latency, which is somewhat higher than the overall effect size of 0.41 reported in the meta-analysis by Pallesen et al. (1998). However, the effect sizes for WASO of 0.36 and 0.44 in this study, are lower than the comparable effect size of 0.61 in the Pallesen et al. (1998) study. These results probably reect a relatively larger number of subjects with sleep onset insomnia in the present study, compared to studies included in the meta-analysis. Compared to the effect size of 0.15 for total sleep time in the meta-analysis, the effect sizes of 0.39 and 0.50 in the present study are superior. For sleep efciency and the SII the data from the present study also indicate distinct treatment gains. It is also worth noticing that the subjects reported improvements in daytime alertness following treatment. This nding runs counter to studies indicating that insomniacs are not sleep deprived (Chambers & Keller, 1993), and to studies indicating that hyperarousal is a central characteristic of insomniacs (Bonnet & Arand, 1997). However, the subjective data on daytime alertness was not corroborated by objective indicators of alertness in this study. Objectively measured daytime sleepiness is generally not elevated in people with insomnia (Riedel & Lichstein, 2000), but as few studies have investigated changes in objective measures of daytime alertness following insomnia treatment, this topic should be fully investigated in future studies. The ndings also indicated improvements in life satisfaction after treatment. Models emphasizing insomnia as a predictor of subsequent psychiatric distress have now been conrmed in prospective studies (Chang, Ford, Meas, Cooper-Patrick, & Klag, 1997). In sum, the results suggest that insomnia may act as a causal agent, inuencing several domains of daily living; underscoring the importance of insomnia prevention and treatment. The reduction in use of medication from preto posttreatment in the present study was signicant, but the effect sizes were small. Considering that the focus of the interventions did not include reduction of hypnotic use, this nding nevertheless indicates a positive side effect of the interventions. Analysis of clinically signicant improvement from pre- to posttreatment also underscores the effects of the interventions, but reveals that

44

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

only a minor portion of the subjects obtain such gains. It should, however, be kept in mind that the criteria for obtaining clinically signicant improvement was relative stringent. For subjects with early morning awakening the interventions did not seem to have any positive effect. Very few studies have addressed this topic, in spite of the fact that early morning awakening is a common problem among the elderly (Pallesen et al., 2001b). Studies of these problems should, therefore, be prioritized in the future, in terms of etiology, treatment and denitions. The relatively large portion of self-referred subjects suffering from sleep onset insomnia in this study was somewhat surprising, as maintenance insomnia and early morning awakening are considered to represent the most urgent problems in the older population (Miles & Dement, 1980; Pallesen et al., 2001b). From pre- to posttreatment there were no differential treatment effects on any parameter between the two interventions (sleep hygiene+stimulus control vs sleep hygiene+relaxation tape), but for two parameters (sleep efciency and life satisfactions) the differences approached signicance in favor of the sleep hygiene+stimulus control condition. Also, stability of clinically signicant improvement approached signicance in favor of sleep hygiene+stimulus control. The relatively lack of differential effects may be due to the fact that both interventions shared a common component (sleep hygiene). Additionally, there is also some overlap between sleep hygiene and stimulus control (Pallesen et al., 1998). In general, studies have shown relaxation procedures and stimulus control to have equal treatment effects, or superior effects for the latter (Morin et al., 1999b). Several patients also reported relatively low compliance to the two specic components of the interventions (stimulus control and relaxation tape), thus lowering the probability of obtaining differential treatment effects. The effect of compliance of clinically signicant improvement at posttreatment was nearly signicant, as was the effect of compliance on stability of clinically improvement. The issue of measurement and effects of compliance in treatment outcome of behavioral interventions for insomnia have received little attention up till now, but results indicate that compliance is positively related to outcome (Riedel & Lichstein, 2001). This topic should clearly be emphasized in future studies, using both self-report and objective measures. Changes from posttreatment to follow-up all were non-signicant, but changes from pretreatment to follow-up in general were signicant, showing that the treatment gains were stable and long-lasting, at least on the group level. The effect sizes obtained at follow-up in this study were 0.52 and 0.53 for sleep onset latency, 0.50 and 0.27 for WASO, and 0.42 and 0.69 for total sleep time, compared to 0.64 (sleep onset latency), 0.59 (WASO) and 0.37 (total sleep time) in the Pallesen et al. (1998) meta-analysis. Thus, the treatment gains seem comparable with the metaanalysis (Pallesen et al., 1998). Again, as the interventions did not aim at reduction in use of medication, such reduction could not be expected. Still, the reduction approached statistical signicance. The fact that changes from posttreatment to follow-up were non-signicant for all chosen parameters, strengthens the assumption that the signicant gains could be attributed to the interventions. The present ndings show that the subjects in the active treatment conditions improved compared to subjects on the waiting-list, and the treatment gains were maintained at 6-month followup, at least at the group level. The results, both at posttreatment and follow-up correspond fairly well to the results reported in the Pallesen et al.s (1998) meta-analysis of non-pharmacological interventions for insomnia in the elderly, despite that a higher proportion of subjects in the present

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

45

study had secondary insomnia or used hypnotic drugs. Thus, the external validity of this study seems relatively high, compared to the majority of studies in the meta-analysis (Pallesen et al., 1998). The results also indicate that subjects with secondary insomnia did obtain clinically signicant improvement at the same degree as subjects with primary insomnia. This nding is in line with studies showing that secondary insomniacs also benet from behavioral interventions. However, a central diagnostic issue that has been pointed out in this regard, is whether and to what degree, a present medical or psychiatric condition is causally related to the insomnia (Lichstein et al., 2000). As the present study only included 10 secondary insomniacs, the statistical power for demonstrating differential treatment outcome for primary and secondary insomniacs is very limited. However, compared to one of the best controlled trials of behavorial interventions for insomnia in the elderly (Morin et al., 1999a) the effects of the present study is substantially smaller, both in terms of effect sizes and in terms of clinical signicance. The reason for this may be that the present study belongs on the effectiveness side of the efcacy-effectiveness continuum (Espie et al., 2001), while the Morin et al. (1999a) study represents a typical efcacy study. Another explanation for the differences in effect may be that the Morin et al. (1999a) study employed a multicomponent approach, while the present study used a more limited set of interventions. The latter interpretation is in line with ndings from the Pallesen et al. (1998) meta-analysis. It seems therefore, that multicomponent intervention yields better results than treatment based on a more limited set of interventions. However, as only two (Epstein, 1998; Morin et al., 1999a) studies employing multicomponent interventions for elderly insomniacs have been conducted to date, such conclusion is in need of further conrming studies. To sum up, in the present study there were no differential effects of the two interventions (sleep hygiene+stimulus control vs sleep hygiene+relaxation tape) at neither posttreatment nor followup. The results indicate that the interventions improved general life satisfaction at posttreatment, but no permanent gains were shown at the follow-up. In general, measures related to daytime consequences of insomnia (daytime alertness and life satisfaction) showed lower treatment gains, expressed as effect sizes, compared to nocturnal variables (sleep onset latency, WASO etc.). Also, behavior not specically targeted by the interventions (medication use) showed relatively small changes at posttreatment and follow-up. It should also be emphasized that the changes were attained by very limited (430 min) interventions; thus the interventions seem to represent manageable approaches that could be employed by broad groups of health practitioners (Espie et al., 2001). Some limitations of the present study should, however, be noted. Findings were all based on self-reports from the participating subjects, while information from bed partners or objective sleep recordings that could validate the subjective reports are missing. This may represent a problem as studies, in general, have demonstrated inconsistencies between subjective and objective measures of sleep (Espie, 1991). However, the subjective data were emphasized because it is the subjective perception of poor sleep that prompts insomniacs to seek treatment in the rst place (Morin et al., 1999b). Likewise, self-reports of daytime alertness were not validated against objective measures. Another limitation of the present study is the fact that several subjects had low compliance to the interventions, thus lowering the studys internal validity. For the same reason the potential treatment effects of the interventions may be underestimated. The fact that 26% of all eligible subjects did not want to participate, an attrition rate of 16.7% during treatment, and

46

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

a further loss of 14.5% of the subjects at follow-up are also reasons for concern. These gures do, however, not deviate strongly from what could be expected in light of reported ndings from other studies (Davies, Lack, Storandt, & Bertelson, 1986; Morin & Azrin, 1988; Morin et al., 1999b; Riedel, Lichstein, & Dwyer, 1995). Due to the modest sample size, differential treatment effects between subgroups would be difcult to detect because of limited statistical power. Based on the present and former studies, some recommendations regarding research on elderly insomniacs seem to be in order. One recommendation is to focus on the possible need of modifying treatment procedures for use with the older population, in order to increase their acceptability for this population (Morin, Blais, & Momeault, 1998). Investigating the effects of multicomponent interventions should also become the focus of research on elderly insomniacs. Such procedures imply more exibility and mimic to greater extent ordinary clinical practice (Seligman, 1995), besides yielding very promising results (Epstein, 1998; Morin et al., 1999a). As effectiveness studies clearly are scarce in the eld, more intervention studies should be done with elderly subjects suffering from secondary insomnia and elderly using hypnotics. To strengthen the effectiveness paradigm more studies should also be conduced in the context of ordinary clinical practice (Espie et al., 2001). As some subjects suffering from chronic insomnia use hypnotics for much longer periods of time than recommended, the potential and tailoring of behavioral interventions for reduction of hypnotic use should be explored. Future studies should also more strongly emphasize the daytime (e.g. daytime alertness) impacts of insomnia treatment of elderly insomniacs, and more attention should be paid to the problem of compliance and patient characteristics related to treatment response. Interventions targeting early morning insomnia should also receive increased attention in future studies.

References
APA (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: American Psychiatric Association. Aragona, M. (2000). Abuse, dependence, and epileptic seizures after zolpidem withdrawal: Review and case report. Clinical Neuropharmacology, 23, 281283. Bech, P., Gudex, C., & Johansen, K. S. (1996). The WHO (ten) well-being index: Validation in diabetes. Psychotherapy and Psychosomatics, 65, 183190. Bliwise, D. L. (1991). Treating insomnia: Pharmacological and nonpharmacological approaches. Journal of Psychoactive Drugs, 23, 335341. Bonnet, M. H., & Arand, D. L. (1997). Hyperarousal and insomnia. Sleep Medicine Reviews, 1, 97108. Bootzin, R. R., & Nicassio, P. M. (1978). Behavioral treatments for insomnia. In M. Hersen, R. Eissler, & P. Miller (Eds.), Progress in behavior modication (Vol. 6) (pp 145). New York: Academic Press. Chambers, M. J., & Keller, B. (1993). Alert insomniacs: Are they really sleep deprived? Clinical Psychology Review, 13, 649666. Chang, P. P., Ford, D. E., Mead, L. A., Cooper-Patrick, L., & Klag, M. J. (1997). Insomnia in young men and subsequent depression. American Journal of Epidemiology, 146, 105114. Davies, R., Lacks, P., Storandt, M., & Bertelson, A. D. (1986). Countercontrol treatment of sleep-maintenance insomnia in relation to age. Psychology and Aging, 1, 233238. Epstein, D. R. (1998). Short- and long term effects of behavioral intervention for insomnia in older adults. Unpublished manuscript. Espie, C. A. (1991). The psychological treatment of insomnia. Chichester: Wiley. Espie, C. A., Inglis, S. J., & Harvey, L. (2001). Predicting clinically signicant responses to cognitive behavior therapy

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

47

for chronic insomnia in general medical practice: Analyses of outcome data at 12 months posttreatment. Journal of Consulting and Clinical Psychology, 69, 5866. First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. B. W. (1995). Structural clinical interview for DSM-IV axis I disorders. New York: Biometrics Research Department. Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). Mini-mental state: A practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12, 189198. Friedman, L., Benson, K., Noda, A., Zarcone, V., Wicks, D. A., OConnell, K., Brokks, J. O., Bliwise, D. L., & Yesavage, J. A. (2000). An actigraphic comparison of sleep restriction and sleep hygiene treatments for insomnia in older adults. Journal of Geriatric Psychiatry and Neurology, 13, 1727. Grad, R. M. (1995). Benzodiazepines for insomnia in the community-dwelling elderly: A review of benet and risk. The Journal of Family Practice, 41, 473481. Hajak, G. (1999). A comparative assessment of the risks and benets of zopiclone a review of 15 years clinical experience. Drug Safety, 21, 457469. Hauri, P. J. (1991). Case studies in insomnia. New York: Plenum Medical Book Company. Hauri, P. J. (2000). Primary insomnia. In M. H. Kryger, T. Roth, & W. C. Dement (Eds.), Principles and practice of sleep medicine (3rd ed.) (pp. 633639). Philadephia: W.B. Saunders. Hening, W., Allen, R., Earley, C., Kushida, C., Picchietti, D., & Silber, M. (1999). The treatment of restless legs syndrome and periodic limb movement disorder. Sleep, 22, 970999. ppler, C., Schramm, E., Riemann, D., Weyerer, S., & Berger, M. (1994). Sleep onset insomnia, sleep Hohagen, F., Ka maintaining insomnia and insomnia with early morning awakening temporal stability of subtypes in a longitudinal study on general practice attenders. Sleep, 17, 551554. Holm, K. J., & Goa, K. L. (2000). Zolpidem an update of its pharmacology, therapeutic efcacy and tolerability in the treatment of insomnia. Drugs, 59, 865889. Holte, A. (1989). The Holte sleeping technique: An experimental study. Scandinavian Journal of Psychology, 30, 4651. Holte, A. (Speaker). (1992). Learning to sleep. Professor Holtes Sleeping Technique. (Cassette Recording). Oslo: Norwegian Psychological Association. Kales, A., Soldatos, C. R., Bixler, E. O., & Kales, J. D. (1983). Rebound insomnia and rebound anxiety: A review. Pharmacology, 26, 121137. Lacks, P., & Morin, C. F. (1992). Recent advances in the assessment and treatment of insomnia. Journal of Consulting and Clinical Psychology, 60, 586594. Lader, M. (1991). History of benzodiazepine dependence. Journal of Substance Abuse Treatment, 8, 5359. Lichstein, K. L., & Riedel, B. W. (1994). Behavioral assessment and treatment of insomnia: A review with an emphasis on clinical application. Behavior Therapy, 25, 659688. Lichstein, K. L., Riedel, B. W., Wilson, B. W., Lester, K. W., & Aguillard, N. (2001). Relaxation and sleep compression for late-life insomnia: A placebo-controlled trial. Journal of Consulting and Clinical Psychology, 69, 227239. Lichstein, K. L., Wilson, N. M., & Johnson, C. T. (2000). Psychological treatment of secondary insomnia. Psychology and Aging, 15, 232240. Miles, L. E., & Dement, W. C. (1980). Sleep and aging. Sleep, 3, 119220. Morin, C. M. (1993). Insomnia. Psychological assessment and management. New York: Guilford Press. Morin, C. M., & Azrin, N. H. (1988). Behavioral and cognitive treatments of geriatric insomnia. Journal of Consulting and Clinical Psychology, 56, 137146. Morin, C. M., Blais, F. C., & Mimault, V. (1998). Sleep disturbances in late life. In M. Hersen, & V. B. van Hasselt (Eds.), Handbook of clinical geropsychology (pp. 273299). New York: Plenum Press. Morin, C. M., Colecchi, C., Stone, J., Sood, R., & Brink, D. (1999a). Behavioral and pharmacological therapies for late-life insomnia. A randomized controlled trial. Journal of American Medical Association, 281, 991999. Morin, C. M., Culbert, J. P., & Schwartz, S. M. (1994). Nonpharmacological interventions for insomnia: A metaanalysis of treatment efcacy. American Journal of Psychiatry, 151, 11721180. Morin, C. M., Hauri, P. J., Espie, C. A., Spielman, A. J., Buysse, D. J., & Bootzin, R. R. (1999b). Nonpharmacological treatment of chronic insomnia. Sleep, 22, 11341156. Morin, C. M., Kowatch, R. A., Barry, T., & Walton, E. (1993). Cognitive-behavior therapy for late-life insomnia. Journal of Consulting and Clinical Psychology, 61, 137146.

48

S. Pallesen et al. / Behaviour Research and Therapy 41 (2003) 3148

Murtagh, D. R. R., & Greenwood, K. M. (1995). Identifying effective psychological treatments for insomnia: A metaanalysis. Journal of Consulting and Clinical Psychology, 63, 7989. National Institutes of Health. (1984). Drugs and insomnia. The use of medication to promote sleep. Journal of American Medical Association, 251, 24102414. Noble, S., Langtry, H. D., & Lamb, H. M. (1998). Zopiclone an update of its pharmacology, therapeutic efcacy and tolerability in the treatment of insomnia. Drugs, 55, 277302. Pallesen, S., Nordhus, I. H., Havik, O. E., & Nielsen, G. H. (2001a). Clinical assessment and treatment of insomnia. Professional Psychology. Research and Practice, 32, 115124. Pallesen, S., Nordhus, I. H., & Kvale, G. (1998). Nonpharmacological interventions for insomnia in older adults: A meta-analysis of treatment efcacy. Psychotherapy, 35, 472482. Pallesen, S., Nordhus, I. H., Nielsen, G. H., Havik, O. E., Kvale, G., Johnsen, B. H., & Skjtskift, S. (2001b). Prevalence of insomnia in the adult Norwegian population. Sleep, 24, 771779. Riedel, B. W., & Lichstein, K. L. (2000). Insomnia and daytime functioning. Sleep Medicine Reviews, 4, 277298. Riedel, B. W., & Lichstein, K. L. (2001). Strategies for evaluating adherence to sleep restriction treatment for insomnia. Behaviour Research and Therapy, 39, 201212. Riedel, B. W., Lichstein, K. L., & Dwyer, W. O. (1995). Sleep compression and sleep education for older insomniacs: Self-help versus therapist guidance. Psychology and Aging, 10, 5463. Roehrs, T., Merlotti, L., Zorick, F., & Roth, T. (1994). Sedative, memory, and performance effects of hypnotics. Psychopharmacology, 116, 130134. Salzman, C. (1982). Key concepts in geriatric psychopharmacology. Psychiatric Clinic of North America, 5, 181190. Schneider-Helmert, D. (1988). Why low-dose benzodiazepine-dependent insomniacs cant escape their sleeping pills. Acta Psychiatrica Scandinavica, 78, 706711. Seligman, M. E. P. (1995). The effectiveness of psychotherapy the consumer reports study. American Psychologists, 50, 965974. Soldatos, C. R. (1994). Insomnia in relation to depression and anxiety epidemiologic considerations. Journal of Psychosomatic Research, 38, 38. Spielman, A. J., Saskin, P., & Thorpy, M. J. (1987). Treatment of chronic insomnia by restriction of time in bed. Sleep, 10, 4556. Wilkinson, L., & the Task Force on Statistical Inference. (1999). Statistical methods in psychology journals: Guidelines and explanations. American Psychologists, 54, 594604. Wooten, V. (1994). Medical causes of insomnia. In M. H. Kryger, T. Roth, & W. C. Dement (Eds.), Principles and practice of sleep medicine (2nd ed.) (pp. 509522). Philadephia: W.B. Saunders. Zammit, G. K., Weiner, J., Damato, N., Sillup, G. P., & McMillan, C. A. (1999). Quality of life in people with insomnia. Sleep, 22(Suppl. 2), 379385. Zarcone, V. P. (2000). Sleep hygiene. In M. H. Kryger, T. Roth, & W. C. Dement (Eds.), Principles and practice of sleep medicine (3rd ed.) (pp. 657661). Philadephia: W.B. Saunders.