【著者(Authors)】 Rengang Wua, Jinfeng Baob, Chungai Zhangc, Jun Dengc, Chunling Longc
【来源(Source)】 Psychotherapy and Psychosomatics 2006; 75(4): 220-8
【关键词(Keywords)】 Cognitive-behavior therapy,Pharmacological therapy,Combined therapy,Chronic insomnia therapies
【摘要(Abstract)】：
Background Previous studies of insomnia focused mainly on the improvement of sleep condition and ignored the effects of sleep-related psychological activity and daytime function after pharmacological and behavioral treatments. We compared the clinical effects of both therapies on sleep condition, sleep-related psychological activity and daytime function in chronic insomnia.
Methods Seventy-one patients with chronic insomnia were randomly divided into 4 groups and either received cognitive-behavior therapy (CBT, n = 19), pharmacological therapy (PCT, n = 17), CBT plus medication (Combined, n = 18) or placebo (n = 17). The treatments lasted for 8 weeks with follow-ups conducted at 3 and 8 months. On the day after treatment ended, all patients were assessed using a polysomnogram (PSG), a sleep diary and a psychological assessment.
Results The three active treatments were more effective than placebo at the time the treatments were completed. Subjective sleep-onset latency, sleep efficacy and total sleep time were better in the PCT group than in the CBT group. At the 3-month follow-up, subjective and objective sleep-onset latency, sleep efficacy and total sleep time were better in the CBT group than in both the PCT and the Combined group. At the 8-month follow-up, the CBT group showed a steady comfortable sleep state, while the PCT and Combined groups were gradually returning to the pre-treatment condition. The Combined group showed a variable long-term effect. On the other hand, pre-sleep arousal at nighttime, dysfunctional beliefs about sleep as well as daytime functioning in the CBT group not only improved, but was better than in the other active treatment groups.
Conclusion Medication and Combined therapy produced a short-term effect on chronic insomnia while CBT had a long-term effect of improved sleep-related psychological activity and daytime functioning.
Keywords: Cognitive-behavior therapy, Pharmacological therapy, Combined therapy, Chronic insomnia therapies.
Table of contents
Introduction
Insomnia, the most common sleep disorder, may involve problems falling asleep, frequent or prolonged nocturnal awakenings or early morning awakenings with an inability to return to sleep. Most insomniacs are treated with various medications when they initially visit their doctors [1,2,3,4]. Short-term use of hypnotic medication is useful and especially indicated for acute insomnia [1, 3, 5, 6]as it has immediate effects that help to shorten patients' sleep-onset latency, nocturnal awakenings, prolong total sleep time and improve sleep efficiency. However, there is little information on the long-term efficacy of hypnotic medication and its role in the management of chronic insomnia [6]. A meta-analysis of 22 placebo-controlled hypnotics trials with 1,894 patients concluded that benzodiazepines and zolpidem produced improvements in sleep-onset latency, number of awakenings, total sleep time and sleep quality [6]; however, drug treatment lasted only 1 week and follow-up was often limited to evaluating withdrawal effects 1 or 2 nights after drug discontinuation. Taking hypnotic medication over long periods of time carries additional risks of physical dependence, withdrawal, and rebound insomnia [7, 8]. The adverse-effect profile of most medications shows daytime sedation, motor incoordination and cognitive impairment such as anterograde amnesia [9]. Therefore, in 1984, The US National Institutes of Health Consensus Conference on Sleeping Pills and Insomnia developed guidelines aimed at discouraging the use of sedative hypnotics beyond 4-6 weeks due to concerns raised over drug misuse, dependency, withdrawal, and the threat of rebound insomnia [10].
Several nonpharmacological interventions have been shown to be effective for the clinical management of insomnia [11,12,13]. Cognitive-behavior therapy (CBT) seeks to change poor sleep habits, alter false beliefs and attitudes about sleep, reduce physical arousal at nighttime and promote sleep hygiene practices [13,14,15]. Two meta-analyses of more than 50 treatment studies (>2,000 patients) concluded that behavioral interventions improve sleep in about 70-80% of patients with primary insomnia. With an average treatment duration of 5 h implemented over a 4-week period, sleep-onset latency and nocturnal wake were reduced to normative values (i.e. <30 min) [16,17,18]. One particular strength of behavioral therapies is that sleep improvement is maintained over time.
Only five studies have directly compared the efficacy of behavioral, pharmacological and combined treatments of insomnia. These studies have shown that drug treatment produced faster improvements while behavioral treatment yielded more durable benefits [19,20,21,22,23]. The finding by Morin [22] indicates that behavioral and pharmacological therapies, alone or in combination, are effective in short-term management of late-life insomnia; follow-ups conducted 3-12 months after treatment showed that behavior therapy yielded the most durable improvements and that pharmacological therapy lost its benefits over time. Smith [24] suggests that CBT is much more effective for both sleep onset and sleep maintenance, although its benefits develop more slowly than those of pharmacotherapy. A trial by Jacobs et al. [23] showed that combined treatment provides no advantage over CBT alone. However, these theses only focused on the improvement of sleep condition and ignored the effects on sleep-related psychological activity and daytime functioning. As we know, chronic insomniacs usually report elevated pre-sleep arousal at nighttime as well as dysfunctional beliefs and attitudes about sleep. For example, many patients feel anxious, depressed and experience intrusive thoughts when they cannot fall asleep. Waters et al. [25] suggested that sleep-related psychological activity is one of the most important contributors to the change of occasional insomnia into chronic insomnia [see also [26]. Hence the effects of CBT and hypnotic medication on psychological activity merit further investigation.
We wanted to test this hypothesis and hence chose chronic insomniacs as trial participants, recorded subjective and objective sleep parameters and screened the psychological activities of our patients. Our trial focused on the following three items: (1) comparison between the effects of CBT and medication, involving both short-term and long-term results; (2) comparison between the effects of CBT and medication on pre-sleep arousal at nighttime, dysfunctional beliefs and attitudes about sleep as well as daytime functioning, and (3) the effect of comprehensive treatment involving CBT and medication.
Methods
Participants
Patients were recruited through newspaper advertisements and letters to physicians. Prospective patients underwent a multi-step screening evaluation that consisted of (1) a sleep history interview by a clinical psychiatrist and a physician; (2) a psychological assessment by a clinical psychologist, and (3) a physician's review of the patient's medical history. Each step of the screening evaluation used ICSD and DSM-IV criteria for primary and chronic insomnia [27, 28]. Diagnosis inclusion criteria were (1) patient complaints that he/she had difficulties in falling or staying asleep, sleep-onset latency and/or waking periods after sleep-onset lasting longer than 30 min per night; (2) that such sleep disorders occurred at least 3 times/week and had lasted >6 months, and (3) that the sleep disturbance caused evident distress or influenced daytime functioning. Exclusion criteria included (1) evidence that the insomnia was directly related to a medical disorder or adverse effects of medication; (2) the presence of sleep apnea or periodic limb movements during sleep; (3) regular use of hypnotic medication or other psychotropic medication with an inability or unwillingness to discontinue medication; (4) current participation in psychotherapy; (5) major depression or other severe psychopathologic condition, as assessed by a brief self-report screening measure, and (6) unresolved life or mental conflicts (excluding a fear towards sleep) within the previous 6 months.
Most (n = 51, 66.2%) patients reported mixed sleep-onset and sleep maintenance staying asleep insomnia, 19 (24.6%) reported sleep maintenance insomnia only, and 7 (9%) reported sleep-onset insomnia only. Seventy-seven voluntary outpatients were selected. He/she had to be willing to accept treatment with hypnotic drugs or psychological therapy for their sleep disorder. All patients provided written informed consent prior to study entry. The 77 patients were randomly divided into 4 groups: the CBT group (n = 19), the pharmacological therapy group (PCT, n = 20), a combined CBT and PCT (Combined, n = 19) and a placebo group (n = 19). There were 36 males and 41 females, average age was 38 ± 12 years.
Treatments
All treatments lasted 8 weeks.
PCT Group. Patients assigned to the active medication group were prescribed with temazepam to be taken 1 h before bedtime, the initial dosage of the first week was 7.5 mg per night, which was gradually increased, up to 30 mg per night (maximum over a 6-week frame), and then reversed to 15 mg in the last week in order to cut down physical dependence at drug withdrawal as much as possible.
CBT Group. Each patient received CBT two times a week. The behavioral content involved stimulus control procedures and sleep restriction therapy [29]. The stimulus control procedures were designed to regulate the sleep-wake schedules and to bring subjects to reassociate the bed/bedroom and bedtime stimuli with sleep rather than with the frustration and anxiety associated with lying in bed trying to fall sleep. Sleep restriction therapy consisted of curtailing the amount of time spent in bed to approximately match the subjective amount of time asleep. The cognitive component was designed to alter the false beliefs and attitudes that often exacerbate insomnia. Sleep hygiene recommendations included a discontinuation of caffeine and nicotine 4-6 h before bedtime, avoidance of alcohol as a sleeping aid, exercising 5-6 h while finishing at last 3 h before bedtime, and minimizing noise, light, and excessive temperature during the sleep period.
Combined Group. Patients received CBT and medication at the same time. Their CBT largely followed that of the CBT group; however, the instructions on taking the prescribed medication were the same as for the PCT group.
Placebo Group. Patients of this group each took placebo tablets made of corn starch that looked identical to the medication of the PCT group.
Therapists and patients were blinded to tablet content in all three tablet-taking groups.
Assessments
Sleep Parameters. Patients slept in the laboratory at their normal bedtimes. Shortly after the introductory/practice day, each subject spent 3 nights and 2 days in the laboratory. During those 3 nights, a standard clinical polysomnogram (PSG) with two eye channels, central and occipital electroencephalographic channels, chin and leg electromyographic as well as electrocardiographic channels was used. Air flow and chest movements were recorded as objective parameters. To avoid CBT effects, bedtime was not prescribed and PCT and placebo patients had a TV in their room at all times, even when the PSG was being recorded. The clinical interview and sleep diaries were used to assess the subjective parameters, which included bedtime, sleep-onset latency, total sleep time and sleep efficiency ratio (defined as the total time spent asleep in contrast to the actual time spent in bed), multiplied by 100.
Psychological and Daytime Functioning Assessment. (1) Pre-sleep arousal scale (PSAS), which includes 16 questions for the assessment of the somatic (questions 1-8) and cognitive subscales (questions 9-16), scored 0-4 [30]; (2) dysfunctional beliefs and attitudes about sleep (DBAS) scale to assess consequences of insomnia (theme 1), sleep control (theme 2), sleep requirement expectations (theme 3), causal attribution of insomnia (theme 4), sleep-promoting activities (theme 5) [31], and (3) a questionnaire from PSQI to assess daytime dysfunction [32].
Therapists
The CBT group was treated by a licensed clinical psychologist, a manual was used during each session. Therapists had previously undergone training in sleep CBT and had independently treated 3 insomniacs using the manual before participating in this study. Two psychiatry residents handled medication and placebo treatment.
Procedures
Subjective and objective sleep parameters were recorded for patients of each group. Parameters included the PSAS, the DBAS, and a daytime dysfunction questionnaire administered just before treatment, on the day treatment stopped as well as during 3- and 8-month follow-ups. Patients were instructed to complete their sleep diaries and record pre-sleep arousal every morning. They had to complete their DBAS and daytime dysfunction questionnaire during the day.
To avoid sleep hygiene untypical for the PCT and placebo groups, these patients were allowed to engage in any activity before going to bed in the sleep lab and there were no rules for bedtime.
Data Analysis
Statistical analyses were performed with SPSS 10.0; ANOVA was used to calculate differences between the four groups. A descriptive examination of the variables was performed, and differences in sleep parameters (sleep-onset latency, sleep efficiency and total sleep time) were recorded. We wanted to determine whether or not the active treatments were more effective than placebo, whether a combined CBT and pharmacological approach was better than either treatment alone, and whether or not there were different degrees of improvement over time across treatment modalities.
Results
Out of the 77 patients who took part in the study, 71 completed the treatment protocol, 6 dropped out prior to the mid-treatment phase (CBT = 0; PCT = 3; Combined = 1; placebo = 2). Of the 6 drop-outs, 3 (PCT) discontinued treatment because of adverse effects, and 3 (1 Combined and 2 placebo) refused to continue medication because of a lack of efficacy. There were no significant differences in demographic or clinical variables between patients who completed and those who dropped out of the study. Thus the results are based on 71 subjects: CBT = 19, PCT = 17, Combined = 18, placebo = 17.
Sleep Data
Table 1 shows that significant differences exist between the subjective and objective sleep parameters during the assessment period. ANOVA analyses confirmed the differences between the four groups. No significant differences were found for sleep-onset latency, sleep efficiency and total sleep time before treatment; however, on the last day of treatment these parameters differed significantly between the four groups. Least significant difference (LSD) tests of both subjective and objective sleep-onset latency showed that the PCT group experienced shorter latency times than the CBT group (p < 0.001 and p < 0.01, respectively) (fig. 1); the subjective and objective sleep efficiency was greater in the PCT than in the CBT group (p < 0.01, p < 0.05), and the subjective and objective total sleep time were longer in the PCT than in the CBT group (p < 0.01, p < 0.004). Post-hoc comparisons revealed that subjects in all three active treatment groups had significantly more improved than those in the placebo group (p < 0.01 for all three groups). Yet sleep-onset latency, sleep efficiency and total sleep time at the third month of follow-up were still significantly improved in all four groups. LSD test of both subjective and objective sleep-onset latency revealed that the CBT group had shorter latency periods than the PCT group (p < 0.003, p < 0.004), that the subjective and objective sleep efficiency of the CBT group was greater than of the PCT group (p < 0.05, p < 0.01) and that the subjective and objective total sleep time was longer in the CBT group than in the PCT group (p < 0.01, p < 0.05) (fig. 2). Similar significances between the four groups were obtained at the 3- and the 8-month follow-ups.
Table 1.
Fig 1.
Fig 2.
Sleep Diaries. There was a significant difference between groups in improved sleep-onset latency from pre-treatment to post-treatment (F3,67 = 4.73, p = 0.005), with the highest (67%) for the Combined group, followed by the PCT (64%), CBT (57%) and placebo group (15%). The proportions of patients who met normal sleep criteria (sleep-onset latency ≤30 min and sleep efficiency ≥85%) after treatment were 9/18 (50%) for the Combined group, 7/19 (36%) for the CBT group, 6/17 (35%) for the PCT group and 2/17 (12%) for the placebo group. There was no significant difference (p > 0.05) between CBT and PCT patients. However, there was a difference (p < 0.04) between CBT and placebo patients.
Sleep-Related Psychological Activity
There were no differences between the four groups in dysfunctional beliefs and attitudes about sleep on the subscale themes 1 and 4 before and after treatment, and on the 3- and 8-month follow-ups (all >0.05).
Table 2 shows patients' changes in pre-sleep arousal, dysfunctional beliefs and attitudes about sleep and daytime dysfunction before and after treatment. ANOVA analyses, which confirmed the differences between the four groups for pre-sleep arousal, dysfunctional beliefs and attitudes about sleep and daytime dysfunction (using the same dependent measures), yielded no significant differences between all groups for pre-sleep arousal on the somatic and cognitive subscales, dysfunctional beliefs and attitudes about sleep or daytime dysfunction before treatment. However, significance was obtained for dysfunctional beliefs and attitudes about sleep for themes 2, 3 and 5 as well as daytime dysfunction immediately after treatment. LSD test for themes 2, 3 and 5 was lower in the CBT than in the PCT group (p < 0.05, p < 0.003, p < 0.001); post-hoc comparisons of the somatic and cognitive subscales of pre-sleep arousal revealed that subjects in all 3 intervention groups had significantly more improved than those on placebo (p < 0.01 for all three treatment groups). Significant differences between the four groups were found at 3- and 8-month follow-up.
Table 2.
Discussion
At the time of treatment completion, CBT and PCT therapies, alone or in combination, were effective in the short-term management of chronic insomnia. The three active treatments were more efficient than placebo. Average sleep-onset latency of the three active treatment groups was below 30 min according to PSG. However, the short-term effect of CBT was lower than that of PCT, subjective and objective sleep-onset latencies in the PCT group were shorter than in the CBT group. Subjective sleep-onset latency in the CBT group was still more than 30 min. As for long-term effects, CBT patients showed the greatest improvements at the 3-month follow-up, and their sleep parameters were better than in the other three groups. The subjective and objective sleep-onset latency in CBT group was less than 30 min, sleep efficiency and total sleep time was higher than 85% and 6 h, respectively. By contrast, these three sleep parameters gradually relapsed to pre-treatment levels in PCT patients: the average sleep-onset latencies were 47.2 min (subjective) and 36 min (objective) and sleep efficiency was lower than 80%, i.e. at the diagnostic level of insomnia. Follow-up results revealed that CBT yielded the most durable improvements in sleep parameters. Our results were similar to Jacobs et al.'s [23] in that their CBT patients also showed no significant change in sleep-onset latency at 1-, 3-, 6-, or 12-month follow-up compared with immediate post-treatment levels, and also showed no change in sleep efficiency at 6-month and 12-month follow-up. PCT loses its clinical benefits over time.
At the 8-month follow-up, the sleep condition of the CBT group still remained at the same level as at 3 months, while PCT patients had returned to their baseline sleeping difficulties. However, there was no evidence that CBT also continued to prolong total sleep time. At all time points after treatment, total sleep time of the CBT group was never more than 7 h. This finding is similar to the results of Morin et al. [17]; either CBT only improves sleep-onset latency and efficiency or, perhaps, insomniacs are a group of people that only need short amounts of sleep.
Apart from the differences in sleeping conditions, the four groups also differed in pre-sleep arousal at nighttime, dysfunctional beliefs and attitudes about sleep as well as daytime dysfunction. Cognitive arousal at nighttime was more strongly associated with sleep-onset latency and waking periods during the night [33, 34]. Our findings indicate that the pre-sleep arousal scores of the CBT group were lower than those of the PCT group after treatment and that CBT patients had a decrease in anxiousness, depression and intrusive thoughts. Though the total sleep time was lower in the CBT than in the PCT group after treatment, the daytime dysfunction scores of the CBT group were similar to the PCT group, indicating that CBT patients had improved sleep quality, resulting in improved daytime functioning that lasted until the 8-month follow-up. Jacobs et al.'s [23] trial showed that there were no significant differences between the groups in changes in daytime mood before and after treatment, which may have contributed to a floor effect. There were no significant differences in the dysfunctional beliefs and attitudes about sleep [for themes 2 (sleep control), 3 (sleep requirement expectations) and 5 (sleep-promoting activities)] in the PCT group before and after treatment, which means that the PCT did not effectively change the dysfunctional beliefs and attitudes about sleep. The remaining high level of pre-sleep arousal and dysfunctional beliefs in the PCT group may cause a relapse once medication is stopped. At the 3- and 8-month follow-ups we found that the CBT patients held lower steady levels of pre-sleep arousal at nighttime and of daytime dysfunction, while PCT patients gradually reverted to their pre-treatment condition of having nervous, tight and tense feelings about their body, worrying about falling asleep at night, spending too much time in bed while not experiencing any drowsiness, trying too hard to sleep while daytime functioning gradually decreased (daytime dysfunction scores increased). Morin et al. [31] suggested that dysfunctional beliefs and attitudes about sleep may underlie and support anxiety and habits that disrupt the sleep process and that, because the PCT has not demonstrated a clear change in the sleep-related psychological activity, its long-term effect may be limited.
Many people are more interested in a combination of CBT and PCT, believing that it optimizes both [21,22,23, 35]. We found that the Combined group showed greater improvement rates than either CBT or PCT alone immediately after completion of treatment. Reduction of sleep-onset latency and increase of sleep efficiency were highest, and Combined treatment also yielded the greatest number of normal sleepers as measured by a subjective and objective sleep-onset latency of 30 min or less and a sleep efficiency of 85% or more. This was different from Jacobs et al.'s [23] results, which indicated that CBT yielded the greatest number of normal sleepers after treatment. We think this was due to the combined effects of the hypnotic drug and the CBT sleep restriction in the Combined group. Nevertheless, the long-term effects in the Combined group were not as good as expected. Sleep levels Between treatment completion and 3-month follow-up, objective sleep levels fell (PSG measured), sleep-onset latency prolonged from 17 to 42 min and sleep efficiency decreased from 87 to 75%, i.e. returned to pre-treatment levels. It seems that the changes in sleep processes in the Combined group are mainly due to medication and that CBT exerted no real long-term influence in this group. Combined therapy might result in negative attribution, with patients inclined to attribute sleep improvement to drug effect but not to CBT, which hampers the development of cognitive-behavior techniques. For example, many patients of the Combined group thought that their sleep-onset latency shortened and pre-sleep arousal at nighttime lessened not because of their own mental regulation but exclusively because of the medication. Jacobs et al. [23] suggested that Combined patients may believe less in CBT and therefore are more vulnerable to relapses. Pre-sleep arousal scores of Combined patients were lower only immediately after treatments finished. At the 3- and 8-month follow-ups the pre-sleep arousal scores increased all over again, and Combined patients again felt emotional confusion and helplessness, entering the vicious circle of sleep disorder. Hauri [21] suggested that insomnia is best treated with a cognitive-behavior approach alone, or a sequential approach for integrating behavior and drug therapies. Medication would be initiated first and behavioral treatment introduced or continued when the drugs are discontinued, and this may prove a more effective method than simultaneous initiation and discontinuation of both treatment modalities.
The difference in treatment cost is likely to be a major consideration in China. CBT is by far the most expensive option. For example, in China, a 56-day trial of temazepam costs approximately USD 30 (office visit once a week for 8 weeks at $16; 56 tablets at USD 0.25/30 mg), compared with CBT at USD 120 (two psychotherapy sessions every week for 8 weeks). However, we must consider the consequences of discontinued treatment and the possibility that the long-term benefits of CBT might offset the short-term premium by reducing indirect costs.
Conclusions
To sum up: in comparison, CBT has better long-term results than medication for sleep condition and daytime functioning; Combined treatment is not as good as the individual therapies alone. At the same time, patients who had received CBT enjoyed healthier attitudes about sleep as well as other improvements, such as less pre-sleep arousal at nighttime and accurate beliefs and attitudes about sleep. Pharmacological therapy cannot effectively change sleep-related psychological activities. Hypnotic medication has beneficial short-term effects, but insomnia symptoms reappear once treatment is withdrawn. Possible reasons may be that hypnotic drugs alter the endogenous biorhythm of the human body and calm psychological distress about sleeping. Still, medication is not as effective as CBT in the long run.
Acknowledgement
This study was supported by the Beijing Institute of Mental Health (grant 2002BMH3872).
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