Secondary insomnia: A heuristic model and behavioral approaches to assessment, treatment, and prevention

Applied & Preventive Psychology 10:107-123 (2002). Cambridge University Press. Printed in the USA. Copyright © 2001 AAAPP 0962-2849/01 $9.50 DOI: 10.1017.S096218490201003X

Secondary insomnia: A heuristic model and behavioral approaches to assessment, treatment, and prevention CHRISTINA S. McCRAE University of Florida KENNETH L. LICHSTEIN The University of Memphis

Abstract

Secondary insomnia (SI), the most common form of insomnia, affects millions of individuals. Unfortunately, SI has rarely been the focus of research, treatment, or preventive efforts because the diagnosis is difficult, and because of the erroneous belief that it is unresponsive to direct treatment. To clarify diagnosis, specific diagnostic guidelines are recommended, and a new heuristic model of SI is presented. To dispel the idea that SI is untreatable, evidence supporting the efficacy of direct psychological treatment is reviewed, and the theoretical basis for behavioral intervention is explained. Common behavioral interventions for sleep are described, and suggestions for prevention are made. Key words: Assessment, Behavioral intervention, Diagnosis, Prevention, Secondary insomnia, Theory, Treatment

Secondary insomnia (SI) poses a threat to public health and is by far the most common form of insomnia. Unfortunately, estimating the costs and consequences of SI is difficult, because research on insomnia has frequently failed to adequately distinguish primary (PI) from secondary insomnia (SI). Based on epidemiological evidence that suggests SI accounts for up to 73% of insomnia cases (Ford & Kamerow, 1989; Klink, Quan, Kaltenborn, & Lebowitz, 1992; Mellinger, Balter, & Uhlenhuth, 1985; Ohayon, Caulet, & Lemoine, 1998), however, a large proportion of the increased health care costs (Bixler, Kales, Soldatos, Kales, & Healey, 1979; Lavie, 1981; Leger & Paillard, 1997; Weyerer & Dilling, 1991), decreased work productivity (Johnson & Spinweber, 1983; Lavie, 1981; Mendelson, Garnett, & Linnoila, 1984), increased absenteeism in the workplace (Leigh, 1991), and increased risk of motor vehicle accidents (Aldrich, 1989; Ancoli-Israel & Roth, 1999; Gillberg & Akerstedt, 1998) related to insomnia is likely attributable to SI. In

this article, we first discuss the difficulties inherent in diagnosing SI and introduce a new heuristic model that we hope promotes a better understanding of this disorder. We then review the sparse treatment-efficacy literature relevant to SI and provide detailed descriptions of the most common behavioral interventions for sleep. We conclude with recommendations for the prevention of SI and their potential application to two common causes of SI--depression and chronic pain. Diagnosis Insomnia can be divided into two main types: primary and secondary. The features of both are identical except for o n e - causality. SI is precipitated by a medical or psychiatric condition or a substance; primary insomnia (P1) is not. SI and PI's shared features include one or a combination of the following: (a) difficulties falling asleep (sleep-onset insomnia), (b) frequent or prolonged awakenings during the night (sleep-maintenance insomnia), or (c) early-morning awakenings with inability to return to sleep (terminal insomnia). In addition, the individual must complain of insomnia and decreased functioning during wakefulness. Diagnostic criteria vary considerably across the three systems used to diagnose sleep disorders--the International Classification of Dis-

This manuscript was supported, in part, by grant AG14738 from the National Institute on Aging and by the Department of Psychology's Center for Applied Psychological Research, part of the State of Tennessee's Center of Excellence Grant Program. Send correspondence and reprint requests to: Christina S. McCrae, Institute on Aging, University of Florida, 1329 SW 16th St., Gainesville, FL 32610-3505. E-mail: [email protected]

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eases (ICD-10; World Health Organization, 1993), the Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric Association, 1994), and the International Classification of Sleep Disorders (ICSD; American Sleep Disorders Association, 1990). Of these three systems, the DSM-IV and the ICSD recognize SI as a distinct disorder. Unfortunately, the diagnostic guidelines provided by these two systems are not consistent. Therefore, we recommend the following diagnostic criteria for SI based on a combination of the ICSD and DSM-IV criteria, and research we recently conducted to establish the most valid quantitative criteria for use in clinical research (Lichstein, Durrence, Taylor, Bush, & Riedel, 2001): (a) difficulty initiating or maintaining sleep of -> 31 minutes, (b) occurring --> 3 nights a week, (c) significant impairment of daytime functioning (job performance, relationships) or marked distress, and (d) the establishment of a primary (causal) condition. The course of SI can be transient ( < 1 month), short term ( > 1 month but < 6 months), or chronic (6 months or more). Typically, however, SI is a chronic problem. SI is often multifactorial and may arise from one or a combination of the following: (a) physiological mechanisms of the primary disorder (particularly true for neurological disorders), (b) secondary symptoms associated with the disease (pain or nocturia), or (c) alerting medications used to treat the primary disorder and/or associated stress (Aldrich, 1993; Hu & Silberfarb, 1991). Table 1 provides specific examples of the disorders and substances that can result in SI and their potential mechanisms. See McCrae and Lichstein (2001) for a more detailed discussion of some common causes of SI.

Table 1. Potential Causes and Mechanisms of $1 Potential causes

Example mechanisms

Psychiatric: depression, anxiety, bipolar disorder, posttraumatic stress disorder (PTSD), schizophrenia

1) abnormalities in neural systems that also regulate sleep 2) psychotropic medications (i.e., SSRIs--selective serotonin reuptake inhibitors)

Medical: asthma, head injury, fibromyalgia, pulmonary disease, arthritis, headaches, Alzheimer's disease, Parkinson's disease, seizures, pain

1) pain 2) associated emotional stress 3) medication (i.e., theophylline~Theodur for asthma) 4) muscle tremors and stiffness (i.e., Parkinson's disease)

Substance: prescription medications (i.e., imipramine, steroids, L-dopa. clonidine) over-the-counter medications (i.e., Anacin, Excedrin, some diet pills, some nasal decongestants) substances of abuse (i.e., alcohol. cocaine, narcotics, amphetamines) common substances (i.e., caffeine, nicotine)

I) arousal 2) disturbance of sleep-wake systems 3) withdrawal side effects

Magnitude of the Problem Prevalence of Sl Epidemiological studies from the United States and western Europe place the prevalence of insomnia in the range of 10%-48% (Ford & Kamerow, 1989; Klink et al., 1992; Mellinger et al., t985; Ohayon, et al., 1998). SI has rarely been the target of such research, but the available evidence suggests it accounts for up to 90% of insomnia in the general population (Ford & Kamerow, 1989; Klink et al., 1992; Mellinger et al., 1985) and up to 73% of insomnia diagnosed (using ICSD criteria) in sleep-disorders centers (Buysse et al., 1994; Coleman et al., 1982; Mendelson, 1997). These data may overestimate the prevalence of SI, however, because most studies are characterized by inadequate definitions of insomnia and inadequate efforts to rule out other sleep disorders. Most studies also fail to distinguish SI from comorbidity (i.e., whether insomnia is caused by another disorder or simply coexists with another disorder). Studies have als6 estimated the prevalence of insomnia associated with particular disorders. Katz and McHorney (1998) studied 3,000 individuals with chronic illnesses (i.e., depression, congestive heart failure, obstructive airway disease, back problems, hip impairment, peptic ulcer) and found significantly elevated rates of insomnia. Monjan and Foley (1996) found older adults with stroke or heart disease were about twice as likely to develop insomnia within the next 3 years than were healthy older adults. Cordoba et al. (1998) found that 47.4% of cirrhotic and 38.6% of chronic renalfailure patients reported disturbed sleep, compared to 4.5% of healthy controls. Several studies report that 50%-70% of pain patients experience insomnia (Atkinson, Ancoli-Israel, Slater, Garfin, & Gillin, 1988; Morin, Gibson, & Wade, 1998; Pilowsky, Crettenden, & Townley, 1985). Most of these studies do not specifically address SI, because they do not establish a causal relationship between the insomnia and the other condition. Morin et al. (1998) is a notable exception, finding that pain was the cause of poor sleep in 90% of pain patients experiencing insomnia. Older Adults SI is more common and more severe in older adults for a multitude of reasons. Older adults spend less time in the deeper stages of sleep (stages 3 & 4) and experience circadian rhythm changes that may make them more vulnerable to sleep disruption. Other reasons include increased rates of illness, including certain neurological diseases (Alzheimer's, Huntington's, and Parkinson's diseases), polypharmacy, and certain age-related psychosocial factors (bereavement, retirement, social isolation, loss of mobility). Older adults who experience psychiatric disorders, particularly depression, may be more vulnerable to SI (Guerrero & Crocq, 1994). Nocturia, coughing, difficulty breathing, and pain are some of the main reasons older adults cite for their sleeping difficulties (Hoch, Buysse, Monk, & Reynolds, 1992).

Secondary. Insomnia

Economic Burden The costs of SI are difficult to determine. There is very little knowledge about the costs of insomnia and even less that is specific to SI. Direct costs of insomnia have been estimated at $10.9 billion in 1990 (Walsh et al., 1995). This includes $1.1 billion for hypnotic medications and $9.8 billion for nursing care for elderly individuals with sleep problems. The indirect costs of insomnia, such as impact on health, work performance and accidents, are extremely difficult to estimate. Research has shown individuals with insomnia visit the doctor twice as often as good sleepers (Weyerer & Dilling, 1991) and are more likely to be hospitalized than good sleepers (Bixler et al., 1979; Lavie, 1981; Leger & Paillard, 1997). It is unclear whether these findings relate to SI, because we do not know whether the insomnia was the cause or the consequence of poor health. Leigh (1991) conducted a survey of 1,308 workers and found insomnia was the best predictor (out of 37) of absenteeism. Insomnia can result in decreased work performance (Johnson & Spinweber, 1983; Lavie, 1981; Mendelson et al., 1984), decreased job satisfaction (Lavie, 1981), and limited job advancement (Johnson & Spinweber, 1983). In 1988, Stoller (1994) estimated the cost of lost work productivity caused by insomnia at $41.1 billion. Insomniacs are also at greater risk for traffic accidents (Aldrich, 1989; Ancoli-Israel & Roth, 1999; Gillberg & Akerstedt, 1998). The cost of accidents resulting from all types of sleep disturbance were estimated at $ 4 6 52 billion in 1988 (Balter et al., 1992). Again, we do not know how much of this cost is attributable to SI. Given that SI accounts for the vast majority of insomnia and research estimating the costs of insomnia has generally made no effort to distinguish PI and SI, it is likely that a majority of these costs are attributable to SI.

Theory Development

Need for Theoretical Development of Sl There is a well-developed and generally accepted behavioral model of PI (Spielman, Caruso, & Glovinsky, 1987) but no such model exists for SI. According to Spielman and colleagues, PI is believed to stem from maladaptive behaviors and cognitions. Specifically, poor sleep arises as a result of some combination of psychological tension (i.e., bedtime worry), conditioned sleep inhibition (i.e., association of the bedroom with activities, thoughts, or emotions that interfere with sleep), and cognitive or physiological arousal related to the preceding factors. According to this model, chronic insomnia develops because some individuals become preoccupied with trying to sleep. Over time, a vicious cycle develops in which the harder the individual tries to sleep, the more frustrated and aroused he or she becomes, and the less he or she is able to sleep. Smith and colleagues (2000, 2001) suggest that although the factors that precipitate PI and SI diffel, the behavioral

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model may provide a good explanation of the factors (maladaptive behaviors, conditioned arousal, worry) that maintain both types of insomnia. These researchers found patients with chronic insomnia secondary to benign pain disorders experienced presleep cognitive arousal similar to that experienced by patients with Pl. Based on their findings, these researchers argue that chronic insomnia secondary to benign pain disorders is more like than unlike PI. Although we agree with Smith and colleagues that the factors that maintain both SI and PI may be similar, we believe a separate model of SI is needed to help explain its development. Although the development of SI may appear straightforward--it is the direct result of some precipitating condition, the causal connection between insomnia and another condition is not always clear-cut. As a result, diagnosing SI can be extremely difficult.

A Heuristic Model of SI The proposed model takes this difficulty into account. The model is not intended to replace existing diagnostic schemes. Instead, we hope it will supplement them and provide both clinicians and researchers alike with a framework for better understanding SI. A theoretically driven consideration of the issues related to SI may promote better understanding of this enigmatic disorder and in turn may result in more effective treatment, and perhaps the development of preventive strategies (which at the present time are virtually nonexistent). Lichstein's (2000) model categorizes SI into three distinct varieties: absolute, partial, and specious. These varieties are not to be confused with the common diagnostic practice of labeling SI based on the three types of predisposing conditions (i.e., psychiatric SI, medical SI, and substance SI). As their names imply, absolute SI occurs when the primary condition is directly responsible for the insomnia, and partial SI occurs when the primary condition is only partially responsible for the insomnia. Specious SI occurs when the primary condition only appears to be related to the insomnia, but in reality is unrelated. The model is based on the causal relationship between the primary condition and the insomnia in terms of two key variables: origin and severity. These variables and the role they play in the model are presented separately for each variety of SI. Figure 1 illustrates the model and the relationships between the two key variables and the three types of SI. Absolute SI requires the insomnia to mimic both the origin and the severity of the primary condition. The insomnia must begin shortly following the primary condition and must be active when the primary condition is active and remit when the primary condition remits. A good example of this would be a cancer patient who always experiences insomnia when the cancer is active and never has problems when the cancer is in remission. We consider this situation to be a naturally occurring single-subject "A-B-A-B" experimental design. Because this design establishes causality when manipulated in the laboratory (Hersen & Barlow, 1976), we can

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ORIGIN

Relationship between the origins of the Insomnia & the Primary Condition (PC) I I

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SEVERITY

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Partial SI*

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Specious SI

origin & severity

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Figure 1. Model of secondary insomnia (SI) depicting the relationship between the insomnia and the primary condition in terms of origin and severity.

presume it does the same when it occurs naturally. Absolute SI is the only variety that allows for a definitive diagnosis of SI. Unfortunately, in clinical settings, the naturally occurring "A-B-A-B" design is an unlikely event• Partial SI occurs when a causal relationship between the insomnia and the primary condition can be established for only one of the key variables. As a result, two versions of partial SI--partial SI (origin) and partial S1 (severity)--are possible. Partial SI (origin) occurs when insomnia that was created by a primary condition develops some degree of functional independence. Over time, a primary component develops as a result of one or more of the mechanisms described in the previous PI model (i.e., psychological tension, conditioning, cognitive or physiological arousal). For example, a recovered alcoholic who developed sleep difficulties 15 years ago as a result of drinking may have continued insomnia despite being sober for the past 5 years. The reverse situation happens in partial SI (severity). Instead of SI developing a PI component, a preexisting PI may be exacerbated by a primary condition, thereby developing an SI corn-

ponent. For example, a patient may have a 20-year history of difficulty falling asleep 2 or 3 nights a week, but may begin experiencing difficulty every night because of the onset of rheumatoid arthritis. Partial SI takes into account that PI and SI are not mutually exclusive conditions. The treatment-andprevention strategies we recommend later in this article are based on the fact that SI and PI often coexist. Specious SI occurs when absolute or partial SI is mistakenly diagnosed. The primary condition and the insomnia appear to be causally related, but in reality are comorbid (both disorders exist but are independent of each other). Because specious SI can never be entirely ruled out, diagnosing SI (whether partial or absolute) is extremely difficult. Fortunately, we can increase our confidence in a SI diagnosis in two ways: (a) by collecting a thorough history from the patient, and (b) by examining the patient's response to treatment of the primary condition• A thorough history helps to establish causality. Regarding treatment, absolute SI can be expected to respond to treatment of the primary condition, whereas partial and specious SI should respond only partial-

Secondary Insomnia

ly or not at all. History-taking and treatment response will be discussed in more detail in the sections on assessment and treatment, respectively.

Assessment

Sleep History A detailed sleep history is essential in the assessment of insomnia (Ohayon et al., 1998). The clinical interview should focus on the nature, duration, and intensity of the sleep complaint; it's longitudinal course; and the individual's sleep habits and response to previous treatments. To differentiate primary insomnia from secondary insomnia, the interview should elicit information pertinent to the two key variables in Lichstein's model: (a) Does the origin of the insomnia shortly follow that of the primary condition? and (b) are variations in the severity of the primary condition over time shortly followed by comparable variations in the insomnia? The sleep history also provides clues as to whether a polysomnographic (PSG) evaluation is indicated. PSG is not recommended for the diagnosis of insomnia, but is often necessary to rule out other potential sources of the sleep disturbance. Apnea is a consideration when the person snores heavily, gasps for breath during the night, awakens with dry mouth, or has headaches on arousal. Restless legs is a consideration when the person (or the bed partner) reports a great deal of leg movement at night, repeatedly kicks a bed partner, or repeatedly awakens to find the bedcovers on the floor. Several versions of structured sleep interviews are available (i.e., Lacks, 1987).

Sleep Diary The Sleep Diary, a log of one's daily sleep patterns, can be used to supplement the information collected during the sleep history. Each morning, the individual records information regarding his or her sleep from the previous night. Although several versions of the Sleep Diary are available, the information recorded typically includes: time to sleep onset, number and duration of nighttime awakenings, total sleep time, and perceived quality of sleep. The Sleep Diary is an essential component of assessment and treatment. During assessment, the diary is often completed for a period of 2 weeks. This pretreatment data provides a baseline measure of the sleep disturbance that can be compared to data collected during and after treatment to determine compliance and response. Examples of sleep diaries are provided in Espie (2000) and McCrae, Durrence, and Lichstein (in press).

Treatment In clinical practice, treatment often focuses solely on the primary condition. Typically, SI receives direct treatment only when the insomnia is severe or does not respond to treatment of the primary condition. This practice is likely based on two

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assumptions: (a) SI will cease to be a problem once the primary condition has been resolved, and (b) SI is unlikely to be responsive to direct intervention. We believe, however, there may he reason to question these assumptions. First, SI frequently has a partial primary component (i.e., partial SI) or is mistakenly diagnosed (i.e., specious SI). In such situations, the insomnia is likely to respond to direct treatment. Second, it has never been demonstrated empirically that SI actually resolves following successful treatment of the primary condition. Third, clinical studies have suggested the relationship between the primary condition and the insomnia may be reciprocal in some cases such that successful treatment of the insomnia may result in improvement in the primary condition (Morin, Kowatch, & O'Shanick, 1990; Morin, Kowatch, & Wade, 1989). Finally, evidence is slowly emerging that suggests SI is responsive to direct psychological intervention (Cannici, Malcolm, & Peek, 1983; Currie, Wilson, Pontefract, & deLaplante, 2000; Lichstein, Wilson, & Johnson, 2000).

Pharmacological vs. Psychological Treatment Hypnotic medications (low doses of benzodiazepines and the benzodiazepine receptor agonists) are the most commonly used form of treatment for insomnia. The benzodiazepines that are often used include temazepam (Restoril) and estazolain (Prosom). In addition, benzodiazepines that are marketed as anxiotytics rather than hypnotics are often used, such as lorazepam (Ativan) and alprazolam (Xanax). The benzodiazepine receptor agonists include zolpidem (Ambien) and zaleplon (Sonata). Sedating antidepressants, such as amitriptyline (Elavil) and doxepin (Sinequan) and antihistamines, such as hydroxyzine (Vistaril) can also be used as hypnotics. Although the efficacy of the sedating antidepressants and antihistamines for the treatment of insomnia has not been well researched, studies have shown that the benzodiazepines and benzodiazepine receptor agonists provide effective shortterm relief of PI. Unfortunately, the clinical effectiveness of these medications decreases over time (after 4 - 8 weeks for the benzodiazepines and after 12-24 weeks for the benzodiazepine receptor agonists), and in the case of the longer acting benzodiazepines, tolerance and dependence can develop (i.e., Woods, Katz, & Winger, 1992). Additional complications can arise from the use of medication in individuals already undergoing treatment for another condition. Patients who are taking multiple medications, such as those with chronic illnesses or the elderly, may be at particular risk for side effects and drug interactions. For example, using a benzodiazepine for insomnia with a patient taking opioids for pain may result in suppressed respiration (Savard & Morin, 2001). Although sleep medications may temporarily improve sleep, they often do not improve daytime performance--memory, concentration, and so on (Johnson & Chernik, 1982). Such impairment of function has been well documented with short-term use, and there is no evidence of resolution with

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long-term use. Persons using long-acting benzodiazepines (flurazepam [Dalmane], quazepam [Doral]) often experience daytime residual effects, including cognitive and psychomotor impairment as well as drowsiness, dizziness, and lightheadedness (Holbrook, Crowther, Lotter, Cheng, & King, 2000; Roth, Hajak, & Ustun, 2001), and older adults may be particularly vulnerable to such effects. For example, older patients are at greater risk for falls and hip fractures when using long-acting agents (Ray, Griffin, & Downey, 1989). Two studies (McClusky, Milby, & Switzer, 1991; Morin, Colecchi, Stone, Sood, & Brink, 1999) have directly compared pharmacological interventions to psychological treatment. McClusky and colleagues (1991) compared 4 weeks of behavioral therapy (Relaxation and Stimulus Control) to triazolam. Sleep Diary measures of sleep latency and total sleep time improved immediately for triazolam (Halcion). Behavioral therapy took 3 weeks to achieve a similar effect. At the 9-week follow-up, however, only the behavioral treatment maintained these improvements. Morin et al. (1999) compared 8 weeks of behavioral treatment (Sleep Hygiene, Sleep Restriction, Stimulus Control, and Cognitive Therapy) to temazepam (Restoril) in older insomniacs. Behavioral intervention alone was found to be more effective in sustaining sleep improvements over time (up to 24 months) than either medication alone or the two treatments combined. A recent meta-analysis has also examined the efficacy of behavioral intervention and medication for the treatment of insomnia. Smith et al. (in press) included 21 studies using within-subjects designs in the analysis: 13 studies evaluated behavioral intervention (stimulus control and/or sleep restriction), 7 studies evaluated medication (benzodiazepines or benzodiazepine receptor agonists), and 1 study compared both. Although behavioral intervention yielded a greater reduction in sleep-onset latency compared to medication, there were no differences between the two treatments on any of the other variables examined (total sleep time, number of awakenings, sleep quality). Thus, the two treatments yielded overall similar short-term outcomes. Cost of treatment is another consideration. Perlis and Youngstedt (2000) recently estimated that psychological intervention costs range from $150-$1000 ($50-$100 per session, for 3-10 sessions). As a result, psychological treatment may initially cost more than pharmacological treatment. In the long run, however, psychological treatment is likely to be more cost-effective than medication, because it produces long-term improvements. To estimate the cost of pharmacological intervention, we calculated the average cost of a 30day supply of 5 mg of zolpidem (Ambien) to be $59 based on price quotes from several on-line pharmacies as well as several nationally recognized pharmacy chains in the Memphis area. Thus, the average yearly cost of zolpidem (Ambien) would be $708. After 5 years the cost of zolpidem (Ambien) rises to $3500, and after 10 years, it rises to $7080 (estimates not adjusted for inflation). We chose zolpidem (Ambien) as our example, because it is currently the most

widely prescribed hypnotic. Although preliminary evidence suggests zolpidem (Ambien) may maintain its effectiveness for up to 3 - 6 months (Scharf, Mendels, Thorpy, & Weiss, 1994; Schlich, L'Heritier, Coquelin, & Attali, 1991), the FDA guidelines recommend it be given for short-term use only. Long-term costs need to be a consideration because insomnia is often a chronic problem, and despite the FDA's recommendation, in practice, many patients continue to take zolpidem (Ambien) and other sleep medications for years. The cost of psychological intervention as calculated previously may be an underestimate, because some patients may require yearly or bi-yearly "booster" sessions of psychological treatment in order to maintain long-term improvements. Despite the potential additional cost of such booster sessions ($50-$200 per year), psychological treatment is likely to remain more cost-effective than medication in the long run. In summary, we believe psychological interventions provide the best treatment option for patients with SI: (a) they provide better long-term maintenance than medication; (b) unlike medication, they do not have the potential for serious, long-term negative consequences; and (c) they are more costeffective in the long run. We believe there is no need for such overreliance on medication when there are safe and effective psychological interventions available. Behavioral treatments provide good long-term maintenance and are unlikely to result in any permanent, serious, unwanted effects. Behavioral interventions may result in temporary increases in daytime sleepiness and memory and concentration problems. Such effects are typically mild, however, and tend to remit after the first or second week of therapy. Overall, when treating SI, first and foremost we recommend aggressive treatment of the primary condition combined with direct psychological treatment of the insomnia. Psychological Treatment There are a variety of psychological or behavioral treatments for insomnia. The efficacy of these treatments has been well documented for PI (Morin et al., 1999; Morin, Culbert, & Schwartz, 1994 and Murtaugh & Greenwood, 1995), and evidence that they are also effective for SI is beginning to accumulate. Psychological treatments work by targeting the behavioral habits and cognitive patterns that perpetuate poor sleep: somatic arousal, cognitive arousal, dysfunctional thoughts, and/or learned maladaptive sleep habits. These behavioral and cognitive factors probably seem familiar, because they were presented earlier in our discussion of the model for PI. The reason treatment targeting these habits is also beneficial for SI is likely caused by the fact that when SI persists for at least a few months, a learned, behavioral component often develops (i.e., partial SI). When patients are unable to sleep, the bedroom may become associated with frustration and arousal rather than with sleep. Similarly, because functioning with little sleep for long periods of time produces stress, obtaining adequate amounts of sleep may become a major preoccupation of these patients. A vicious cycle can

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thus develop in which the more one needs to sleep; the less he or she is able to sleep. Thus, behavioral components (i.e., PI) may develop even in SI (i.e., partial SI). There are a wide variety of cognitive and behavioral treatments for insomnia including: cognitive, cognitive behavioral, relaxation, stimulus control, sleep hygiene, sleep restriction, and imagery. Each of these treatments involves an interactive process between the therapist and the patient. A brief overview is provided for each of these treatments. Several excellent sources are available for readers interested in greater explanation of each of these treatments (Bootzin & Perlis, 1992; Lichstein & Morin, 2000). Sleep Hygiene. Sleep hygiene is a straightforward intervention, consisting of a set of five instructions intended to eliminate or limit five behaviors that interfere with sleep (alcohol and caffeine use, smoking, napping, and exercise). It is often the first form of intervention used. In our clinical experience, it is also the behavioral intervention with which nonspecialists are most familiar. The patient is encouraged to comply with a set of five instructions. The instructions and the rationale for each are presented in Table 2. We believe the rationale given for each instruction is extremely important and helps to increase compliance. As discussed earlier, behavioral interventions often use a Sleep Diary to monitor treatment progress and compliance. Likewise, the patient can maintain a Sleep Hygiene log to monitor which of the five instructions he or she was able to follow each day. The thera-

Table 2, Sleep Hygiene Instructions and the Rationale for Each Instruction

Rationale

1. Avoidcaffeine after noon Caffeine is a stimulant that can lead to increased arousal and difficultyfalling and staying asleep. Some people are very sensitive to the effects of caffeine, and use of caffeine after noon may disrupt sleep. For Instructions 2-5, avoid the followingbehaviors within 2 hours of bedtime: Exercising too close to bedtime may put 2. Exercise your body in an aroused state when you need to be relaxing. However, participation in regular exercise that occurs earlier in the day may improve sleep. 3. Nicotine Nicotine. like caffeine, is a stimulant that can make falling and staying asleep difficult. 4. Alcohol Although you may initially feel sleepy after drinking alcohol, alcohol use near bedtime usually leads to more awake time during the night. Heavy meals close to bedtime put a strain 5. Heavy meals on your digestive system while you are trying to sleep. Heavy meals may produce physical discomfortor metabolic changes that interfere with sleep.

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pist and patient can then review this log together. Any instructions the patient is having trouble following can be targeted and strategies for improving compliance can be discussed. Although research has shown sleep hygiene alone is not particularly effective, multicomponent treatments including sleep hygiene have been shown to be effective (Morin et al., 1994). For more detailed information on sleep hygiene see Riedel (2000). Stimulus Control. Stimulus control, the most effective single behavioral intervention (Morin et al., 1994), is based on the idea that insomnia is caused by the association of the bed and bedroom with activities other than sleep (i.e., eating, watching television, reading, worrying). This intervention was developed by Bootzin (1972, 1975). The main goal of stimulus control is to break sleep-incompatible associations and to strengthen the association of the bed and bedroom with sleep. Stimulus control consists of a set of six instructions (more detailed information is available in Bootzin & Epstein, 2000). The instructions and the rationale for each are presented in Table 3. As with sleep hygiene, a Sleep Diary and a Stimulus Control log can be used to monitor the individual's treatment progress and target problems with compliance. Sleep Restriction. Sleep restriction limits or restricts the time allowed for sleep each night (Spielman, Saskin, & Thorpy, 1987). The therapist encourages the patient to eliminate napping and to restrict the amount of time spent in bed (TIB) at night. Typically, the patient keeps a Sleep Diary for 2 - 3 weeks to establish how much time each night is actually spent sleeping (i.e., time spent awake in bed trying to sleep is excluded). Based on the average amount of time the person sleeps each night, the therapist determines a prescribed sleep amount for the patient. This amount is typically equal to either the person's average total sleep time (TST) or to the TST plus 30 minutes (Wohlgemuth & Edinger, 2000). In the latter case, 30 minutes are added to take into account the amount of nightly awake time considered to be normal. This amount should not be less than 5 hours per night in most cases. Once the TIB has been set, the therapist and patient set the desired bedtime and wake time. Because the initial TIB is based on pretreatment data, it is likely that it is an underrepresentation of the individual's actual sleep need. Sleep restriction takes this into account by raising the TIB in 1 5 - 3 0 minute increments each week until the individual's sleep efficiency reaches 90% or higher. Sleep efficiency refers to the percentage of time spent in bed at night that is actually spent sleeping (TST/TIB × 100%). When the individual's sleep efficiency falls below 85% in a given week, the TIB is lowered by 1 5 - 3 0 minutes. The goal of sleep restriction is to regulate the sleep-wake cycle by tailoring the time spent in bed to the patient's true sleep need. It does this by influencing the homeostatic system, which along with the circadian system is thought to regulate sleep (Borbely, 1982). Although the circadian system maintains the internal body clock that regulates sleep and

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Table 3. Stimulus-Control Instructions and the Rationale for Each Instruction

Rationale

1. Do not use your bed or bedroom for anything (any time of the day) but sleep (or sex).

When you do other things in bed, you are "misusing" the bed. Doing other things reinforces the notion that a variety of actions are appropriate in that setting (e.g., if you pay bills while in bed or in the bedroom, going to bed will become a cue to begin thinking about your finances and worrying about money. This may be particularly true for individuals with SI who may have large medical bills). When your bed is reserved for sleep alone, then going to bed at night will be a strong cue for you to fall asleep. Your body will tell you when it is tired; let it. When you go to bed when you are sleepy, you are more likely to go to sleep right away, reinforcing the association between your bed and sleep. When you are not sleepy, you are more likely to toss and turn. You are also more likely to begin thinking and become mentally and physically aroused. By establishing a fixed time for getting up and allowing your bedtime to vary, you allow your body to determine how much sleep yon need to function well. Your body will let you know this by getting tired when it is time for you to go to bed. Although this instruction may appear counterintuitive (i.e., How is getting out of bed going to help you sleep better?), it helps to strengthen the association of the bed and the bedroom with sleep if you do not spend long periods of awake time in bed. By getting out of bed when you have not fallen asleep after 15-20 minutes, you promote the association of the bed with sleep.

2. Go to bed only when sleepy.

3. If you do not fall asleep within about 15-20 minutes, leave the bed and do something in another room. Go back to bed when you feel sleepy again. Clock watching with regard to the 15-20 minute rule is not recommended. If you do not fall asleep within 20 minutes on returning to bed, repeat this instruction as many times as needed. 4. If you wake up during the night and do not fall back to sleep within 20 minutes, follow rule 3 again. 5. Use your alarm to leave your bed at the same time every morning regardless of the amount of sleep obtained. 6. Avoid napping.

You acquire new habits with repeated practice. When first beginning this treatment, you may have to get up many times each night before falling asleep. This will help your body acquire a constant sleep rhythm. When you vary your wake-up time each day, you do not allow your internal body clock to acquire a stable rhythm. Naps meet some of your sleep need and throws your body rhythm off schedule, making it less likely that you will fall asleep quickly at night. When you do not nap, you help to ensure that any sleep deprivation you feel from last night will increase your likelihod of falling asleep quickly tonight. If you absolutely must nap, do not nap past 3 vM.

wakefulness, the h o m e o s t a t i c s y s t e m causes progressively increasing desire to sleep the l o n g e r one is wakeful. By restricting the time in bed each night, sleep restriction initially results in sleep deprivation. O v e r time, the patient b e c o m e s progressively sleep d e p r i v e d and as a result, the homeostatic system places increasing pressure on the individual to sleep. Then, as the prescribed TIB is adjusted, the individual eventually reaches the p o i n t where his or her true sleep needs are being met. N u m e r o u s studies, i n c l u d i n g two meta-analyses support the efficacy o f sleep restriction (i.e., Bliwise, 1993; Lichstein & Riedel, 1998; M o r i n et al., 1994; M u r t a g h & G r e e n w o o d , 1995). See W o h l g e m u t h and E d i n g e r (2000) for a m o r e detailed discussion o f sleep restriction. Sleep Compression. The g o a l of sleep c o m p r e s s i o n is similar to that of sleep r e s t r i c t i o n - - t o limit or restrict the time a l l o w e d for sleep each night. Instead of i m m e d i a t e l y restricting the individual's T I B , sleep c o m p r e s s i o n involves gradually reducing T I B until it m o r e closely matches the ind i v i d u a l ' s actual sleep need. A S l e e p Dairy is kept for 2 - 3 w e e k s in order to establish h o w m u c h time the patient is spending in bed e a c h night (TIB) versus h o w m u c h time is actually spent sleeping (TST). T h e therapist calculates the difference b e t w e e n the TIB and T S T and r e c o m m e n d s the pa-

tient r e d u c e TIB by a specified a m o u n t based on the length of treatment. F o r a 5 - w e e k treatment, TIB w o u l d be r e d u c e d by a p p r o x i m a t e l y one fifth o f this difference during e a c h session. F o r e x a m p l e , an individual with an average TIB o f 8 hours (480 minutes) and an average T S T o f 5 hours (300 m i n utes) spends a p p r o x i m a t e l y 3 hours (180 minutes) a w a k e in bed each night [480 minutes (TST) - 300 minutes (TIB) = 180 minutes a w a k e in bed] and w o u l d reduce his or her TIB by a p p r o x i m a t e l y 35 minutes each w e e k for 5 w e e k s [180 m i n u t e s / 5 w e e k s -- 35 m i n u t e s / w e e k ] . I f the individual adheres to this schedule, his or her TIB should a p p r o x i m a t e l y equal his or her T S T of 300 minutes by the end o f w e e k 5. To allow for a n o r m a l a m o u n t of night a w a k e time, the final T I B goal m a y be adjusted by 1 5 - 2 0 minutes. Thus, in the preceding e x a m p l e , the final TIB goal c o u l d be adjusted to 3 1 5 320 minutes. If the patient's sleep efficiency reaches 9 0 % or higher during a g i v e n week, the TIB can be raised by 1 5 - 2 0 minutes. T y p i c a l l y the therapist and the patient c h o o s e specific retiring and arising times during each session. O v e r the course o f treatment, the reduction in TIB is a c c o m p l i s h e d through a c o m b i n a t i o n o f delaying retiring time and advancing arising time. R e s e a r c h has s h o w n sleep c o m p r e s s i o n to be effective for older adults with i n s o m n i a (Lichstein, R i e -

Secondary Insomnia

del, Wilson, Lester, & Aguillard, 2001; Riedel, Lichstein, & Dwyer, 1995). Relaxation. Relaxation refers to a variety of techniques used to target mental or physical arousal or both. Common techniques include progressive muscle relaxation, passive relaxation, visual imagery, and autogenic training. For each technique, the client is encouraged to sit back and get comfortable, close the eyes, and become mentally prepared to relax. The therapist may dim the lights in the room to create a relaxed atmosphere. The therapist initially guides the person through the relaxation using a soothing voice. The procedure typically takes 10-20 minutes. When used for insomnia, the individual is instructed to practice the relaxation at home just prior to bedtime and during nighttime awakenings. Often, the individual is also asked to incorporate a daily practice session. Practice is extremely important, because relaxation is a skill that takes time to master. The more the person practices, the deeper the level of relaxation achieved. We provide an overview of four common relaxation techniques (more detailed information is available in Lichstein, 1988). Progressive muscle relaxation involves alternately tensing and releasing different muscle groups throughout the body. Tension is used in order to produce relaxation because sometimes simply trying to relax does not result in the maximal drop in tension. The initial production of tension results in a deeper relaxation once the tension is released. Typically, 15 different muscle groups are tensed and relaxed in a specific order: hands, wrists, arms, shoulders, feet, ankles, thighs, buttocks, abdomen, shoulders, neck, forehead, face, jaw, and shoulders. Particular attention is given to the way one's muscles feel when relaxed. The person is to compare and contrast the way the muscles feel when they are relaxed versus when they are tense. In this way, a greater understanding of what relaxation feels like develops. Throughout the relaxation, the person is to focus on abdominal or diaphragmatic breathing (i.e., inhaling slowly, taking air in and all the way down to the abdomen, and then exhaling slowly). For each muscle group, the person tenses for 4 - 5 seconds, focusing on the way the muscles feel when tense. Then, the muscles are relaxed for 2 0 - 3 0 seconds while the person focuses on the way the muscles feel when relaxed compared to the way they felt when tensed. Passive relaxation is a variation of progressive muscle relaxation in which the muscle tensing is eliminated. Instead, the person Sequentially thinks about each muscle group and focuses on mentally releasing any tension in the muscles. Although this procedure does not involve actively tensing the muscles, mentally focusing on the release of muscular tension can elicit micro-activation of the muscles and increase regional blood flow, resulting in feelings of deep relaxation. We frequently employ a hybrid passive relaxation procedure in our research with older adults. This hybrid procedure only takes 10 minutes to administer. We believe this procedure may be more effective for older adults because it is shorter and less physically demanding than progressive muscle re-

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laxation. Older adults and certain patient groups may have difficulty tensing certain muscle groups (i.e., hands, neck) because of arthritis, back problems, or other physical difficulties. Visual imagery involves creating a visual picture or a mental image of a relaxing scene, object, or situation. The therapist may suggest an image or the person may already have a relaxing image in mind. The more involved the image, the less attention the person can give to other thoughts (i.e., worries about illness, anxiety related to illness). The person is encouraged to involve as many senses (sights, sounds, smells, tastes) as possible, as this will enhance the relaxation. For example, a beach scene might involve the smell of suntan lotion, the warmth of the sun on one's skin, the salty smell of the ocean, and the sounds of seagulls just off the shoreline. Other popular images include the mountains, space, a cabin or other vacation spot, and fishing. The image can also be one that is uniquely relaxing for the person. Although the typical image is a relaxing one, neutral images are also occasionally used. Autogenic training combines imagery with focus on heaviness and warmth in one's extremities. Specifically, the person focuses on heaviness and warmth in one's arms and legs while repeating statements, such as "My right arm feels heavy and warm." This is done first for the right arm, then the left arm, then the right leg, and finally the left leg. This procedure works by releasing the vasoconstriction that often accompanies anxiety and arousal. By imaging warmth in the limbs, the person can actually cause an increase in blood flow to the arms and legs. This vasodilation results in feelings of relaxation. Cognitive. Cognitive therapy targets thoughts maladaptive to sleep. When insomnia persists over a period of time, many individuals develop dysfunctional thoughts and beliefs about their sleep and its consequences. They often worry about the negative effects of sleep loss or fear they may never sleep well again. For example, some individuals have unrealistic beliefs about how much sleep they need and become focused on obtaining 8 hours of sleep each and every night. In reality, sleep need varies with some individuals needing as little as 3 hours (Jones & Oswald, 1968) and others requiring 12 or more hours. Many older individuals may not realize sleep decreases with age (Bliwise, 1993) and may expect to get the same amount of sleep they got when they were younger. These thoughts are a normal reaction to sleep loss. Unfortunately, they often lead to performance anxiety, which heightens arousal (cognitive, emotional, physiological) and over time perpetuate the insomnia. The goal of the therapist is to guide the individual in (a) identifying maladaptive thoughts, (b) challenging their validity, and (c) replacing them with thoughts more conducive to sleep. For an individual with unrealistic beliefs about sleep need, a more adaptive thought would be, "Even if I do not sleep 8 full hours, I will still be able to function. I may feel a little tired, but almost everyone occasionally feels tired during the day." Table 4

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Table 4. Examples of Maladaptive Thoughts Regarding Sleep and More Adaptive Alternatives Maladaptive thought If I do not try harder to get enough sleep, my cancer (insert any other condition) will get worse. I have lost control over my ability to sleep. Insomnia is destroyingmy entire life. I am never going to get a good night's sleep again.

More adaptive thought Poor sleep does have an effect on my health. However, trying harder is probably not the best solution as it is likely to make sleep more difficult. My effort would be better spent exploring other options for coping with my sleep problems with my therapist. My ability to sleep has been affectedby my condition, and I may have lost some control. There still may be some things I can do to improve my sleep, however. It is true that my inability to sleep is having an impact on my life. There are still parts of my life that I enjoy (i.e., family, friends, reading), however. My condition has caused me to sleep poorly. I may or not sleep as well as I did prior to my condition. Regardless, there are things I can do to make sure I get the best night of sleep possible (i.e., practicing good sleep hygiene, talking to my physicianto make sure the medications I am taking will have the least possible impact on my sleep).

lists some maladaptive thoughts that may develop as a result of SI and examples of how these thoughts may be made more adaptive during therapy. In order to identify the person's faulty beliefs, the therapist frequently has the individual maintain a daily log of his or her maladaptive thoughts, the situations in which they occur, and how he or she reacted to them (angry, upset, frustrated). Improvement in sleep occurs, because the more adaptive belief reduces the individual's arousal. A more thorough discussion of cognitive therapy is provided in Morin, Savard, and Blais (2000). Cognitive Behavioral. Cognitive behavioral therapy (CBT) combines cognitive therapy (previously described) with one or more behavioral techniques, such as sleep hygiene, stimulus control, sleep restriction, and relaxation. By combining several techniques, the therapist can tailor the intervention to target the various factors that may be maintaining the insomnia (cognitive and physiological arousal, conditioning, worry).

Treatment Efficacy Each of the interventions just described has been found to be effective either alone or as part of multicomponent treatments. Two meta-analyses indicate behavioral intervention significantly improves sleep, resulting in patients falling asleep approximately 30 minutes sooner, sleeping approximately 30 minutes longer, and having approximately one less awakening per night (Morin et al., 1994; Murtagh & Greenwood, 1995). Sleep restriction and stimulus control produced the largest improvements, and overall, treatment gains were either maintained or enhanced at follow-ups ranging from 3 weeks to 3 years. Although the majority of research has focused on PI, we believe the frequent overlap between PI and SI (i.e., partial SI) suggests behavioral interventions may also be useful in treating SI. Research targeting the treatment of SI has been scarce, consisting of only a handful of case studies and a few randomized group studies. The results of such studies have been

highly encouraging, however. For example, case studies have shown insomnia improves following behavioral treatment for SI due to canc6r (Stam & Bultz, 1986), chronic pain (French & Tupin, 1974), depression and pain (Morin et al., 1990), hemophilia (Varni, 1980), and multiple medical problems (Kolko, 1984). These studies used a variety of treatments (i.e., relaxation, slow deep breathing, sleep restriction, stimulus control, visual imagery). Using a multiple baseline design, Morin et al. (1989) administered 6 weeks of stimulus control and sleep restriction to three chronic pain patients. Each patient reported sleeping better, and polysomnographic evaluation confirmed improved sleep (i.e., decreased time to fall asleep, fewer and shorter awake times at night) at posttreatment and maintained improvement at 6 months followup. Tan et al. (1987) treated 20 psychiatric inpatients with SI for an average of 5 weeks using some combination of individual psychotherapy, group psychotherapy, marital therapy, occupational therapy, sleep medication, progressive relaxation, stimulus control, and biofeedback. The patients rated their overall quality of sleep on a 0 to 8 scale and demonstrated significant improvement from pretreatment (M -- 1.6, SD = 0.2) to posttreatment (M = 6.0, SD = 0.4). These gains were maintained at 6 months follow-up (M = 6.9, SD = 0.4). Only three randomized studies of SI have been conducted, but their results are equally promising (Cannici et al., 1983: Currie et al., 2000; Lichstein et al., 2000). Cannici and colleagues assigned 30 cancer patients to either usual medical care for their cancer or usual care plus three consecutive sessions of progressive relaxation. Patients in the progressive relaxation group fell asleep approximately 90 minutes sooner after treatment, and this improvement was maintained at 3 month follow-up. The control group evidenced no improvement at either posttreatment or follow-up. Although the improvement in the time it took patients to fall asleep in the progressive relaxation group was large and clinically meaningful, this was the only measure demonstrating statistically significant treatment gains. However, the insignificant dif-

Secondary Insomnia

ferences for the other sleep measures (e.g., total sleep time, number of awakenings during the night, rated sleep satisfaction) and for pain ratings may be attributable to low power resulting from the study's small sample size. Currie et aL (2000) treated chronic pain patients (primarily back pain) with cognitive behavioral therapy. Thirty-two participants were assigned to 7 weeks of group-administered cognitive behavioral therapy, consisting of sleep restriction, stimulus control, and relaxation. The remaining 28 participants were assigned to a wait-list control. At both posttreatment and 3 month follow-up, treated participants experienced significant improvements in sleep compared to the control participants. On average, the treated group fell asleep 26.6 minutes sooner, experienced a 48.7-minute reduction in time spent awake during the night, and experienced an increase in sleep efficiency from 72% to 85% following treatment. There was no significant difference between the treated and control groups in total number of awakenings or total time spent sleeping following treatment. The treated participants also demonstrated a significant reduction in nocturnal movement (i.e., tossing and turning, arm and leg movements) from baseline to posttreatment, suggesting their sleep was more restful. Lichstein et al. (2000) recently conducted a randomized study focusing specifically on older adults. Forty-four older adults (58 years or older) who were not taking sleep medication and had at least a 6-month history of insomnia participated. Medical and psychiatric SI were equally represented; depression and chronic pain were the most common primary disorders. Participants were assigned to either treatment or a wait-list control group. The treatment group received 4 weeks of hybrid passive relaxation, stimulus control, and sleep hygiene. At posttreatment and follow-up, the treated group improved significantly on three sleep measures: wake time during the night, sleep efficiency (ratio of time slept to time spent in bed × 100), and rated quality of sleep (1 = very good to 5 = excellent). From baseline to follow-up, the treated group had 30.9 minutes less unwanted awake time (from 87.3 to 56.4 minutes), experienced a 10% increase in sleep efficiency (from 66.7 to 77.0%), and reported improved sleep quality (from 2.7 to 3.2). There were no differences in treatment response for medical versus psychiatric SI. We believe these results are highly encouraging as older adults with insomnia can be particularly difficult to treat. Selecting a Behavioral Intervention Stimulus control, sleep restriction, and multicomponent treatments have been found to be the most effective behavioral interventions (Morin et al., 1994). Careful consideration of the factors maintaining a person's sleep problems can help in the selection of an intervention or the best combination of interventions. For example, stimulus control may be most appropriate for patients who spend considerable time in the bedroom performing a variety of activities from television

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watching to reading to paying bills to talking on the telephone. Some individuals with SI, however, may be forced to spend considerable time in bed because of illness, and for such individuals, one of the other interventions may be more practical (i.e., cognitive therapy, relaxation). Other individuals (i.e., older adults) simply spend too much unnecessary time in bed, and sleep restriction may be particularly effective for them. Some older adults spend a great deal of time in bed attempting to sleep, because they erroneously believe they need a full 8 hours of sleep each night. Cognitive therapy targeting this erroneous belief may also be useful, and the therapist may wish to combine sleep restriction and cognitive therapy in such cases. For individuals with high levels of physiological and cognitive arousal, relaxation procedures may be helpful (Morin et al., 1994). In some cases, however, relaxation may have a paradoxical effect, increasing performance anxiety and arousal (Morin, 1993) and possibly, precipitating panic attacks (Ley, 1988). Combining techniques is useful, because often more than one factor is maintaining the insomnia. Information collected during the sleep history should assist the therapist in determining which factors in addition to the primary condition are maintaining the insomnia. Treatment Response As Post Hoc Diagnostic Indicator Earlier, we suggested that treatment response was one way to increase our confidence in our diagnosis of SI. If the insomnia remits following treatment of the primary condition, we can be fairly confident of a diagnosis of absolute SI. ff the insomnia improves but does not completely remit, this supports partial SI. The true secondary component of the insomnia has responded, but the primary (or behavioral) component remains. Specious SI occurs when there is no change in the insomnia following treatment of the primary disorder. In such situations, the insomnia is actually PI. The response to direct sleep treatment also provides post hoc diagnostic evidence. If direct treatment of the insomnia eliminates the sleep disturbance, a diagnosis of specious SI (i.e., PI) is warranted. If the response is only partial, the diagnosis is partial SI. When there is no change in the insomnia following sleep intervention, the most likely diagnosis is absolute SI. We realize that such post hoc support for diagnosis may not appear to have any immediate practical utility. However, a large component of clinical skill develops as a result of clinical experience, and careful consideration of treatment response may add to such experience. Prevention A literature search using PsychLit and MEDLINE revealed no published research on the prevention of SI. Given the number of individuals affected by SI, this is an area well deserving of attention. The simplest and most direct way to prevent SI is to either cure or prevent the primary condition from occurring in the first place. For example, once a cure for can-

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cer is developed, individuals will no longer suffer from SI resulting from cancer-related pain. Unfortunately, SI results from such a wide variety of illnesses and substances that it is unrealistic to think we will be able to eliminate all precipitating conditions. Therefore, we make several practical suggestions for prevention. First and foremost, we believe preventive efforts should be implemented on diagnosis with a condition likely to result in SI and should be integrated with the overall treatment of the primary condition. Preventive efforts might include: (a) minimizing the impact that treatment of the primary condition has on the individual's sleep, (b) sleep education and training in the behavioral management of sleep, (c) creating a bedroom environment that is conducive to sleep (i.e., reducing unwanted light and noise), and (d) aggressive behavioral treatment for individuals with preexisting PI. Finally, the development of reliable SI risk-assessment methods to identify patients who are most likely to develop insomnia and also most likely to benefit from prevention would help to ensure the cost-effectiveness of prevention. Minimize Impact of Precipitating Condition Treatment on Sleep When an individual is diagnosed with a primary condition likely to result in SI, we recognize that the primary condition should be treated aggressively. In doing so, however, it is important to try to minimize the impact of such treatment on sleep. As we mentioned earlier, SI can result when the medication used to treat the primary condition has an alerting effect (Aldrich, 1993; Hu & Silberfarb, 1991). Medications that can cause insomnia include: fluoxetine (Prozac) for depression, clonidine (Catapres) for high blood pressure, theophylline (Theodur) for asthma, and levodopa (Sinemet) for Parkinson's disease. For a more thorough listing of medications likely to cause insomnia see Lichstein (2000). In some cases, it may be possible to substitute a nonalerting or less alerting medication. For example, there is evidence that mirtazapine (Remeron), an antidepressant that alleviates insomnia and improves sleep architecture (Thase, 1999), could be used in place of fluoxetine (Prozac). When there is no appropriate substitute, there are other steps that can be taken to minimize the impact of the medication on sleep. For example, the dose can be manipulated such that the lowest effective amount of the drug is used. Time of administration can also be altered. For example, it may be possible for the individual to take the alerting medication in the morning, so that it will be less likely to interfere with sleep. Behavioral Interventions As Preventive Measures Early education about sleep and the risk that certain primary disorders and their treatments pose to sleep may help circumvent the development of SI. Although behavioral interventions as preventive measures for insomnia have not been systematically studied, a recent study found cognitive

behavioral techniques to be effective in the prevention of anxiety and depression (Seligman, Schulman, DeRubeis, & Hollon, 1999). In this study, university students at risk for depression had fewer episodes of generalized anxiety disorder and showed a trend toward fewer major depressive episodes following a cognitive behavioral prevention program than did controls. Thus, we feel there is reason to believe behavioral interventions may also prove effective in preventing SI. On diagnosis with a primary condition, the patient could be encouraged to adopt good sleep hygiene. One or more of the other behavioral techniques could also be taught before sleep ever becomes a problem. Many patients experience a great deal of stress as a result of their illness. Relaxation or cognitive training may help such patients to manage this stress, thereby preventing it from interfering with sleep. These techniques may offer additional benefits because they can also be used throughout the day as often as needed, and as a result, may lower the individual's overall level of stress and anxiety. The clinician may also consider having the patient maintain a Sleep Diary in order to monitor sleep. The Sleep Diary serves a dual purpose: (a) it would help to raise the individual's awareness of his or her sleep pattern, and (b) if the patient begins to develop a problem sleeping despite preventive efforts, the clinician can identify and treat it before it develops into a chronic problem. For some patients, education about the risk of SI and behavioral training may result in performance anxiety that may interfere with sleep. When there is reason to believe a particular patient is likely to become unduly anxious about sleep, the clinician can first assure him or her that minor changes in sleep are expected. If this assurance does not reduce the patient's anxiety, it may be best to avoid the behavioral techniques and to try one or more of the other recommended preventative strategies. Bedroom Environment Environmental factors that may interfere with sleep include noise, light, the activity of others, an uncomfortable sleep surface, and a bedroom that is too warm or too cold. Of the factors mentioned, only noise has been systematically studied. Research suggests both white noise and earplugs may help reduce the effects of environmental noise on sleep. Williamson (1992) randomly assigned 60 coronary artery bypass graft (CABG) patients to either a white-noise treatment or a no-treatment control condition. The treatment group heard ocean sounds for 3 consecutive nights following transfer from intensive care. Compared to the control group, the treatment group awoke less during the night and reported sleeping better. Another study found earplugs increased the total amount of sleep and reported quality of sleep of female surgical and gynecological patients (Haddock, 1994). Unfortunately, the results of this study are limited, because the pa-

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tients were allowed to choose whether or not they wanted to wear the earplugs. Despite this, both white noise and the use of earplugs hold promise as preventive measures and warrant additional research. Other steps that can be taken to improve the bedroom environment include adjusting the temperature in the room and reducing interruptions, a major problem in clinical settings (Floyd, 1999). Unwanted light can be reduced by fitting the bedroom windows with blackout curtains. If the bed itself is uncomfortable, measures that may make it more comfortable include finding a mattress or pillows of the preferred firmness, switching to an adjustable bed, and selecting sheets that have the desired texture and softness.

Preexisting PI For individuals who have insomnia prior to diagnosis with another disorder, it is particularly important to directly target the sleep disorder before it worsens (i.e., partial SI develops). One of the first considerations is whether the insomnia is already being treated. If so, how is it being treated, and how effective is the treatment? If the individual is taking hypnotic medication yet still experiencing insomnia, withdrawal from the medication and the implementation of behavioral treatment may prove helpful. Treatment of the PI needs to be considered within the context of the newly diagnosed condition. Thus, another reason to consider hypnotic withdrawal is potential interaction with treatment of the newly diagnosed condition. Regardless of hypnotic usage, behavioral interventions can be implemented as they are unlikely to exacerbate the primary condition. Careful consideration of the environmental factors discussed previously may also help to not only improve the preexisting PI but also prevent the development of SI (i.e., partial SI). Potential Benefits to Primary Condition Successful prevention of SI may reduce the severity of the primary condition, because there is often a reciprocal relationship between SI and the primary condition (Moldofsky, 1989; Paiva, Batista, Martins, & Martins, 1995). For example, in the case of chronic back pain, the insomnia that originates because of the pain can result in fatigue and lowered pain thresholds that in turn further erode sleep quality. By preventing SI, we can help to ensure the patient gets the best possible night's sleep and as a result, may be better able to cope with the pain. If the patient does not have to deal with the additional stress of insomnia, more of his or her resources can be devoted to dealing with the primary condition. Application to Two Common Causes of SI We provide examples of how the strategies we suggest may be used to prevent SI in depression and chronic pain. Of the wide variety of disorders that can cause SI, we have chosen to discuss depression and chronic pain, because they are extremely common and are likely to be encountered by the

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largest number of health professionals in the widest variety of settings. Depression. Depression is the most common psychiatric cause of SI (Walsh & Sugerman, 1989). Insomnia occurs in approximately 50% of depressed outpatients and up to 90% of depressed inpatients (American Psychiatric Association, 1994). When the primary disorder is depression, minimizing the impact of treatment is extremely important, because many popular antidepressants disturb sleep. In a recent review, Gursky and Krahn (2000) report that the most commonly prescribed antidepressants, fluoxetine (Prozac) and other selective serotonin reuptake inhibitors (SSRIs), often fragment sleep. Thase (1999) suggests the SSRIs interfere with sleep by stimulating serotonin-2 (5-HT-sub-2) receptors. Thus, one way to prevent SI would be to select an antidepressant that blocks rather than stimulates these serotonin2 receptions, such as mirtazapine (Remeron; Thase, 1999) or trazodone (Desyrel; Brunello et al., 2000). For patients who do not respond well to antidepressants other than the SSRIs, time of administration can be manipulated to limit the impact of the medication on sleep. For example, the patient may be advised to take fluoxetine (Prozac) in the morning rather than at bedtime. Using the lowest effective dose may also help. For a more detailed discussion of the effects of various antidepressants on sleep, see Brunello et al. (2000). Many depressed individuals also experience considerable stress and anxiety (American Psychiatric Association, 1994). Behavioral interventions that target stress and anxiety (relaxation, cognitive therapy) may prove beneficial in such cases. To reduce the likelihood of behavioral factors contributing to poor sleep, sleep hygiene and stimulus control could be implemented. Some depressed patients may not want to get out of bed or feel they do not have the energy to get out of bed, potentially contributing to insomnia by straining the association between their bed and sleep. Encouraging such patients to get out of bed during the day and implementing stimulus control at night may help. Sleep restriction or sleep compression could also be used to reduced excess bed time. It is not uncommon for depressed individuals to present with preexisting insomnia. In Ford and Kamerow's (1989) well-cited epidemiological study, complaints of insomnia during the initial interview predicted the development of depression by 1 year follow-up. In such cases, insomnia may be a prodromal symptom of depression; however, it is also possible that PI may be a risk factor for depression. Regardless, we believe sleep is an issue that should be addressed early in the assessment of depressed patients. Early treatment may improve the preexisting insomnia, prevent any further worsening of sleep, and according to Thase (1999), may also help to improve the patient's prognosis. Chronic Pain. Pain, one of the most frequent sources of SI, can result from a variety of conditions, including back or neck injury, osteoarthritis, fibromyalgia, and headache

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(Haythornthwaite, Hegel, & Kerns, 1991; Morin, Gibson, & Wade, 1998). Pain often shares a reciprocal relationship with insomnia. For example, in women with fibromyalgia, research has demonstrated that pain during the day tended to disturb nighttime sleep; the reverse was also found--poor sleep tended to intensify daytime pain (Affieck, Urrows, Tenhen, Higgins, & Abeles, 1996). We believe combining aggressive pain management with SI preventive efforts may prove beneficial. Often, it may not be possible to completely eliminate sleep disturbance altogether; in such cases, early SI prevention may prove helpful in circumventing the reciprocal escalation of symptoms. There are a variety of effective treatment options available for pain, such as pain facility treatment, medication, physical therapy, and cognitive behavioral treatments (Fishbain, 2000). Medication is often the primary treatment for pain, and there are a wide range of pharmacological options, including simple analgesics, adjuvant agents (antidepressants, anticonvulsants, N-methyl-Daspartate-receptor agonists, muscle relaxants), and opioids (Holmquist, 2001). Many of these agents have sedating effects and as a result help to improve both sleep and pain--at least in the short term. For example, research has demonstrated that both amitriptyline (Elavil--a sedating antidepressant) and cyclobenzaprine (Flexeril--a skeletal muscle relaxant) were more effective than placebo in producing improvements in sleep, fatigue, and pain in individuals with fibromyalgia after 1 month of treatment (Carette et al., 1994). Unfortunately, long-term maintenance was a problem as these improvements were not maintained at 3- and 6-month follow-ups. We believe nonpharmacological SI preventive efforts merit consideration as they may provide long-term results. They can also be easily combined with both pharmacological and nonpharmacological methods of pain management. Cognitive behavioral treatment is often included in multidisciplinary chronic pain programs (Burns, Johnson, Mahoney, Devine~ & Pawl, 1998). Combining cognitive behavioral treatment for insomnia with that for chronic pain may help prevent the development of SI. Because depression often accompanies chronic pain and is also associated with insomnia, cognitive behavioral treatment targeting pain, depression, and insomnia may prove to be an efficient and effective approach to the prevention of both SI and depression in chronic pain patients. The suggestions made earlier for depressed patients regarding the bedroom environment may also prove helpful for pain patients. Cognitive therapy and relaxation techniques may help reduce anxiety. For some individuals with chronic pain, progressive muscle relaxation may not be the best option as a preventive strategy as the tensing and releasing of certain muscle groups may aggravate their pain. In such cases, passive relaxation (which drops the muscle-tension component of progressive muscle relaxation) may prove useful. Because there are such a wide variety of sources of chronic pain, it is possible that different preventive strategies may prove beneficial for different types of

chronic pain. For example, light to moderate exercise may improve both pain and sleep in individuals with fibromyalgia, yet further aggravate pain and disturb sleep in individuals with osteoarthritis or back pain. Therefore, research on preventive efforts for the various types of chronic pain is needed. Summary SI is a serious disorder that is associated with significant health, safety, and economic consequences. SI arises from a wide variety of medical and psychiatric disorders and substances and is by far the most common form of insomnia. Estimates indicate SI may affect as much as one third of the general population. SI can be difficult to diagnosis, because it is often difficult to determine whether the primary condition is causing the insomnia or is simply comorbid. A thorough clinical interview that establishes the relationship between the origin and severity of the primary disorder and the insomnia can help clarify diagnosis. Lichstein's heuristic model represents the first step toward a clearer theoretical conceptualization of SI. The three types of insomnia recognized by the model (absolute, partial, and specious) take into account the fact that SI and PI often coexist. Treatment has typically focused on the primary disorder, because it is frequently assumed that the insomnia will resolve following successful treatment of the primary disorder. In reality, however, SI is often refractory to such treatment. Although pharmacological treatment is currently the most popular method of treating sleep disturbance, this approach has serious limitations (i.e., potential side effects, drug interactions, tolerance, dependence). Fortunately, evidence in favor of direct behavioral intervention is beginning to emerge. Because behavioral interventions offer better long-term maintenance and a lower risk of adverse consequences than medication, it represents the best treatment option for S1. A variety of behavioral interventions have been shown to effectively treat insomnia. Some target the habits that perpetuate poor sleep (sleep hygiene, stimulus control, sleep restriction), whereas others target physiological and psychological arousal (relaxation, cognitive therapy). A very popular and effective approach to behavioral intervention is to combine several of these techniques. Cognitive behavioral therapy refers to the combination of cognitive therapy, which targets thoughts maladaptive to sleep, and one or more of the other behavioral techniques. Presently, there are no empirically tested preventive strategies for SI. However, treating the primary disorder with nonalerting medications when possible and when not, using the lowest possible dose and morning administration may help to inhibit the development of insomnia. In addition, early education about the risk of SI and the habits and thinking patterns that may contribute to sleeping difficulties may prove helpful. The behavioral techniques used to treat insomnia may prove preventative when taught on initial diagnosis with the primary condition.

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