J Behav Med (2009) 32:244–254 DOI 10.1007/s10865-008-9198-8
Non-pharmacological treatments for insomnia Matthew R. Ebben Æ Arthur J. Spielman
Accepted: December 22, 2008 / Published online: January 24, 2009 Ó Springer Science+Business Media, LLC 2009
Keywords Insomnia Behavioral treatments Sleep restriction Stimulus control Sleep hygiene CBT-I
the population suffers with insomnia (Ohayon 2007). According to the criteria of the International Classification of Sleep Disorders (American Academy of Sleep Medicine 2005), insomnia is defined by a complaint of difficulty initiating or maintaining sleep, waking up too early or sleep that is consistently unrefreshing. Of course, the individual needs to have set aside an ample opportunity to sleep. The sleeping difficulty should also be accompanied by daytime impairment, such as difficulty concentrating, memory difficulties, fatigue, stomach problems, irritability and/or reduced motivation. Studies investigating the impact of chronic insomnia have shown, reduced quality of life, higher absenteeism, impaired job performance, and higher healthcare utilization (Kuppermann et al. 1995; Simon and VonKorff 1997).
Definition and prevalance of insomnia
Co-morbidity of insomnia
Insomnia is one of the most prevalent health concerns worldwide. Current estimates indicate that 6% to 15% of
Co-morbidity of insomnia and psychiatric illness has long complicated the treatment of insomnia. In fact, insomnia is a common symptom in many psychiatric disorders such as anxiety disorders, depression, bipolar disorder, and psychosis (to name just a few) (Ebben and Fine in press). A thorough evaluation of the association between insomnia and psychiatric illness is beyond the scope of this paper. However, we would like to briefly touch on the association between insomnia and its relationship with anxiety and depression because it is commonly seen in clinical practice. Anxiety is one of the most frequent associated features of insomnia. Insomniacs have a 17 times greater risk of suffering from anxiety than those without insomnia (Taylor et al. 2005). Moreover, generalized anxiety disorder is present in 44% of insomniacs (Ohayon and Roth 2003). In Benca et al. meta-analysis (1992) (with a combined
Abstract Insomnia is a common disorder effecting millions of people worldwide. Currently most individuals suffering from insomnia take medications to help them sleep. However, there are a variety of behavioral treatments, which have been shown to be effective in empirical studies that offer many advantages over medications. In addition, behavioral treatments have been shown to be more effective long-term than medication. This paper reviews the principles and practice of these behavioral treatments. At the end of the paper there is also a brief discussion of circadian rhythm disorders that can mimic insomnia.
M. R. Ebben (&) Department of Neurology and Neuroscience, Center for Sleep Medicine, Weill Medical College of Cornell University, 525 East 68th Street, Room k-615, New York, NY 10065, USA e-mail:
[email protected] A. J. Spielman Cognitive Neuroscience Doctoral Program, The City College of the City University of New York, 138th Street and Convent Ave., NAC 7/120, New York, NY 10031, USA A. J. Spielman New York Methodist Hospital, Center for Sleep Disorders Medicine and Research, 519 Sixth Street, Brooklyn, NY 11215, USA
123
J Behav Med (2009) 32:244–254
N = 7,151) investigating the relationship between psychiatric illness and sleep quality, they found that anxiety level was associated with a reduction in total sleep time, and sleep efficiency (the ratio of total sleep time over time in bed), as well as an increase in sleep latency. This study primarily looked at sleep architecture; therefore causation between insomnia and psychiatric illness was not addressed. However, a study by Ohayon and Roth (2003) found that anxiety appeared before insomnia in 43% of cases and that insomnia co-occurred with anxiety in 39% of cases. A recent study of adolescents, found that insomnia presented before anxiety in 16% of cases, and that anxiety occurred before insomnia in 73% of cases (Johnson et al. 2006). This study also found that in 11% of cases, insomnia and anxiety occurred at the same time. In a study specifically looking at the causal relationship between psychiatric illness and insomnia, Ohayon (1997) came to the conclusion that insomnia is mostly an associated symptom of another psychiatric disorder. Together these data indicate that in both adults and adolescents anxiety often is a prodromal feature of insomnia. The common co-morbidity of insomnia and depression has also been a challenge to clinicians. In the context of major depression, sleep disturbance is present in almost 80% of cases (Ohayon et al. 2000; Weissman et al. 1996). Historically, the predominant view has been to treat the presumptive cause of the insomnia, the mood disorder. However, clinical experience and at least one study have shown that the most typical residual symptoms following successful treatment of depression are disturbed sleep and fatigue (Nierenberg et al. 1999). This can be conceptualized as an incomplete resolution of the depression or alternatively that insomnia has become autonomous from its origin. Therefore, in cases in which acute insomnia is related to depression, when the depression is in remission and yet sleep disturbance is still present, treatment must necessarily aim beyond the depression. A number of epidemiological studies have shown that the common sequence of depression predating the development of insomnia is not invariant. These studies have shown that insomnia is a risk factor for depression. Insomnia not only precedes depression in these studies, but successful treatment of the sleep problem lessens the risk of future depression (Ford and Kamerow 1989; Breslau et al. 1996). The most recent study that bears on the tangled web of insomnia and depression targeted both depression and insomnia from the start of treatment (Fava et al. 2006). In this study an SSRI medication is combined with either a hypnotic or placebo in patients with major depression. In the group with the hypnotic medication, depression was more quickly relieved and sleep disturbance was more effectively addressed. Therefore, the consensus from the community of sleep clinicians is that insomnia should not be considered
245
secondary to depression, but rather both disorders should be diagnosed. Furthermore, in cases of co-morbid depression and insomnia attention to both disorders is warranted. Chronic medical illness is also commonly associated with insomnia. In fact, Katz and McHorney 1998 found that patients with a number of medical conditions had increased odds of insomnia. They found that hip impairment, congestive heart failure, obstructive airway disease, back pain, and prostate problems all significantly increased the chances of insomnia. In addition, in the majority of these cases the insomnia continued to be present at a 2-year follow-up. Insomnia associated with medical conditions offers a unique challenge to clinicians, and is often very difficult to successfully treat. Success in these cases is typically contingent on improvement of the underlying medical condition.
The 3 P model of insomnia It order to understand the therapeutic targets of many of the non-pharmacological treatments, it is helpful to consider the 3 P model of insomnia (see Fig. 1) (Yang et al. 2006). The 3P’s in this model stand for predisposing, precipitating, and perpetuating factors. Predisposing characteristics may be genetic or underlying personality traits such as basal level of anxiety or hyperarousal. According to this model, individuals with high levels of anxiety or hyperarousal are at increased risk of developing insomnia (Drake et al. 2004). Precipitating events such as work and educational stress, health and emotional problems, induce periods of difficulty sleeping (Bastien et al. 2004). Acute insomnia may become chronic because of perpetuating habits, practices and worrying. Perpetuating activities commonly include maladaptive practices, such as prolonged time in bed, eating, surfing the web or watching television in bed, and drinking alcohol to help promote sleep. When patients are asked why they began to spend more time in bed, for example, they frequently report that they do so because they want to increase their opportunity to sleep. The extra time in bed may on occasion permit more sleep. However, tossing and turning in bed, lighter more fragmented sleep, and worrying about daytime impairment while trying to sleep are all negative consequences of spending too much time in bed. Other perpetuating factors include daytime activities aimed at reducing tiredness associated with insomnia, such as drinking more caffeinecontaining beverages or napping. Appreciating the potency of the patient’s thinking, worrying and planning about their problems has yielded a paradigm shift in the understanding and therapeutics of insomnia. An early portrayal of the role of worry in maintaining sleep disturbance focused on stirring up
123
246
J Behav Med (2009) 32:244–254
Fig. 1 Graphical representation of the 3 P’s Model (Adapted from ‘‘A behavioral perspective on insomnia treatment’’ by A. J. Spielman, L. Caruso, and P. Glovinsky) Morin 1993
emotional arousal (Kales and Kales 1984). When the patient’s apprehension of the upcoming night produces emotional arousal, a vicious cycle can begin, which makes it harder for the patient to fall asleep. More recent work has delineated how the types of maladaptive cognitions (e.g., myths about sleep and distortions or catastrophizing about the consequences of poor sleep), the decision to engage in safety behaviors (e.g., getting into bed early) and the abnormal processes of attending to sleep, intending to sleep and trying to sleep are counterproductive (Ree and Harvey 2004; Espie et al. 2006; Morin 1993). As illustrated in Fig. 1, over time, the importance of each of these three factors can change with perpetuating habits and practices frequently gaining in importance. The non-pharmacological treatments often aim at these perpetuating features to improve the sleep disturbance. The predominant treatment for insomnia is sedative hypnotic medications (Walsh and Schweitzer 1999). In general, these medications are effective in improving sleep. However, the emergence of side effects, the development of drug tolerance, drug dependency and discontinuation effects and the unknown long-term effects of these medications are limitations of this therapeutic approach. Furthermore, as symptomatic treatment, hypnotics do not address the presumed mechanism responsible for insomnia, therefore symptoms typically return once treatment is discontinued (Walsh and Schweitzer 1999; Greenblatt 1992; Johnson and Chernik 1982; Kales et al. 1974). Hypnotics may also be contraindicated because of a patient’s current medication usage, a history of substance abuse, or existing medical conditions. On the other hand, behavioral treatments, which address mechanisms contributing to insomnia, have been shown to be as effective as sedative
123
hypnotic medication and the benefits are more durable (Edinger et al. 2001; Morin et al. 1994, 1999; Murtagh and Greenwood 1995). Of the behavioral treatments for insomnia stimulus control, sleep restriction, cognitive-behavior therapy, progressive muscle relaxation, and paradoxical intention have the most empirical support for their efficacy (2005; Edinger et al. 2001; Morin et al. 1994, 1999; Engle-Friedman et al. 1992; Espie et al. 1989, 2001; Guilleminault et al. 1995; Gustafson 1992; Jacobs et al. 1993; Lacks et al. 1983; Ladouceur and Gros-Louis 1986; Lichstein and Johnson 1993; Lick and Heffler 1977; McClusky et al. 1991; Mitchell 1979; Morin and Azrin 1987; Morin et al. 1993; Nicassio and Bootzin 1974; Sanavio 1988; Smith et al. 2002; Stanton 1989; Turner and Ascher 1979; Turner and Ascher 1982; Woolfolk and McNulty 1983; Friedman et al. 1991; Riedel et al. 1995). Sleep hygiene (used in conjunction with other techniques) and biofeedback have less empirical support than the previously cited techniques, but also appear to be effective in treating insomnia (Sanavio 1988; Friedman et al. 1991; Hauri 1991; Coursey et al. 1980; Freedman and Papsdorf 1976; Hauri 1981; Hauri et al. 1982; Nicassio et al. 1982; Spielman et al. 1987). In this paper we will discuss each of these cognitive and behavioral techniques for treating insomnia. We will briefly describe the theoretical background on which the technique is based and how the technique is used in practice. The empirical evidence regarding efficacy and effectiveness are mentioned, but are not the focus of this review. In addition to these well-known approaches, we will also describe biofeedback techniques. There will also be a brief discussion of the most common circadian rhythm disorders that can present as insomnia.
J Behav Med (2009) 32:244–254
Stimulus control Developed in the early 1970s, stimulus control therapy has been shown to be effective in a considerable number of research studies (Bootzin 1972). This treatment involves five basic instructions (Bootzin et al. 1991). 1. 2. 3.
4. 5.
Don’t get into bed unless you are sleepy. Don’t use the bed for anything except sleep and, of course, sex. If you are unable to fall asleep within 10–20 min of either getting into bed or after waking up during the night, get up and go to another room. Get up at the same time each morning. Don’t nap during the day.
The goal of stimulus control therapy is to help the patient associate the bedroom environment and nighttime rituals with rapid sleep onset and thus bring sleep under the control of antecedent conditions. Stimulus control therapy has been conceptualized within the framework of learning theory. The struggle to fall asleep or go back to sleep during the night are unpleasant and associated with disturbing thoughts that are themselves arousing. The individual with insomnia is tossing and turning, worried that mood and performance will be impaired tomorrow because s/he cannot fall asleep tonight. These experiences are recurrent, night-after-night and can be seen as learning trials. Unfortunately, what is learned is that the set of stimuli in the bedtime environment lead to sleeplessness. Stimulus Control therapy was developed to break the maladaptive association between the bedroom environment and activities in bed and being awake struggling to go to sleep. There are some individuals with insomnia who report that they sleep better on their couch, or when sleeping away from home. They may be surprised that they sleep well in the sleep laboratory with all of its intrusive paraphernalia. This makes sense in the view of learning theory, because sleeping in a novel environment does not have the same stimulus conditions as the individual’s typical sleep setting. Absent the cues that usually precede the struggle to sleep, the learned mechanism is not triggered in the novel environment and the person has less difficulty sleeping. Like sleep restriction, the instructions of Stimulus Control Therapy promote the retraining of sleep by establishing conditions that lead to the experience of rapid sleep onset after getting in bed.
Sleep restriction therapy Sleep restriction therapy is a technique developed in the mid 1980s (Spielman et al. 1987) and, as the name implies,
247
is based on restricting the patient’s time in bed. Excess time in bed is viewed as perpetuating insomnia in numerous ways. Prolonged, distressing and unsuccessful struggles to fall asleep, lying in bed worrying that performance will suffer the next day and the fragmentation of sleep are all negative consequences of too much time in bed. Sleep Restriction Therapy reduces time in bed and limits these distressing experiences that perpetuate insomnia. In addition, reduced time in bed produces sleep loss at the start of Sleep Restriction. The well-known effects of sleep deprivation, including rapid sleep onset, deeper sleep and sustained sleep are triggered and thus sleep is promoted. The Sleep Restriction protocol requires the patient to fill out a sleep log (see Fig. 2) for 2-weeks. Based on the sleep log, a sleep/wake schedule is set. The average amount of nighttime sleep is calculated from the sleep log and the time in bed is prescribed to match this amount. An individual, for example, who sleeps on average 6 h per night, as documented on the sleep log, is scheduled to be in bed for 6 h at the start of Sleep Restriction. The patient is scheduled to wake-up, by alarm clock seven days per week, at the typical time s/he wakes during work days. In our example, the individual who wakes-up at 6:30 am on work days and 9:30 am on weekends will be scheduled to go to sleep at 12:30 am and get up 7 days per week at 6:30 am. The understanding that sleep, as well as many biological functions, are regulated by the biological or circadian clock informs the clinician that in addition to the amount of sleep, the timing of sleep needs to be controlled to promote good sleep. In addition, no napping is permitted. Patients are told to expect increased fatigue and sleepiness and decreased performance at the start of treatment due to the sleep loss that occurs. Of note, the lower limit for the assigned time in bed is typically 5 h. As treatment proceeds sleep continues to be monitored with the help of the sleep log and time in bed is changed according to how well the patient sleeps. When sleep occupies 90% or more of the time in bed (also called sleep efficiency, total sleep time/time in bed 9 100%) time in bed is increased by 15–30 min. If sleep efficiency is lower than 85%, then time in bed is reduced by 15 min. Sleep efficiency in the 85 to \90% range does not trigger any change in schedule. In older individuals the criterion is lower, equal to or greater than 85% to increase time in bed and \80% to decrease time in bed. Another way to decide when to change time in bed is the patient’s daytime performance, mood, and alertness. If the patient is able to sleep successfully on a particular schedule, but reports sleepiness, additional time in bed is scheduled. Sleep restriction is difficult to comply with in the first few weeks, although sleep rapidly improves. A typical course of treatment is usually 6–8 weeks.
123
248
J Behav Med (2009) 32:244–254
Fig. 2 A version of the CCNY sleep log. Patients are instructed to complete this log upon awakening in the morning. The black dot indicates the time the patient got into bed, and the black lines represent periods of sleep. The black circle shows time out of bed. The numeral prior to the black dot indicates when medications were taken (if any were taken before bedtime). Medications taken at other times of the day are listed below the chart. c indicates time of caffeine consumption. Daily alcohol consumption for each day is listed below medications
Progressive muscle relaxation
Cognitive therapy for insomnia
Developed in the 1920s Progressive Muscle Relaxation was based on the idea that muscular tension was at the root of anxiety. As a natural extension of this theory, it was thought that teaching patients to reduce muscle tension would also reduce anxiety. However, more recent studies have shown that the act of relaxing muscles does not necessarily reduce psychological anxiety. In one interesting study patients with insomnia and without muscular tension, slept worse with progressive muscle relaxation (Hauri et al. 1982). However, in general, this technique has been shown to be helpful for sleeping difficulty (Nicassio et al. 1982). The progressive muscle relaxation technique is simple and starts with training during the day or evening. The patient is asked to sit comfortably in a chair during the therapy session. The patient is told to purposely tense a muscle and then relax it and to focus on the changing experience of tension. Typically they are asked to tense for 10–15 s and relax for the same period of time. As the patient becomes more proficient at this technique they will become more aware of their muscular tension throughout the day. Once the patient’s becomes fully comfortable and confident using this technique, they are asked to use it at bedtime to help promote sleep. Some practitioners screen patients using frontalis muscle monitoring to measure whether they will be good candidates for progressive muscle relaxation (Hauri 1991). This may be important with this technique, because as previously mentioned; sleep may not improve or might be made worse in patients who are not physiologically tense.
The major proponents of cognitive therapy were originally trained in the psychodynamic school. Disillusioned at the ineffectiveness of that approach, their innovative theorizing produced therapies largely based on correcting perceived cognitive errors. Common cognitive errors include minimizing positive events and maximizing negative events, and/or overgeneralization of negative events, to name just a few. Over the decades since its inception, cognitive approaches have become a mainstay of treatment for a range of mental health disorders. There is only one study we are aware of in which cognitive therapy has been used effectively as a stand-alone treatment of insomnia (Harvey et al. 2007). Most commonly, the cognitive approach is a core component of multimodal approaches to insomnia. Applying cognitive therapy to the treatment of insomnia targets unrealistic and maladaptive beliefs that fuel the sleep disturbance and also helps to reformulate anxiety-provoking thoughts regarding sleep. Patients with difficulty sleeping, for example, worry that their insomnia will significantly impair their immune system and catastrophize that daytime deficits are devastating. Identifying the irrational beliefs and counterproductive thinking is the first task in cognitive therapy for insomnia. Morin 1993 has identified categories of maladaptive cognitions. These include (1) attribution of transient sleep difficulties as a chronic problem, (2) believing that most daytime problems are the result of poor sleep, (3) unrealistic expectations regarding an individual’s sleep need, (4) general cognitive errors such as
123
J Behav Med (2009) 32:244–254
overgeneralization, rumination, and magnification, (5) high anxiety regarding sleep, which is often associated and/or initiated with bedtime activities. In order to help identify these types of thoughts the Dysfunctional Beliefs and Attitudes about Sleep scale (DBAS) was developed (Morin et al. 1993). This scale consists of 30-questions which tap into the person’s attitude regarding sleep and sleep-related issues. Once these insomnia-perpetuating beliefs are identified, a combination of reassurance, education, and disputation of the irrational beliefs is used to help reduce anxiety and improve sleep. Sessions devoted to didactic training in the principles of sleep regulation or assigned readings reassure patients of the considerable understanding of sleep that informs their treatment. Incorrect ideas about what constitutes normal sleep are addressed. For example, patients are relieved that individuals with no sleep problem wake multiple times per night. The job of treatment is therefore not to prevent awakenings, but to help the patient resume sleep more easily. In other cases, for example in patients who say ‘‘I can’t function because of my insomnia’’. An empirical approach is used and data is collected on the dayto-day variation in performance. Such data is used to reassure patients that their daytime problems are not so absolutely invariant. Increasingly the term cognitive behavioral therapy for insomnia (CBT-I) is used in the field of sleep medicine. Basically this term means using a combination of cognitive therapy with the other behavioral approaches described in this paper (stimulus control, sleep restriction, progressive muscle relaxation and so on). Many clinicians find it more helpful for patients to use the CBT-I approach than using treatments serially.
Biofeedback The majority of research on biofeedback in insomnia was performed in the early 1980s and showed that this treatment modality is effective in improving insomnia (Hauri 1981; Nicassio et al. 1982). However, biofeedback has never caught on as a main treatment option, because of the expense of the equipment, and difficulty in training some patients. Most commonly, frontalis electromyogram (EMG), temperature and sensory motor rhythm biofeedback have been used. Although these techniques vary in their exact procedures, they all involve the patient’s monitoring physiological functions through some type of electronic or computerized interface. Using this interface, patients are taught to increase or decrease the displayed parameter (brain wave frequencies [sensory motor rhythm], muscle tension [EMG], or limb temperature). Most commonly the
249
change is brought about through guided imagery, diaphragmatic breathing, and/or other types of relaxation techniques. With some of these methods, the degree of effectiveness correlates with the ability to learn the technique. This is particularly true with sensory motor rhythm biofeedback (Hauri 1981).
Other approaches Originally developed as a therapeutic technique to treat compulsive disorders and anxiety Paradoxical Intention has been used for insomnia and although it has been shown to be helpful, it is not a commonly employed strategy (Morgenthaler et al. 2006). In its original form, paradoxical intention consisted of instructing patients to exaggerate problematic symptoms in order for them to gain insight into the problem. In the treatment of insomnia, the basic theory is the same; however the practice has been modified accordingly. The patient is told to attempt to stay awake, while remaining in bed at night. The patient is instructed not to use drastic methods to remain awake, such as pinching or poking oneself. This method is thought be effective because it eliminates the stress and challenge of trying to go to sleep. This technique does not appeal to all patients; therefore proper patient selection for this treatment appears to be rather important (Espie and Lindsay 1985). Sleep hygiene is a term coined to describe a set of rules meant to improve sleep (Hauri 1991). There is no single list of these do’s and don’ts about sleep and practices of everyday living. There was a time when a snack before bedtime, for example, was often recommended, but this item has dropped off most lists these days. In general, sleep hygiene ‘‘tips’’ have face validity and are consistent with our understanding of sleep regulation. Although sleep hygiene has not been found to independently improve sleep in the few empirical studies of this approach, the recommendations are thought to be helpful when integrated with other techniques. The following is an outline of the typical sleep hygiene instructions. 1.
2.
Consistent sleep and wake times Abiding by a regular sleep schedule is the most common sleep hygiene recommendation and one of the most important. Variable sleep schedules result in varying exposure to time cues, which may produce a fluctuating influence on sleep timing. Adhering to a regular sleep schedule coordinates and synchronizes the interaction of sleep and biological clock regulation, a mutually beneficial relationship. Limit time in bed See above description of ‘‘Sleep restriction therapy’’.
123
250
3.
4.
5.
6.
J Behav Med (2009) 32:244–254
Do not nap Napping during the day results in reduced sleep need at night. A few exceptions are noteworthy. Individuals who cannot set aside enough time to sleep at night would be advised to avoid sleep deprivation by napping during the day. In older individuals who cannot sustain a long enough bout of sleep during the night may consider a trial of daytime napping and perform a cost benefit analysis. Finally, shift workers frequently suffer from difficulty sleeping and impaired alertness during work hours. Many such individuals benefit from a nap before their shift or during work hours. Remove the clock from the bedroom Regardless of whether monitoring the time at night makes an individual more anxious or gives them some sense of mastery over the sleeping process, watching the clock is activating and counter-productive for sleep. Avoid caffeine Caffeine is a well-known stimulant and often disrupts sleep (Karacan et al. 1976). While the elimination half-life of caffeine is about 4.5 h, it is significantly longer in older individuals. Furthermore, with increased dose the activation effects will last for many more hours. Most sleep hygiene lists suggest caffeine-containing substances should not be taken after noon. We suggest that caffeine ingestion be limited to a morning dose, at most in those suffering with insomnia. Avoid alcohol Many individuals report using alcohol to help them fall asleep. However, what many people do not know is that during the night, as alcohol is metabolized, it produces awakenings and sleep is fragmentated (Adamson and Burdick 1973). Therefore, reducing or discontinuing alcohol can be particularly helpful for those individuals who complain of light unrefreshing sleep and/or early morning awakenings. Because of the health benefits of regular, modest alcohol use we tell patients that once their insomnia is improved we will slowly permit alcohol use. In our view (and the 3 Ps model of insomnia) addressing all the contributions to insomnia may be necessary to improve sleep. Once sleep is more robust the addition of alcohol may not be disruptive.
Circadian rhythms disorders that can mimic insomnia It may seem odd to specifically address circadian rhythm disorders that mimic insomnia, given that a much larger percentage of patients suffer from insomnia as part of an underlying psychiatric disorder. However, we would like to address this issue in this review because most practitioners reading this have extensive experience treating mood disorders, and are therefore less likely to confuse co-morbid
123
insomnia. Moreover, for those without an extensive background in sleep medicine, deciphering insomnia from circadian rhythm disorders can be particularly tricky. Often patients will come to a sleep center assuming that they suffer from insomnia, however after taking a thorough clinical history and reviewing the sleep/wake patterns of the individual it becomes apparent that a circadian rhythm disorder, not insomnia, is actually at the root of the problem. This differentiation between insomnia and circadian disorders is not just semantic, because the treatment strategies for circadian rhythm problems are quite different than the ones typically used for insomnia. The essential feature differentiating circadian rhythm disorders and insomnia is the sleep/wake pattern. For example, if a patient reports a long history (usually since childhood or adolescence) of difficulty both falling asleep at night and waking up in the morning, there is a very good chance that the patient suffers from Delayed Sleep Phase Syndrome (DSPS). It is quite common for insomniacs to report difficulty falling asleep. However, it is much less common that insomnia sufferers report difficulty waking up in the morning. This condition is frequently seen in teenagers and young adults, with a reported prevalence in this population of 7–16% (American Academy of Sleep Medicine 2005). Although it can also be present in older individuals, however the prevalence is significantly lower at 3% (Ando et al. 2002). Very often parents of teens with DSPS report that it is extremely difficult to wake their child for school. College students can often adapt their schedules to their delayed phase by avoiding morning classes. However, once they enter the work force the DSPS typically resurfaces as a problem. Therefore, both high school students and young adults just starting their careers are commonly seen in sleep clinics seeking treatment. Genetic factors also seem to play a role in DSPS; in fact a family history is present in approximately 40% of cases (American Academy of Sleep Medicine 2005). In other cases, the patient may report a history of falling asleep or getting sleepy early in the evening and then waking up too early, unable to fall back to sleep. These individuals may be suffering from Advanced Sleep Phase Syndrome (ASPS). This disorder has an estimated prevalence of approximately 1% and is more frequently seen in the elderly (Ando et al. 1995). It is not uncommon to hear patients with ASPS report bedtimes of 7 pm with wake times of 3 am. This disorder can often be seen in retirees, who complain that they don’t know what to do with themselves when they awaken at 3 am in the morning. In both DSPS and ASPS, if the individual has an adequate opportunity to sleep at their preferred time, total sleep time is generally within normal limits and daytime sleepiness is usually not reported. However, particularly in cases of DSPS, because of constant social and work constraints that limit the person’s ability to sleep into the
J Behav Med (2009) 32:244–254
late morning or early afternoon on a regular basis, they often report daytime sleepiness. In addition to DSPS and ASPS, numerous other circadian sleep disorders exist, however these are the most common disorders to be confused with insomnia. Generally circadian rhythm disorders are treated with a combination of bright light, melatonin (only for DSPS), and/or a customized sleep/wake schedule, not the typical cognitivebehavioral treatments listed previously in this paper. A detailed review of the various treatment options for these disorders is beyond the scope of this paper, for a thorough review on this topic please refer to Zee’s 2006 review. However, we will briefly discuss how bright light is used for both DSPS and ASPS and how melatonin can be used to treat DSPS. This section will be capped off with a brief description of chronotherapy. In order to understand the use of bright light and melatonin in circadian rhythm disorders it is important to understand the phase response curve. The phase response curve basically describes the delaying or advancing effects that a stimulus (usually bright light or melatonin) will have on shifting an individual’s circadian rhythms. The circadian time is frequently measured by using either the core body temperature or the plasma melatonin levels of the patient. Bright light administered before the nadir of core body temperature has a phase delaying effect (Khalsa et al. 2003), which means that the patient will tend to fall asleep later and wake up later. Therefore, treatment of ASPS typically involves exposure to bright light before the nadir of core body temperature (Morgenthaler et al. 2007). In most cases, this will involve exposing the patient to bright light in the evening. Conversely, bright light administered after the nadir of core body temperature has a phase advancing effect (Khalsa et al. 2003). Allowing the patient to fall asleep earlier and wake up earlier, making it ideal for the treatment of DSPS (Morgenthaler et al. 2007). In cases of DSPS, bright light is delivered either in the morning or afternoon depending on the degree of delay in the patients circadian rhythms. The strength of the response to bright light is, in part, determined by the proximity of the light pulse to the nadir of the core body temperature. Therefore, light pulses closer to the nadir will have a stronger effect than pulses further away from the nadir. The intensity and duration of the light also have an impact on the strength of the response (Czeisler et al. 2005). In other words, the higher the intensity of the light and the longer the duration of exposure to the light, the stronger the effect on the patients’ circadian rhythms. Bright light with an intensity between 2,500 and 10,000 Lux has consistently been shown to phase shift circadian rhythms, with higher intensity light producing larger phase shifts (Boivin et al. 1996). We generally suggest that patients in treatment for DSPS get at least 1-h of bright light exposure immediately upon waking
251
each morning and patients treated for ASPS are typically exposed to 1-h of bright light in the evening. There is also a phase response curve to melatonin, which is nearly the opposite of the phase response curve for bright light. Therefore, melatonin administered before the nadir of core body temperature will advance circadian rhythms, and a dose given after the nadir will have a phase delaying effect. Large scale studies investigating the clinical benefits of melatonin are lacking. However, a few studies have shown melatonin treatment to be beneficial for the treatment of DSPS (Dahlitz et al. 1991; Oldani et al. 1994; Nagtegaal et al. 1998). There is currently debate in the field of sleep medicine whether morning melatonin administration is helpful for the treatment of ASPS. One of the first treatments developed for DSPS is called chronotherapy. This treatment involves the progressive delaying of the patient’s sleep/wake schedule by 3 h each day. Although this treatment has been shown to be effective in treating DSPS (Czeisler et al. 1981), it is not commonly used. This is most likely because it is difficult to put aside ones work and social schedule for the time required to complete the treatment protocol. However, this treatment can be used with teenagers and college students with DSPS during their summer break. In conclusion, although hypnotic medications are the most common treatment for insomnia, most patients will benefit from either the addition of cognitive-behavioral treatments to the medication regimen or stopping the medication and beginning these cognitive-behavioral techniques, it is currently unclear which procedure is most effective (stopping medication and then starting CBT-I, or starting CBT-I before the medication has been stopped). Studies employing both psychological approaches (most commonly CBT) and pharmacological therapies has yielded mixed results (Morin et al. 1999a, b; Jacobs et al. 2004). A soon to be published Clinical Guideline of the AASM recommends combining these two modalities only after a significant sequence of trials within one modality or the other has not reached optimum effectiveness (SchutteRodin et al. 2008). In general, patients prefer CBT to pharmacologic treatments for insomnia, if given the option (Morin et al. 1992). However, like drug therapy, when using these methods is it very important to give the patient a through clinical evaluation in order to help select the appropriate treatment option. A purely behavioral approach, such as sleep restriction, may be employed initially as a tactic to reduce cognitive concerns before direct work on cognitive contributions is begun. Conversely, in patients reluctant to curtail time in bed because of a preoccupation with sleep duration, a cognitive approach may be a good way to start. If the patient is found to sleep better away from home, then stimulus control
123
252
therapy may be the best option. In some cases, patients will refuse the traditional cognitive-behavioral therapies because it lacks face validly, in these cases it can be helpful to use a method like biofeedback, which shows the patient concrete feedback on the progress of the therapy. Often patients do not fall neatly into one treatment category; therefore a combination of treatments is necessary. Although the implementation of these therapies can take considerable clinical skill and may take several sessions in order to implement properly, if used correctly they can give the patient long-term resolution and management of their sleep problems. Therefore, non-pharmacological treatments are a helpful addition to the treatment options of any practitioner treating insomnia.
References Adamson, J., & Burdick, J. A. (1973). Sleep of dry alcoholics. Archives of General Psychiatry, 28(1), 146–149. American Academy of Sleep Medicine. (2005). The international classification of sleep disorders: Diagnostic and coding manual (xviii, 297 pp). Westchester, IL: American Academy of Sleep Medicine. Ando, K., Kripke, D. F., & Ancoli-Israel, S. (1995). Estimated prevalence of delayed and advanced sleep phase syndromes. Sleep Research, 24, 509. Ando, K., Kripke, D. F., & Ancoli-Israel, S. (2002). Delayed and advanced sleep phase symptoms. The Israel Journal of Psychiatry and Related Sciences, 39(1), 11–18. Bastien, C. H., Vallieres, A., & Morin, C. M. (2004). Precipitating factors of insomnia. Behavioral Sleep Medicine, 2(1), 50–62. doi:10.1207/s15402010bsm0201_5. Benca, R. M., Obermeyer, W. H., Thisted, R. A., & Gillin, J. C. (1992). Sleep and psychiatric disorders. A meta-analysis. Archives of General Psychiatry, 49(8), 651–668. discussion 669–70. Boivin, D. B., Duffy, J. F., Kronauer, R. E., & Czeisler, C. A. (1996). Dose–response relationships for resetting of human circadian clock by light. Nature, 379(6565), 540–542. doi:10.1038/ 379540a0. Bootzin, R. R. (1972). A stimulus control treatment for insomnia. In Proceedings of the American Psychological Association (pp. 395–396). Bootzin, R. R., Epstein, D., & Wood, J. M. (1991). Stimulus control instructions. In P. Hauri (Ed.), Critical issues in psychiatry: Case studies in insomnia (pp. 19–28). New York: Plenum Medical Book. Breslau, N., Roth, T., Rosenthal, L., & Andreski, P. (1996). Sleep disturbance and psychiatric disorders: A longitudinal epidemiological study of young adults. Biological Psychiatry, 39(6), 411–418. doi:10.1016/0006-3223(95)00188-3. Coursey, R. D., Frankel, B. L., Gaarder, K. R., & Mott, D. E. (1980). A comparison of relaxation techniques with electrosleep therapy for chronic, sleep-onset insomnia a sleep-EEG study. Biofeedback and Self-Regulation, 5(1), 57–73. doi:10.1007/BF00999064. Czeisler, C. A., Buxton, O. M., & Khalsa, S. B. S. (2005). The human circadian timing system and sleep-wake regulation. In M. H. Kryger, T. Roth, & W. C. Dement (Eds.), Principles and practice of sleep medicine (4th ed., xxxiii, 1517 pp). Philadelphia, PA: Elsevier/Saunders.
123
J Behav Med (2009) 32:244–254 Czeisler, C. A., Richardson, G. S., Coleman, R. M., Zimmerman, J. C., Moore-Ede, M. C., Dement, W. C., et al. (1981). Chronotherapy: Resetting the circadian clocks of patients with delayed sleep phase insomnia. Sleep, 4(1), 1–21. Dahlitz, M., Alvarez, B., Vignau, J., English, J., Arendt, J., & Parkes, J. D. (1991). Delayed sleep phase syndrome response to melatonin. Lancet, 337(8750), 1121–1124. doi:10.1016/01406736(91)92787-3. Drake, C., Richardson, G., Roehrs, T., Scofield, H., & Roth, T. (2004). Vulnerability to stress-related sleep disturbance and hyperarousal. Sleep, 27(2), 285–291. Ebben, M. R., & Fine, L. (2009). Insomnia: A risk for future psychiatric illness. In S. R. Pandi-Peumal & M. Kramer (Eds.), Sleep and mental illness. Cambridge: Cambridge University Press (in press). Edinger, J. D., Wohlgemuth, W. K., Radtke, R. A., Marsh, G. R., & Quillian, R. E. (2001). Cognitive behavioral therapy for treatment of chronic primary insomnia: A randomized controlled trial. Journal of the American Medical Association, 285(14), 1856–1864. doi:10.1001/jama.285.14.1856. Engle-Friedman, M., Bootzin, R. R., Hazlewood, L., & Tsao, C. (1992). An evaluation of behavioral treatments for insomnia in the older adult. Journal of Clinical Psychology, 48(1), 77–90. doi:10.1002/1097-4679(199201)48:1\77::AID-JCLP2270480112 [3.0.CO;2-J. Espie, C. A., & Lindsay, W. R. (1985). Paradoxical intention in the treatment of chronic insomnia: Six case studies illustrating variability in therapeutic response. Behaviour Research and Therapy, 23(6), 703–709. doi:10.1016/0005-7967(85)90070-1. Espie, C. A., Lindsay, W. R., Brooks, D. N., Hood, E. M., & Turvey, T. (1989). A controlled comparative investigation of psychological treatments for chronic sleep-onset insomnia. Behaviour Research and Therapy, 27(1), 79–88. doi:10.1016/0005-7967 (89)90123-X. Espie, C. A., Inglis, S. J., Tessier, S., & Harvey, L. (2001). The clinical effectiveness of cognitive behaviour therapy for chronic insomnia: Implementation and evaluation of a sleep clinic in general medical practice. Behaviour Research and Therapy, 39(1), 45–60. doi:10.1016/S0005-7967(99)00157-6. Espie, C. A., Broomfield, N. M., MacMahon, K. M., Macphee, L. M., & Taylor, L. M. (2006). The attention-intention-effort pathway in the development of psychophysiologic insomnia: A theoretical review. Sleep Medicine Reviews, 10(4), 215–245. doi:10.1016/j. smrv.2006.03.002. Fava, M., McCall, W. V., Krystal, A., Wessel, T., Rubens, R., Caron, J., et al. (2006). Eszopiclone co-administered with fluoxetine in patients with insomnia coexisting with major depressive disorder. Biological Psychiatry, 59(11), 1052–1060. doi:10.1016/j. biopsych.2006.01.016. Ford, D. E., & Kamerow, D. B. (1989). Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? Journal of the American Medical Association, 262(11), 1479–1484. doi:10.1001/jama.262.11.1479. Freedman, R., & Papsdorf, J. D. (1976). Biofeedback and progressive relaxation treatment of sleep-onset insomnia: A controlled, allnight investigation. Biofeedback and Self-Regulation, 1(3), 253– 271. doi:10.1007/BF01001167. Friedman, L., Bliwise, D. L., Yesavage, J. A., & Salom, S. R. (1991). A preliminary study comparing sleep restriction and relaxation treatments for insomnia in older adults. Journal of Gerontology, 46(1), 1–8. Greenblatt, D. J. (1992). Pharmacology of benzodiazepine hypnotics. The Journal of Clinical Psychiatry, 53(Suppl), 7–13. Guilleminault, C., Clerk, A., Black, J., Labanowski, M., Pelayo, R., & Claman, D. (1995). Nondrug treatment trials in psychophysio-
J Behav Med (2009) 32:244–254 logic insomnia. Archives of Internal Medicine, 155(8), 838–844. doi:10.1001/archinte.155.8.838. Gustafson, R. (1992). Treating insomnia with a self-administered muscle relaxation training program: A follow-up. Psychological Reports, 70(1), 124–126. doi:10.2466/PR0.70.1.124-126. Harvey, A. G., Sharpley, A. L., Ree, M. J., Stinson, K., & Clark, D. M. (2007). An open trial of cognitive therapy for chronic insomnia. Behaviour Research and Therapy, 45(10), 2491–2501. doi:10.1016/j.brat.2007.04.007. Hauri, P. (1981). Treating psychophysiologic insomnia with biofeedback. Archives of General Psychiatry, 38(7), 752–758. Hauri, P. (1991). Sleep hygiene, relaxation therapy, and cognitive interventions. In P. Hauri (Ed.), Critical issues in psychiatry: Case studies in insomnia (pp. 65–84). New York: Plenum Medical Book. Hauri, P. J., Percy, L., Hellekson, C., Hartmann, E., & Russ, D. (1982). The treatment of psychophysiologic insomnia with biofeedback: A replication study. Biofeedback and Self-Regulation, 7(2), 223–235. doi:10.1007/BF00998785. Jacobs, G. D., Rosenberg, P. A., Friedman, R., Matheson, J., Peavy, G. M., Domar, A. D., et al. (1993). Multifactor behavioral treatment of chronic sleep-onset insomnia using stimulus control and the relaxation response. A preliminary study. Behavior Modification, 17(4), 498–509. doi:10.1177/01454455930174005. Jacobs, G. D., Pace-Schott, E. F., Stickgold, R., & Otto, M. W. (2004). Cognitive behavior therapy and pharmacotherapy for insomnia: A randomized controlled trial and direct comparison. Archives of Internal Medicine, 164(17), 1888–1896. doi:10.1001/archinte. 164.17.1888. Johnson, L. C., & Chernik, D. A. (1982). Sedative-hypnotics and human performance. Psychopharmacology, 76(2), 101–113. doi: 10.1007/BF00435262. Johnson, E. O., Roth, T., & Breslau, N. (2006). The association of insomnia with anxiety disorders and depression: Exploration of the direction of risk. Journal of Psychiatric Research, 40(8), 700–708. doi:10.1016/j.jpsychires.2006.07.008. Kales, A., & Kales, J. D. (1984). Evaluation and treatment of insomnia (xi, 324 pp). New York: Oxford University Press. Kales, A., Bixler, E. O., Tan, T. L., Scharf, M. B., & Kales, J. D. (1974). Chronic hypnotic-drug use. Ineffectiveness, drug-withdrawal insomnia, and dependence. Journal of the American Medical Association, 227(5), 513–517. doi:10.1001/jama. 227.5.513. Karacan, I., Thornby, J. I., Anch, M., Booth, G. H., Williams, R. L., & Salis, P. J. (1976). Dose-related sleep disturbances induced by coffee and caffeine. Clinical Pharmacology and Therapeutics, 20(6), 682–689. Katz, D. A., & McHorney, C. A. (1998). Clinical correlates of insomnia in patients with chronic illness. Archives of Internal Medicine, 158(10), 1099–1107. doi:10.1001/archinte.158.10. 1099. Khalsa, S. B., Jewett, M. E., Cajochen, C., & Czeisler, C. A. (2003). A phase response curve to single bright light pulses in human subjects. The Journal of Physiology, 549(Pt 3), 945–952. doi: 10.1113/jphysiol.2003.040477. Kuppermann, M., Lubeck, D. P., Mazonson, P. D., Patrick, D. L., Stewart, A. L., Buesching, D. P., et al. (1995). Sleep problems and their correlates in a working population. Journal of General Internal Medicine, 10(1), 25–32. doi:10.1007/BF02599573. Lacks, P., Bertelson, A. D., Sugerman, J., & Kunkel, J. (1983). The treatment of sleep-maintenance insomnia with stimulus-control techniques. Behaviour Research and Therapy, 21(3), 291–295. doi:10.1016/0005-7967(83)90211-5. Ladouceur, R., & Gros-Louis, Y. (1986). Paradoxical intention vs stimulus control in the treatment of severe insomnia. Journal of
253 Behavior Therapy and Experimental Psychiatry, 17(4), 267–269. doi:10.1016/0005-7916(86)90062-5. Lichstein, K. L., & Johnson, R. S. (1993). Relaxation for insomnia and hypnotic medication use in older women. Psychology and Aging, 8(1), 103–111. doi:10.1037/0882-7974.8.1.103. Lick, J. R., & Heffler, D. (1977). Relaxation training and attention placebo in the treatment of severe insomnia. Journal of Consulting and Clinical Psychology, 45(2), 153–161. doi:10.1037/ 0022-006X.45.2.153. McClusky, H. Y., Milby, J. B., Switzer, P. K., Williams, V., & Wooten, V. (1991). Efficacy of behavioral versus triazolam treatment in persistent sleep-onset insomnia. The American Journal of Psychiatry, 148(1), 121–126. Mitchell, K. R. (1979). Behavioral treatment of presleep tension and intrusive cognitions in patients with severe predormital insomnia. Journal of Behavioral Medicine, 2(1), 57–69. doi:10.1007/ BF00846563. Morgenthaler, T., Kramer, M., Alessi, C., Friedman, L., Boehlecke, B., Brown, T., et al. (2006). Practice parameters for the psychological and behavioral treatment of insomnia: An update. An american academy of sleep medicine report. Sleep, 29(11), 1415–1419. Morgenthaler, T. I., Lee-Chiong, T., Alessi, C., Friedman, L., Aurora, R. N., Boehlecke, B., et al. (2007). Practice parameters for the clinical evaluation and treatment of circadian rhythm sleep disorders. An American Academy of Sleep Medicine report. Sleep, 30(11), 1445–1459. Morin, C. M. (1993). Cognitive therapy Component. Insomnia: Psychological assessment and management. Treatment manuals for practitioners (pp. 126–144). Guilford Press: New York. Morin, C. M., & Azrin, N. H. (1987). Stimulus control and imagery training in treating sleep-maintenance insomnia. Journal of Consulting and Clinical Psychology, 55(2), 260–262. doi: 10.1037/0022-006X.55.2.260. Morin, C. M., Gaulier, B., Barry, T., & Kowatch, R. A. (1992). Patients’ acceptance of psychological and pharmacological therapies for insomnia. Sleep, 15(4), 302–305. Morin, C. M., Kowatch, R. A., Barry, T., & Walton, E. (1993a). Cognitive-behavior therapy for late-life insomnia. Journal of Consulting and Clinical Psychology, 61(1), 137–146. doi:10.1037/ 0022-006X.61.1.137. Morin, C. M., Stone, J., Trinkle, D., Mercer, J., & Remsberg, S. (1993b). Dysfunctional beliefs and attitudes about sleep among older adults with and without insomnia complaints. Psychology and Aging, 8(3), 463–467. doi:10.1037/0882-7974.8.3.463. Morin, C. M., Culbert, J. P., & Schwartz, S. M. (1994). Nonpharmacological interventions for insomnia: A meta-analysis of treatment efficacy. The American Journal of Psychiatry, 151(8), 1172–1180. 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 the American Medical Association, 281(11), 991–999. doi:10.1001/jama.281.11.991. Morin, C. M., Hauri, P. J., Espie, C. A., Spielman, A. J., Buysse, D. J., & Bootzin, R. R. (1999b). Nonpharmacologic treatment of chronic insomnia. An American Academy of Sleep Medicine review. Sleep, 22(8), 1134–1156. Murtagh, D. R., & Greenwood, K. M. (1995). Identifying effective psychological treatments for insomnia: A meta-analysis. Journal of Consulting and Clinical Psychology, 63(1), 79–89. doi: 10.1037/0022-006X.63.1.79. Nagtegaal, J. E., Kerkhof, G. A., Smits, M. G., Swart, A. C., & Van Der Meer, Y. G. (1998). Delayed sleep phase syndrome: A placebo-controlled cross-over study on the effects of melatonin administered five hours before the individual dim light melatonin
123
254 onset. Journal of Sleep Research, 7(2), 135–143. doi: 10.1046/j.1365-2869.1998.00102.x. Nicassio, P., & Bootzin, R. (1974). A comparison of progressive relaxation and autogenic training as treatments for insomnia. Journal of Abnormal Psychology, 83(3), 253–260. doi: 10.1037/h0036729. Nicassio, P. M., Boylan, M. B., & McCabe, T. G. (1982). Progressive relaxation, EMG biofeedback and biofeedback placebo in the treatment of sleep-onset insomnia. The British Journal of Medical Psychology, 55(Pt 2), 159–166. Nierenberg, A. A., Keefe, B. R., Leslie, V. C., Alpert, J. E., Pava, J. A., Worthington, J. J., III, et al. (1999). Residual symptoms in depressed patients who respond acutely to fluoxetine. The Journal of Clinical Psychiatry, 60(4), 221–225. NIH State-of-the-Science Conference Statement on manifestations and management of chronic insomnia in adults. NIH Consensus and State-of-the-Science Statements, 22(2), 1–30 (2005). Ohayon, M. M. (1997). Prevalence of DSM-IV diagnostic criteria of insomnia: Distinguishing insomnia related to mental disorders from sleep disorders. Journal of Psychiatric Research, 31(3), 333–346. doi:10.1016/S0022-3956(97)00002-2. Ohayon, M. M. (2007). Prevalence and comorbidity of sleep disorders in general population. La Revue du Praticien, 57(14), 1521– 1528. Ohayon, M. M., & Roth, T. (2003). Place of chronic insomnia in the course of depressive and anxiety disorders. Journal of Psychiatric Research, 37(1), 9–15. doi:10.1016/S0022-3956(02)000 52-3. Ohayon, M. M., Shapiro, C. M., & Kennedy, S. H. (2000). Differentiating DSM-IV anxiety and depressive disorders in the general population: Comorbidity and treatment consequences. Canadian Journal of Psychiatry, 45(2), 166–172. Oldani, A., Ferini-Strambi, L., Zucconi, M., Stankov, B., Fraschini, F., & Smirne, S. (1994). Melatonin and delayed sleep phase syndrome: Ambulatory polygraphic evaluation. NeuroReport, 6(1), 132–134. Ree, M. J., & Harvey, A. G. (2004). Investigating Safety Behaviours in Insomnia: The Development of the Sleep-related Behaviours Questionnaire (SRBQ). Behaviour Change, 21, 26–36. doi: 10.1375/bech.21.1.26.35971. 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(1), 54–63. doi:10.1037/0882-7974.10.1.54. Sanavio, E. (1988). Pre-sleep cognitive intrusions and treatment of onset-insomnia. Behaviour Research and Therapy, 26(6), 451–459. doi:10.1016/0005-7967(88)90139-8. Schutte-Rodin, S., Broch, L., Buysse, D., Dorsey, C., & Sateia, M. (2008). Evaluation and management of chronic insomnia in
123
J Behav Med (2009) 32:244–254 adults: An American Academy of Sleep Medicine clinical guideline. Journal of Clinical Sleep Medicine, in press. Simon, G. E., & VonKorff, M. (1997). Prevalence, burden, and treatment of insomnia in primary care. The American Journal of Psychiatry, 154(10), 1417–1423. Smith, M. T., Perlis, M. L., Park, A., Smith, M. S., Pennington, J., Giles, D. E., et al. (2002). Comparative meta-analysis of pharmacotherapy and behavior therapy for persistent insomnia. The American Journal of Psychiatry, 159(1), 5–11. doi: 10.1176/appi.ajp.159.1.5. Spielman, A. J., Caruso, L. S., & Glovinsky, P. B. (1987a). A behavioral perspective on insomnia treatment. The Psychiatric Clinics of North America, 10(4), 541–553. Spielman, A. J., Saskin, P., & Thorpy, M. J. (1987b). Treatment of chronic insomnia by restriction of time in bed. Sleep, 10(1), 45–56. Stanton, H. E. (1989). Hypnotic relaxation and the reduction of sleep onset insomnia. International Journal of Psychosomatics, 36(1–4), 64–68. Taylor, D. J., Lichstein, K. L., Durrence, H. H., Reidel, B. W., & Bush, A. J. (2005). Epidemiology of insomnia, depression, and anxiety. Sleep, 28(11), 1457–1464. Turner, R. M., & Ascher, L. M. (1979). Controlled comparison of progressive relaxation, stimulus control, and paradoxical intention therapies for insomnia. Journal of Consulting and Clinical Psychology, 47(3), 500–508. doi:10.1037/0022-006X.47.3.500. Turner, R. M., & Ascher, L. M. (1982). Therapist factor in the treatment of insomnia. Behaviour Research and Therapy, 20(1), 33–40. doi:10.1016/0005-7967(82)90006-7. Walsh, J. K., & Schweitzer, P. K. (1999). Ten-year trends in the pharmacological treatment of insomnia. Sleep, 22(3), 371–375. Weissman, M. M., Bland, R. C., Canino, G. J., Faravelli, C., Greenwald, S., Hwu, H. G., et al. (1996). Cross-national epidemiology of major depression and bipolar disorder. Journal of the American Medical Association, 276(4), 293–299. doi: 10.1001/jama.276.4.293. Woolfolk, R. L., & McNulty, T. F. (1983). Relaxation treatment for insomnia: A component analysis. Journal of Consulting and Clinical Psychology, 51(4), 495–503. doi:10.1037/0022006X.51.4.495. Yang, C. M., Spielman, A. J., & Glovinsky, P. (2006). Nonpharmacologic strategies in the management of insomnia. The Psychiatric Clinics of North America, 29(4), 895–919. doi: 10.1016/j.psc.2006.09.005. abstract viii. Zee, P. C. (2006). Circadian rhythm sleep disorders. Primary Psychiatry, 13(8), 58–67.
