Assessment and treatment of insomnia in adults a guide for clinicians.
Insomnia has severe consequences for those who have it. It is associated with daytime fatigue; greater use of medical services; use of over-the-counter medication and alcohol; functional impairment; work absenteeism; impaired concentration and memory; decreased enjoyment of relationships; and increased risk of medical illness, traffic accidents, and work accidents (Sateia & Nowell, 2004). Lundh (1998) reported that laboratory-based measures indicated that people with insomnia showed no impairment on tasks that relied on automatic or habitual processing, but impairment was seen on tasks requiring attention and mental effort. Thus, insomnia is a debilitating disorder for a large number of people, affecting both social and occupational roles.
People with insomnia frequently seek treatment from sleep specialists, who are typically physicians (Edinger & Means, 2005). However, as discussed later in this article, psychological interventions are usually the treatment of choice. Moreover, it is probable that many psychotherapy clients grapple with insomnia in addition to the mental health issue on which they originally focused. Therefore, there is a treatment gap that could potentially be filled by counselors. This article provides clinicians with the tools they need to effectively assess and treat clients for insomnia.
* Assessment of Insomnia
Diagnosis and Classification
Insomnia is defined in the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association [APA], 2000) as "a complaint of difficulty initiating or maintaining sleep or of nonrestorative sleep that lasts for at least 1 month (Criterion A) and causes clinically significant distress or impairment in social, occupational, or other important areas of functioning (Criterion B)" (p. 599). This definition refers to primary insomnia, which does not occur as a result of another sleep disorder or mental disorder and is not due to the physiological effects of a substance or medical condition (APA, 2000). Although the DSM-IV-TR may serve various functions, including education, establishing criteria for research, and providing criteria for clinical diagnosis, the American Academy of Sleep Medicine (AASM; 2005), in its second edition of the International Classification of Sleep Disorders (ICSD), offers a more detailed classification of insomnia. The ICSD lists three subtypes of insomnia that may be described as primary because they are not attributable to external factors: psychophysiological insomnia, paradoxical insomnia, and idiopathic insomnia. Table 1 lists the primary features associated with each of these three types of primary insomnia.
However, the definitions published by the DSM-IV-TR and the ICSD have not ended debates about how insomnia should be classified. In the sleep research literature, insomnia has been commonly divided into four categories: difficulty falling asleep, midsleep awakenings, early-morning awakenings, and nonrestorative sleep (Hauri, 2000). However, we concur with Hauri that this classification is undesirable for two reasons: (a) there is a great deal of overlap in these categories (e.g., someone may have difficulty falling asleep and experience midsleep awakenings) and (b) these categories reflect normative age-related changes in sleep (e.g., increasing age is often normally associated with early-morning awakenings). Moreover, this differentiation may serve little clinical utility because the inability to sleep at any point in the night can lead to the same frustrations and daytime functional impairments. Hauri suggested that a better way to subdivide insomnia is to categorize it based on its duration: transient (a few days), short-term (weeks), or chronic (months and years). Transient and short-term insomnia are caused by situational stress (e.g., job loss), medical or psychological disorders, or circadian factors (e.g., jet lag; Sateia & Nowell, 2004). Treatment of transient and short-term insomnia is focused on eliminating the precipitating stress, educating clients about sleep, providing sleep hygiene instructions, and perhaps by prescribing short-term use of hypnotics (Sateia & Nowell, 2004). To treat chronic insomnia, these methods are combined with cognitive and behavioral therapies.
Mental health professionals are not close to a consensus on how best to classify insomnia. Therefore, in addition to providing a diagnosis, the clinician's efforts are best directed not to classification but to clients' responses to two questions: What is the extent of the sleep disturbance and consequent daytime deficits? and What factors contribute to the insomnia? Although the latter question gives some guidance to treatment approaches, the former question provides baseline data against which the efficacy of treatment can be tested.
Assessment of Extent of Sleep Disturbance
When assessing the extent of the client's sleep disturbance problem, there are generally two considerations: (a) the client's perception of the quality of his or her sleep and (b) the client's perceptions of the impact of insomnia on his or her function when awake. When assessing sleep quality, a common strategy is to have the client fill out a sleep diary for 1 to 2 weeks. An example of a typical sleep diary is provided by Morin (1993); however, sleep diaries can be tailored to suit the needs of each clinician and client. The sleep diary generally provides information on sleep onset latency (i.e., time needed to fall asleep), awakenings after falling asleep, early-morning awakenings, total sleep and awake times, time in bed, and sleep efficiency (i.e., time asleep per time in bed; Morin, 1993). As a benchmark, sleep efficiency for healthy sleepers tends to range around 95% (e.g., Carskadon & Dement, 2000).
Although a sleep diary has the advantage of avoiding the problems with memory that are always a concern with retrospective measures, there are a wide variety of self-report measures that can be used. Many of these questionnaires can be easily viewed, including the Sleep History Questionnaire (Edinger, 1987), the Sleep Disturbance Questionnaire (Espie, Brooks, & Lindsay, 1989), the Sleep Impairment Index (Morin, 1993), the Beliefs and Attitudes About Sleep Scale (Morin, 1993), the Pittsburgh Sleep Quality Index (PSQI; Buysse, Reynolds, Monk, Berman, & Kupfer, 1989), and the Epworth Sleepiness Scale (Johns, 1991).
Assessment of Factors Contributing to Insomnia
Although sleep diaries and questionnaires are useful in quantifying the amount of sleep disruption, an assessment interview is particularly helpful for exploring factors that contribute to insomnia. Morin (1993) has developed the Insomnia Interview Schedule, which is a semistructured interview aimed at identifying the presence of insomnia and its contributing factors (the framework for this interview can be accessed in Morin, 1993). Through this interview, the client provides possible causes for his or her insomnia, thus directing treatment that should address the client's foremost complaint(s). Clinicians should take particular note of the symptoms described by the client, including descriptions of impairments in daytime functioning (A. G. Harvey & Tang, 2003); these are the symptoms that should be the targets of any intervention. Once the clinician has a good understanding of the factors that have caused and that still maintain the insomnia, he or she should then redefine the problem for the client. The clinician should guide the client to see relationships between behaviors and poor sleep (Hauri, 1989), and in doing so, can outline the treatment for the client. In general, there are numerous factors that may cause, maintain, or exacerbate insomnia (see Table 2 for an overview of these factors). A few of these factors merit further comment.
Hyperarousal, maladaptive beliefs, and maladaptive conditioning. Given that recent research has pointed to the role of both cognitive and physiological arousal in insomnia, assessing the degree of hyperarousal in clients is important. Cognitive and emotional hyperarousal are common to many people with insomnia. A. G. Harvey (2005) noted that intrusive thoughts, worry, and rumination characterize people with insomnia both at bedtime and throughout the day. Moreover, empirical studies have confirmed a correlation between worry and sleep length, that is, individuals who worry more sleep less (e.g., Kelly, 2002).
Bonnet and Arand (1995) have shown that, in addition to experiencing cognitive hyperarousal, many people with insomnia have a higher level of physiological arousal (as measured by metabolic rate) both at night and throughout the day, suggesting that this hyperarousal is responsible both for sleep difficulties and for concomitant daytime problems (see also Sateia & Nowell, 2004). People with insorrmia also tend to have a higher body temperature than normal (Bonnet & Arand, 1996) and increased fast brain wave activity (as measured by an electroencephalogram) before sleep (Lamarche & Ogilvie, 1997). Hyperarousal may be caused either by stressful life events (Healey et al., 1981) or by internal experiences (e.g., memories of traumatic experiences) that Rachman (1980, p. 55) described as unsuccessful emotional processing. The tendency of individuals with insomnia to underestimate their total sleep time (Edinger & Finns, 1995) may be related to this hyperarousal.
One factor that can fuel hyperarousal is worry about sleep itself. Many people with insomnia tend to have maladaptive and incorrect beliefs about sleep. Although it has been shown that sleep deprivation affects performance (for a thorough review, see Monk, 1991), people with insomnia tend to greatly exaggerate the extent of their sleep difficulty and the impact that sleep loss has on their performance. Older clients are particularly prone to this exaggeration (Morin, Stone, Trinkle, Mercer, & Remsberg, 1993).
This worry about sleep can then become associated with stimuli associated with bedtime (e.g., the bed itself, brushing teeth before going to bed, donning nightwear), thereby promoting wakefulness at bedtime. That is, these learned associations result from overconcern about one's inability to sleep, which then leads to cycles in which seeing the stimulus (e.g., the bed) prompts worry about lack of sleep, leading to more agitation, and consequently less ability to sleep (AASM, 2005).
Other sleep disorders. The clinician should be sensitive to symptoms such as snoring or periodic leg movements that may indicate the presence of a sleep disorder other than insomnia. It is useful to seek information from a client's bed partner about such symptoms. In addition, complaints of severe daytime fatigue (e.g., falling asleep in meetings or when stopped at red lights) may indicate the presence of narcolepsy, a chronic neurological sleep disorder characterized by excessive daytime sleepiness. (The National Sleep Foundation provides online information and resources about these other sleep disorders at www.sleepfoundation.org, while the Canadian Sleep Society provides similar information at www.css.to)
Circadian rhythm phase shifts. Disrupted circadian rhythms also lead to both temporary and chronic sleep disturbance. Circadian rhythms are biological functions, including the timing of sleep and wakefulness, that follow approximately 24-hour cycles (Lack & Bootzin, 2003). Shift work (Hauri, 2000; Sateia & Nowell, 2004),jet lag (Hauri, 2000), and both adolescence and advancing age (Sateia & Nowell, 2004) can upset these circadian rhythms, creating difficulty with sleeping. Individuals who report sleep-onset insomnia (i.e., trouble with falling asleep) may have a delayed sleep phase. Their trouble with falling asleep is caused by trying to sleep at a time that is inconsistent (i.e., earlier) with their circadian rhythm (Morris, Lack, & Dawson, 1990). Older adults typically experience advanced circadian rhythms, such that the phase of older adults' circadian rhythms occurs earlier than that of their younger counterparts. Although phase delays make it difficult to fall asleep, phase advancement makes it difficult to maintain sleep in the early morning (Akerstedt, 1988).
Natural aging. In addition to phase advancement, the sleep of older individuals is normally fragmented and involves more sleep stage shifts (indicating poorer sleep), more Stage 1 sleep (light sleep), a longer latency to sleep Stages 3 and 4 (deep sleep), less deep sleep, and more midsleep awakenings (Williams, Karacan, Thornby, & Salis, 1972). These changes all result in reduced sleep efficiency and reduced total sleep time and, therefore, also cause decreased daytime alertness and cognitive deficits.
Because it is normal for older adults to have difficulty initiating and maintaining sleep, older adults represent one population that may be particularly susceptible to complaints of insomnia. Furthermore, older adults tend to exacerbate the problem through excessive worrying. Later-life insomnia is a concern because, if left unmanaged, it is related to poor health, depression, angina, limitations to activities of daily living, and long-term use of sedative, or hypnotic, drugs (Newman, Enright, Manolio, Haponik, & Wahl, 1997). Fortunately, there are treatment strategies for older adults that can be readily implemented.
* Treatment for Insomnia
It must be noted at the outset that there are some substantial problems with research into the efficacy of treatment for insomnia. The principal problem is how improvement is measured. In many studies, success is based on changes to clients' sleep, either as measured by a polysomnograph or based on subjective report. However, preliminary research has shown that distress about sleep can have little relation to actual sleep disruption (Belicki, Chambers, & Ogilvie, 1997). These findings buttress Edinger and Wohlgemuth's (1999) suggestion that treatment success should be based on clients' subjective reports of improved sleep, independent of objective measures of sleep quantity. Furthermore, Mendelson (1993) has argued that the benefit of treatment may be in changing the client's perception of sleep, rather than sleep itself. Moreover, although the definition of insomnia includes a component of altered daytime functioning, research rarely takes improvements to daytime functioning into account (Edinger & Wohlgemuth, 1999; A. G. Harvey & Tang, 2003).Yet, in our experience, the desire to improve daytime functioning is ultimately what propels clients to seek help. Therefore, much of the literature has perhaps been misdirected in its focus on the extent of sleep disruption.
That said, the consistent picture from the literature is that there are treatment approaches that can successfully address complaints of insomnia in many clients. Moreover, these approaches can be successfully applied not only to primary insomnia but also to insomnia that is comorbid with other conditions. We first briefly review some of the principal medical, or physical, treatments available, then turn to the techniques that can be used by counselors.
Physical Approaches to the Treatment of Insomnia
There are two main approaches to the physical treatment of insomnia: pharmacotherapy and bright light treatment. Although some literature has shown that these methods are helpful in alleviating the symptoms of insomnia, there are certain risks associated with each type of treatment.
Pharmacological treatment. Hypnotic and antidepressant drugs are the most common form of treatment for insomnia (Walsh & Schweitzer, 1999). Antidepressants such as trazadone and amitriptyline are among the top four drugs prescribed for insomnia. Although they may induce sedation, there is no research supporting their use for insomnia, and they are known to have numerous side effects (National Institutes of Health, 2005). In fact, a recent state-of-the-science review suggested that the off-label use (i.e., practice of prescribing pharmaceuticals for a purpose outside the scope of a drug's approved label) of antidepressants for insomnia occurs too frequently, citing the fact that little evidence indicates that antidepressants are efficacious in this context (National Institutes of Health, 2005).
Benzodiazepines, such as flurazepam and temazepam, have been found to be effective on a short-term basis (Hauri, 2000). However, long-term use of these drugs may cause addiction and/or tolerance, decreased daytime functioning, poor sleep quality, and rebound insomnia (i.e., insomnia that reoccurs and worsens) upon discontinuation (Hauri, 2000). Therefore, recent research has dictated that benzodiazepines be prescribed less frequently; newer, nonbenzodiazepine medications have replaced older benzodiazepine medication as the drug of choice for insomnia.
Nonbenzodiazepine hypnotics (i.e., benzodiazepine receptor agonists), such as zolpidem (Ambien), zaleplon (Sonata), and eszopiclone (Lunesta), have thus far proven effective in the treatment of insomnia. In general, their shorter half-life makes these drugs less likely to cause dependence, rebound insomnia, and medication "hangovers" (e.g., malaise and cognitive difficulty) the following day (National Institutes of Health, 2005). Zolpidem, in particular, is associated with decreased time to fall asleep, increased total sleep time, decreased total wake time, and more efficient sleep (Kryger, Steljes, Pouliot, Neufeld, & Odynski, 1991). However, eszopiclone is the only one of these drugs that has been studied for its long-term effects, and even it has only been studied over 6 months (Hair, McCormack, & Curran, 2008; National Institutes of Health, 2005). Clinicians should note, however, that people with insomnia are often prescribed hypnotics for many years, not just 6 months, and the long-term effects of this practice remain unknown.
Furthermore, there is evidence that in the long term, psychological therapies are more effective in treating insomnia than pharmacotherapy. For example, Wu, Zhang, Deng, and Long (2002), in a comparison of four groups (i.e., pharmacotherapy, cognitive behavioral therapy [CBT], pharmacotherapy combined with CBT, and placebo control), found that pharmacotherapy was only effective in the short term, while psychological treatments were effective over the long term (Wu et al., 2002). In a more recent study, Vallieres, Morin, Guay, Bastien, and LeBlanc (2004) showed that when pharmacotherapy was used only for a short duration and overlapped slightly with the introduction of CBT, improvements were superior to using the two sequentially (i.e., pharmacotherapy, then CBT) or concurrently. In particular, it should be noted that most improvements occurred after the introduction of CBT (Vallieres et al., 2004).
Bright light therapy. For individuals with insomnia resulting from circadian factors, bright light therapy may be of some use. Campbell, Dawson, and Anderson (1993) showed that for older adults with sleep maintenance insomnia, 12 evenings of bright light therapy increased sleep efficiency. Subsequently, Suhner, Murphy, and Campbell (2002) demonstrated that the same bright light treatment delayed the body temperature rhythm an average of 94 minutes. Thus, this treatment may be successful in alleviating sleep maintenance difficulties by realigning body temperature rhythms with sleep and wake times. This therapy should allow people with insomnia to remain awake longer, thus consolidating subsequent sleep. Because the body temperature minimum is delayed following evening bright light therapy, sleep should be easier to maintain in the early morning. Suhner et al. found, however, that when bright light exposure was reduced to twice a week, changes to circadian rhythms were not maintained. This result indicates that daily exposure, a time-consuming and cumbersome procedure, is needed to preserve changes to circadian rhythms.
For individuals with sleep-onset insomnia, bright light therapy should be administered in the morning (Lack & Bootzin, 2003). Early morning bright light exposure advances the circadian rhythm (Lack & Bootzin, 2003), making the person with insomnia feel tired earlier. Any individuals planning to use this technique should be educated about possible side effects, such as increased cataract risk (Reme, Rol, Grothmann, Kaase, & Terman, 1996), and should investigate the costs and other potential disadvantages of this technique.
Clearly there are disadvantages to the various physical approaches to the treatment of insomnia. Fortunately, as discussed in the following section, numerous studies have shown that psychological approaches to managing sleep complaints can be effective.
Psychological Approaches to the Treatment of Insomnia
Numerous studies have demonstrated the usefulness of CBT in treating insomnia, although empirical research has indicated that some components of CBT are more effective than others. CBT for insomnia is typically a short treatment, with success being reported for treatment approaches ranging from two to six sessions (e.g., Backhaus, Hohagen, Voderholzer, & Riemann, 2001; Verbeek, Schreuder, & Declerck, 1999). Even a self-administered program of bibliotherapy involving six booklets mailed weekly to participants has been shown to be effective (see Mimeault & Morin, 1999, for a complete description of this program). Bastien, Morin, Ouellet, Blais, and Bouchard (2004) recently investigated CBT delivered in different modalities (i.e., face-to-face individual sessions, group sessions, telephone calls) and found that all modalities led to gains (when compared with baseline self-reports) that were maintained at a 6-month follow-up. Moreover, one does not need a high level of expertise to effectively use CBT. Espie, Inglis, Tessier, and Harvey (2001) found that CBT could be effectively delivered in six group sessions by specially trained, primary care nurses.
In sum, CBT is not only useful, it is also quite cost-effective for the client and can be accomplished with ease and in a timely manner, thereby requiring minimal obligation on the part of the clinician. It typically involves certain components: sleep education, sleep hygiene, sleep restriction, stimulus control, and cognitive therapy.
Sleep education. Sleep education simply provides clients with information about sleep. For instance, Verbeek et al. (1999) stressed that clients should be aware of what constitutes good and poor sleep, how much sleep is needed, how age affects sleep, and how insomnia develops and is maintained. Sleep education may be especially important for older adults who need to recognize and adapt to developmental changes to sleep through such means as building nap times into their daily schedule and finding tasks or hobbies to complete in the early morning.
Sleep hygiene. Sleep hygiene is a self-regulation technique that addresses the poor sleep habits that interfere with good sleep (Gatchel & Oordt, 2003). Sleep hygiene instructions (see Appendix) provide commonsense instructions for making small lifestyle changes that may aid the client in initiating and maintaining sleep. This intervention is very popular; however, although it may suffice for some clients, Espie et al. (1998) reported that sleep education and sleep hygiene instructions were not enough to lead to improvements and that sleep scheduling (i.e., sleep restriction) was necessary for treatment gains to be evident.
Sleep restriction. Sleep restriction therapy was developed in response to the observation that chronic insomnia is perpetuated by an excessive amount of time spent in bed (Spielman, Saskin, & Thorpy, 1987). Often, people with insomnia try to compensate for lost sleep or for boredom by remaining in bed longer; this extra time in bed simply causes more wake time, less deep sleep, and more light sleep (Hauri, 2000; Wohlgemuth & Edinger, 2000). The purpose of this treatment is to consolidate clients' sleep, decreasing both the time to fall asleep and awakenings after sleep onset. Clients' need to sleep is increased by the slight sleep deprivation that is imposed, thereby deepening and consolidating sleep (Wohlgemuth & Edinger, 2000). Nevertheless, it is this sleep deprivation that makes compliance with this treatment difficult for some clients. However, Wohlgemuth and Edinger noted that this treatment also lessens the frustration that is associated with remaining in bed for extended periods and inability to sleep, which may encourage clients to comply with it. This treatment component is recommended for clients when their napping and/or excessive time in bed seem to be contributing to sleep difficulties (Wohlgemuth & Edinger, 2000). (For details of the typical sleep restriction prescription, see Appendix.)
Stimulus control. L. Harvey, Inglis, and Espie (2002) recommended combining stimulus control therapy with sleep restriction therapy to maximize benefits because they found that stimulus control therapy was the best predictor of improvements in sleep. Stimulus control therapy was originally used to change problem behaviors (e.g., overeating). Applied to treating insomnia, stimulus control therapy (Bootzin, 1975) was designed to reassociate the bed, the bedroom, and bedtime activities with sleep, rather than with arousal. Stimulus control is based in operant conditioning learning theory, where the bedroom has become a discriminative stimulus associated with an absence of reinforcement, specifically reduced sleep (i.e., the bedroom has become an antecedent following which sleep is less likely to occur). Therefore, all activities other than sleep (and sex) are not permitted in the bedroom in order to reestablish the bedroom as a positive discriminative stimulus signalling the availability of reinforcement, specifically sleep (Bootzin, 1975). (For stimulus control instructions to the client, see Appendix.)
Cognitive restructuring. Cognitive interventions are based on cognitive therapy techniques used with depression and anxiety. Cognitive restructuring attempts to change the belief that poor sleep will lead to devastating consequences (Smith, Smith, Nowakowski, & Perlis, 2003). The goal of cognitive restructuring is to have clients realize that their beliefs about sleep and the consequences of poor sleep are distorted. (See Appendix for one approach to cognitive restructuring for insomnia.)
Paradoxical intention. This cognitive strategy is used to alleviate difficulty with falling asleep (Broomfield & Espie, 2003). Because individuals with insomnia often experience anxiety at sleep onset, paradoxical intention is thought to work by eliminating the effort to sleep and its associated cognitive and affective arousal, thereby reducing anxiety. Broomfield and Espie found, as expected, that this technique reduced both sleep effort and bedtime anxiety; it also reduced subjective sleep-onset latency. Moreover, a shorter sleep-onset latency was correlated with anxiety reduction, indicating that it is through the reduction of anxiety at sleep onset that paradoxical intention reduces insomnia (Broomfield & Espie, 2003). However, it may be equally true that the reduction in sleep-onset latency consequently reduced clients' anxiety. (See Appendix for different ways for a client to implement this technique.)
Relaxation therapy. Although it is a common technique used in the treatment of insomnia, no evidence exists to suggest that the sole use of relaxation training effectively relieves insomnia (e.g., Edinger, Wohlgemuth, Radtke, Marsh, & Quillian, 2001). Relaxation techniques are purported to reduce physiological tension prior to sleep onset and to be useful when clients wake up in the middle of the night (Gatchel & Oordt, 2003). However, the current findings in the current literature indicate that relaxation therapy is not an essential strategy and is best used in combination with other components of CBT.
In summary, insomnia is a prevalent disorder that can have negative consequences in terms of clients' health, well-being, and performance. Many individuals seeking psychotherapy may be wrestling with insomnia and its effects. In addition, when insomnia is the sole complaint, many who are affected by this disorder seek medical help. However, in the course of our brief review of biological therapies for insomnia (i.e., pharmacotherapy, bright light therapy), we argue that although these therapies may have some clinical utility on a short-term basis, they are often not the treatments of choice, especially as a long-term solution. When clients report difficulty with sleep, the components of CBT, when applied to insomnia, are an important aid for providing quick treatment with lasting effects. Furthermore, CBT is the treatment that is preferred by clients (Morin, Gaulier, Barry, & Kowatch, 1992). It is easy to see why because psychological treatments have no side effects; have no tolerance or dependency issues; are relatively quick and cost effective; and, most important, are efficacious over the long term. Given that the psychological treatment of insomnia is recommended, we urge clinicians to have greater involvement in both the assessment and the treatment of insomnia.
Cognitive Behavioral Therapy Components to Treat Insomnia
Sleep hygiene instructions to the client (Hauri, 1982; Modn, 1993)
* Sleep only as much as needed to feel refreshed.
* Maintain a regular sleep/wake schedule, even on weekends.
* Exercise regularly, but not close to bedtime.
* Fat regular meals, avoid going to bed hungry, and avoid excessive liquids in the evening.
* Plan time for worrying well before bedtime.
* Avoid trying to fall asleep, and turn the clock so the numbers are not showing.
* Make the bedroom free from light and noise, and set a comfortable temperature.
* Avoid long naps.
* Cut down on caffeine, alcohol, and smoking.
Sleep restriction prescription (Spielman et al., 1987)
* Client completes sleep diary for 2 weeks (provides information about bed/wake times, length of time to fall asleep, and number/ duration of awakenings).
* Clinician calculates the average total sleep time according to sleep diary data.
* Clinician assigns time in bed equal to average total sleep time (no less than 4.5 hours/night).
* Clinician helps client to decide on appropriate bed/wake times for this amount of sleep.
* Each week, the client's average sleep efficiency (time asleep/ time in bed) is calculated.
* If sleep efficiency is above 90%, clinician increases client's time in bed by 15 minutes; if below 85%, it is decreased by 15 minutes.
* Clinician continues to adjust time in bed until client reports satisfaction with sleep/daytime function, sleep efficiency is 85%-90%.
Client's time in bed remains at last adjusted value.
Stimulus control instructions to the client (Bootzin, 1975)
* Keep a regular sleep/wake schedule every day, regardless of how much sleep you get.
* Use the bed and bedroom only for sleep (and sex).
* Sleep only in the bedroom, not elsewhere in the house.
* If awake, leave the bedroom.
* Return to bed only when sleepy.
* Recognize internal cues for sleepiness (e.g., yawning).
* Refrain from napping.
Cognitive restructuring (Harvey & Greenall, 2003; Smith et al., 2003)
* Client constructs list of all potential negative consequences of poor sleep (5-10 items).
* He/she rates the odds of each consequence actually occurring (not likely to very likely).
* He/she calculates how often sleep is poor and how often these consequences have occurred.
* Clinician displays the large discrepancy between beliefs (#2) and actual outcome (#3).
Paradoxical intention options for the client (Broomfield & Espie, 2003)
* At bedtime, relax with the lights out, but keep the eyes open.
* At bedtime, try to read for as long as possible.
Test to Earn CE Credit
Note: Correctly completing 3 of 3 test questions earns 1 continuing education contact hour.
* Examination Questions
1. What percentage of the population is estimated to suffer from the consequences of insomnia?
 a. One tenth
 b. One quarter
 c. One third
 d. One half
2. Which of the following physical treatments have been found to be helpful in alleviating the symptoms of insomnia?
 a. Pharmacotherapy
 b. Bright-light treatment
 c. Group psychotherapy
 d. a and b.
3. What counseling approach is advanced by the authors as being useful in the psychological treatment of clients with insomnia?
 a. Existential therapy
 b. Cognitive-behavioral therapy
 c. Gestalt theraphy
 d. Human, person-centered therapy
Akerstedt, T. (1988). Sleepiness as a consequence of shift work. Sleep, 11, 17-34.
Aldrich, M. S. (1993). Insomnia in neurological diseases. Journal of Psychosomatic Research, 37(Suppl. 1), 3-11.
American Academy of Sleep Medicine. (2005). International classification of sleep disorders: Diagnostic and coding manual (2nd ed.). Westchester, IL: Author.
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.
Backhaus, J., Hohagen, F., Voderholzer, U., & Riemann, D. (2001). Long-term effectiveness of a short-term cognitive-behavioral group treatment for primary insomnia. European Archives of Psychiatry & Clinical Neuroscience, 251, 35-41.
Bastien, C. H., Morin, C. M., Ouellet, M.-C., Blais, F. C., & Bouchard, S. (2004). Cognitive-behavioral therapy for insomnia: Comparison of individual therapy, group therapy, and telephone consultations. Journal of Consulting and Clinical Psychology, 72, 653-659.
Belicki, K., Chambers, E., & Ogilvie, R. (1997). Sleep quality and nightmares. Sleep Research, 26, 637.
Bliwise, D. L. (2005). Normal aging. In M. H. Kryger, T. Roth, & W C. Dement (Eds.), Principles and practice of sleep medicine (pp. 24-38). Philadelphia, PA: Elsevier.
Bonnet, M. H., & Arand, D. L. (1995). 24-hour metabolic rate in insomniacs and matched normal sleepers. Sleep, 18, 581-588.
Bonnet, M. H., & Arand, D. L. (1996). The consequences of a week of insomnia. Sleep, 19, 453-461.
Bootzin, R. R. (1975). Behavior modification and therapy: An introduction. Cambridge, MA: Winthrop.
Bootzin, R. R. (2000). Cognitive-behavioral treatment of insomnia: Knitting up the ravell'd sleeve of care. In D. T. Kenny & J. G. Carlson (Eds.), Stress and health: Research and clinical applications (pp. 243-266). Amsterdam, Netherlands: Harwood Academic Publishers.
Broomfield, N. M., & Espie, C. A. (2003). Initial insomnia and paradoxical intention: An experimental investigation of putative mechanisms using subjective and actigraphic measurement of sleep. Behavioral and Cognitive Psychotherapy, 31, 313-324.
Buysse, D. J., Reynolds, C. F., Kupfer, D. J., Thorpy, M. J., Bixler, E., Kales, A., ... Stapf, D. (1997). Effects of diagnosis on treatment recommendations in chronic insonmia--A report from the APA/NIMH DSM-IV field trial. Sleep, 20, 542-552.
Buysse, D. J., Reynolds, C. F., Monk, T. H., Berman, S. R., & Kupfer, D. J. (1989). The Pittsburgh Sleep Quality Index: A new instrument for psychiatric practice and research. Psychiatry Research, 28, 193-213.
Campbell, S. S., Dawson, D., & Anderson, M. W. (1993). Alleviation of sleep maintenance insomnia with timed exposure to bright light. Journal of the American Geriatrics Society, 41, 829-836.
Carskadon, M. A., & Dement, W. C. (2000). Normal human sleep: An overview. In M. H. Kryger, T. Roth, & W. C. Dement (Eds.), Principles and practice of sleep medicine (pp. 15-25). Toronto, Ontario, Canada: Saunders.
Currie, S. R., Wilson, K. G., Pontefract, A. J., & deLaplante, L. (2000). Cognitive-behavioral treatment of insomnia secondary to chronic pain. Journal of Consulting and Clinical Psychology, 68, 407-416.
Edinger, J. D. (1987). Sleep history questionnaire for evaluating insomnia complaints. In P. A. Keller & S. R. Heyman (Eds.), Innovations in clinical practice: A sourcebook (Vol. 6, pp. 295-303). Sarasota, FL: Professional Resource Exchange.
Edinger, J. D., & Finns, A. I. (1995). The distribution and clinical significance of sleep time misperceptions among insomniacs. Sleep, 18, 232-239.
Edinger, J. D., & Means, M. K. (2005). Cognitive-behavioral therapy for primary insomnia. Clinical Psychology Review, 25, 539-558.
Edinger, J. D., & Wohlgemuth, W. K. (1999). The significance and management of persistent primary insomnia: The past, present and future of behavioral insomnia therapies. Sleep Medicine Reviews, 3, 101-118.
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. Journal of the American Medical Association, 285, 1856-1864.
Espie, C. A., Brindle, S., Tessier, S., Dawson, S., Hepburn, T., McLellan, A., ... McColl, J. (1998). Supervised cognitive-behavior therapy for insomnia in general medical practice--Preliminary results from the West of Scotland program. In E. Sanavio (Ed.), Behavior and cognitive therapy today: Essays in honor of Hans J Eysenck (pp. 67-86). Oxford, England: Elsevier Science.
Espie, C. A., Brooks, D. N., & Lindsay, W. R. (1989). An evaluation of tailored psychological treatment of insomnia. Journal of Behavior Therapy & Experimental Psychiatry, 20, 143-153.
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, 45-60.
Gatchel, R. J., & Oordt, M. S. (2003). Insomnia. In R. J. Gatchel & M. S. Oordt (Eds.), Clinical health psychology and primary care: Practical advice and clinical guidance for successful collaboration (pp. 135-148). Washington, DC: American Psychological Association.
Hair, P I., McCormack, P. L., & Curran, M. P. (2008). Eszopiclone: A review of its use in the treatment of insomnia. Drugs, 68, 1415-1434.
Harvey, A. G. (2005). Unwanted intrusive thoughts in insomnia. In D. A. Clark (Ed.), Intrusive thoughts' in clinical disorders: Theory. research, and treatment (pp. 86-118). New York, NY: Guilford Press.
Harvey, A. G., & Greenall, E. (2003). Catastrophic worry in primary insomnia. Journal Of Behavior Therapy and Experimental Psychiatry, 34. 11-23.
Harvey, A. G., & Tang, N. K. Y. (2003). Cognitive behaviour therapy for primary insomnia: Can we rest yet? Sleep Medicine Reviews, 7, 237-262.
Harvey, L., Inglis, S. J., & Espie, C. A. (2002). Insomniacs' reported use of CBT components and relationship to long-term clinical outcome. Behaviour Research and Therapy, 40, 75-83.
Hauri, P. J. (1982). Sleep disorders. In R. J. Gatchel, A. Baum, & J. E. Singer (Eds.), Handbook of psychology and health: Vol. 1. Clinical psychology and behavioral medicine: Overlapping disciplines (pp. 211-260). Hillsdale, NJ: Erlbaum.
Hauri, P. J. (1989). The cognitive-behavioral treatment of insomnia. In A. J. Stunkard & A. Baum (Eds.), Eating, sleeping, and sex. Perspectives in behavioral medicine (pp. 181-194). Hillsdale, N J: Erlbaum.
Hauri, P. J. (2000). The many faces of insomnia. In D. I. Mostofsky & D. H. Barlow (Eds.), The management of stress and anxiety in medical disorders (pp. 143-159). Needham Heights, MA: Allyn & Bacon.
Healey, E. S., Kales, A., Monroe, L. J., Bixler, E. O., Chamberlain, K., & Soldatos, C R. (1981). Onset of insomnia: Role of life-stress events. Psychosomatic Medicine, 43, 439-451.
Johns, M. W. (1991). A new method for measuring daytime sleepiness: The Epworth Sleepiness Scale. Sleep, 14, 540-545.
Kelly, W. E. (2002). Worry and sleep length revisited: Worry, sleep length, and sleep disturbance ascribed to worry. Journal of Genetic Psychology, 163, 296-304.
Kryger, M. H., Steljes, D., Pouliot, Z., Neufeld, H., & Odynski, T. (1991). Subjective versus objective evaluation of hypnotic efficacy: Experience with zolpidem. Sleep, 14, 399-407.
Lack, L. C., & Bootzin, R. R. (2003). Circadian rhythm factors in insomnia and their treatment. In M. L. Perlis & K. L. Lichstein (Eds.), Treating sleep disorders: Principles and practice of behavioral sleep medicine (pp. 305-343). New York, NY: Wiley.
Lamarehe, C. H. & Ogilvie, R. D. (1997). Electrophysiological changes during the sleep onset period of psychophysiological insomniacs, psychiatric insomniacs, and normal sleepers. Sleep, 20, 724-733.
Lichstein, K. L., McCrae, C. S., & Wilson, N. M. (2003). Secondary insomnia: Diagnostic issues, cognitive-behavioral treatment, and future directions. In M. L. Perlis & K. L. Lichstein (Eds.), Treating sleep disorders: Principles and practice of behavioral sleep medicine (pp. 286-304). New York, NY: Wiley.
Lundh, L.-G. (1998). Cognitive-behavioral analysis and treatment of insomnia. Scandinavian Journal of Behaviour Therapy, 27, 10-29.
Mendelson, W. B. (1993). Pharmacologic alteration of the perception of being awake or asleep. Sleep, 16, 641-646.
Mimeault, V., & Morin, C. M. (1999). Self-help treatment for insomnia: Bibliotherapy with and without professional guidance. Journal of Consulting and Clinical Psychology, 67, 511-519.
Monk, T. H. (Ed.). (1991). Sleep, sleepiness, and performance. New York, NY: Wiley.
Morin, C. M. (1993). Insomnia: Psychological assessment and management. New York, NY: Guilford Press.
Morin, C. M., Gaulier, B., Barry, T., & Kowatch, R. A. (1992). Patients' acceptance of psychological and pharmacological therapies for insomnia. Sleep, 15, 302-305.
Morin, C. M., Stone, J., Trinkle, D., Mercer, J., & Remsberg, S. (1993). Dysfunctional beliefs and attitudes about sleep among older adults with and without insomnia complaints. Psychology & Aging, 8, 463-467.
Morris, M., Lack, L., & Dawson, D. (1990). Sleep-onset insomniacs have delayed temperature rhythms. Sleep, 13, 1-14.
National Institutes of Health. (2005, June). National Institutes of Health state-of-the-science conference statement on manifestations and management of chronic insomnia in adults. Retrieved from National Institutes of Health website: http://consensus.nih. gov/2005/2005InsomniaSOS026main.htm
Newman, A. B., Enright, P. L., Manolio, T. A., Haponik, E. F., & Wahl, P. W. (1997). Sleep disturbance, psychosocial correlates, and cardiovascular disease in 5,201 older adults: The Cardiovascular Health Study. Journal of the American Geriatrics Society, 45, 1-7.
Rachman, S. (1980). Emotional processing. Behaviour Research and Therapy, 18. 51-60.
Reid, K. J., & Zee, P. C. (2005). Circadian disorders of the sleep-wake cycle. In M. H. Kryger, T. Roth, & W. C. Dement (Eds.), Principles and practice of sleep medicine (pp. 691-701). Philadelphia, PA: Elsevier.
Reme, C. E., Rol, P, Grothmann, K., Kaase, H., & Terman, M. (1996). Bright light therapy in focus: Lamp emission spectra and ocular safety. Technology and Health Care, 4, 403-413.
Sateia, M. J., & Nowell, P. D. (2004). Insomnia. The Lancet, 364, 1959-1973.
Smith, M. T., Smith, L. J., Nowakowski, S., & Perlis, M. L. (2003). Primary insomnia: Diagnostic issues, treatment, and future directions. In M. L. Perlis & K. L. Lichstein (Eds.), Treating sleep disorders: Principles and practice of behavioral sleep medicine (pp. 214-261). New York, NY: Wiley.
Spielman, A. J., Saskin, P., & Thorpy, M. J. (1987). Treatment of chronic insomnia by restriction of time in bed. Sleep, 10, 45-56.
Suhner, A. G., Murphy, P. J., & Campbell, S. S. (2002). Failure of timed bright light exposure to alleviate age-related sleep maintenance insomnia. Journal of the American Geriatrics Society, 50, 617-623.
Vallieres, A., Morin, C. M., Guay, B., Bastien, C. H., & LeBlanc, M. (2004). Sequential treatment for chronic insomnia: A pilot study. Behavioral Sleep Medicine, 2, 94-112.
Verbeek, I., Schreuder, K., & Declerck, G. (1999). Evaluation of short-term nonpharmacological treatment of insonmia in a clinical setting. Journal of Psychosomatic Research, 47, 369-383.
Walsh, J. K., & Schweitzer, P. K. (1999). Ten-year trends in pharmacological treatment of insomnia. Sleep, 22, 371-375.
Williams, R. L., Karacan, I., Thornby, J. I., & Salis, P. J. (1972). The electroencephalogram sleep patterns of middle-aged males. The Journal of Nervous and Mental Disease, 154, 22-30.
Wohlgemuth, W. K., & Edinger, J. D. (2000). Sleep restriction therapy. In K. L. Lichstein & C. M. Morin (Eds.), Treatment of late-life insomnia (pp. 147-166). Thousand Oaks, CA: Sage.
Wu, R., Zhang, C., Deng, J., & Long, C. (2002). Comparison between cognitive-behavior therapy and medication on chronic insomnia. Chinese Mental Health Journal, 16, 677-680.
Catherine E. Milner and Kathryn Belicki, both at Department of Psychology, Brock University, St. Catharines, Ontario, Canada. Correspondence concerning this article should be addressed to Kathryn Belicki, Department of Psychology, Brock University, St. Catharines, Ontario, Canada L2S 3A1 (e-mail: email@example.com).
TABLE 1 Classifications of Insomnia for Formal Diagnoses Type/Subtype Description Primary DSM-IV-TR Difficulty initiating or maintaining sleep or experiencing nonrestorative sleep; duration of at least 1 month; clinically significant distress or impairment of functioning ICSD Psychophysiological Arousal * cognitive (e.g., racing thoughts) * emotional (e.g., anxiety, anger, worry) * physiological (e.g., higher metabolic rate) Learned associations that disrupt sleep Clients with insomnia report more sleep disturbance than is confirmed by objective measures Paradoxicala Clients with insomnia report poor sleep and may show evidence of hyperarousal despite * no objective evidence of sleep problems * no impairment in waking performance Idiopathic Rare form of insomnia Characterized by objectively poor quality of sleep Begins in childhood, even infancy Absence of factors contributing to insomnia Insomnia related to other Sleep disruption that co-occurs with disordersb physical or psychological illness Note. DSM-IV-TR = Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.; American Psychiatric Association, 2000); ICSD = Internal Classification of Sleep Disorders: Diagnostic and Coding Manual (American Academy of Sleep Medicine, 2005). (a) Formerly pseudoinsomnia or sleep state misperception. (b) Also referred to as comorbid or secondary insomnia. TABLE 2 Overview of Factors That Contribute to Insomnia Problem Description/Impact on Sleep General medical problems (Hauri, Symptoms (e.g., tremors, 2000; Lichstein et al., 2003; breathing difficulties, pain) Sateia & Nowell, 2004) directly impair sleep Medications indirectly impair sleep Worry about disease increases arousal and disrupts sleep Neurodegenerative disorders Frequent awakenings throughout (Aldrich, 1993) the night Chronic pain (Currie et al., Bidirectional relationship with 2000) sleep, such that pain impairs ability to sleep and pain is exacerbated by poor sleep Other sleep disorders (Bootzin, 2000; Hauri, 2000; Sateia & Nowell, 2004 Sleep apnea Periodic cessation of breathing, snoring Periodic limb movements in Periodic kicking of the legs, sleep restless sleep Restless leg syndrome "Creepy-crawly" sensation in the legs at bedtime, relieved by moving the legs Narcolepsy Excessive daytime sleepiness, uncontrollable sleep attacks Circadian phase shifts (e.g., those caused by jet lag, shift work; Reid & Zee, 2005) Delayed circadian rhythms Trouble falling asleep Advanced circadian rhythms Early morning awakenings Natural aging (Bliwise, 2005) Light and fragmented sleep, difficulty initiating and maintaining sleep Psychological problems (Bootzin, Symptoms directly impair sleep 2000; Buysse et al., 1997; Medications may impair sleep Hauri, 2000 Lifestyle factors (Bootzin, Poor sleep hygiene (e.g., 2000; Hauri, 2000; Sateia & extended time in bed, daytime Nowell, 2004) naps, caf-feine use) reduces the drive for sleep, thereby impairing the ability to both fall asleep and stay asleep Hyperarousal (Bonnet & Arand, 1995, 1996; Harvey, 2005; Lamarche & Ogilvle, 1997) Physiological Higher metabolic rate, increased body temperature, and increased fast brain waves impair the ability to fall asleep and stay asleep Cognitive Worry and rumination shorten sleep time Maladaptive beliefs about sleep Maladaptive beliefs about sleep (Morin et al., 1993) can increase hyperarousal Beliefs that poor sleep will negatively affect physical and mental health Unrealistic expectation of catastrophic consequences of not sleeping Unrealistic beliefs about the amount of sleep needed Overestimation of sleep disruption Bias for remembering only poor nights of sleep Maladaptive conditioning (Morin Worry about sleep associated et al., 1993) with bedtime stimuli (e.g., bed, brush-ing teeth), thereby increasing hyperarousal
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|Title Annotation:||Assessment & Diagnosis|
|Author:||Milner, Catherine E.; Belicki, Kathryn|
|Publication:||Journal of Counseling and Development|
|Date:||Mar 22, 2010|
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