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Dr. Erman is clinical professor in the Department of Psychiatry at the University of California, San Diego School of Medicine, is a staff scientist for the Scripps Research Institute Department of Neuropharmacology, and is the president of Pacic Sleep Medicine Services. Disclosures: Dr. Erman is a consultant to Cephalon, Mallinckrodt, Neurocrine, sano-aventis, and Takeda; is on the speakers bureaus of Forest, sano-aventis, and Takeda; is on the advisory boards of Cephalon, Neurocrine, sanoaventis, and Takeda; has received grant/research support from Arena, Cephalon, Eli Lilly, GlaxoSmithKline, Mallinckrodt, Merck, Organon, Pzer, Pharmacia, ResMed, sano-aventis, Schwarz Pharma, and Takeda; and owns stock in Cephalon, Forest, Merck, Neurocrine, Pzer, sano-aventis, and Sepracor. The best cure for insomnia is to get a lot of sleep. W. C. Fields1 Understanding insomnia and how it can most effectively be treated continues to challenge psychiatrists and other clinicians. Insomnia may be acute or chronic, but the majority of patients presenting for evaluation to treating physicians complain of chronic insomnia. Acute (transient or short-term) insomnia may be extremely disruptive and troubling to patients, but usually can be understood in the context of recent stresses that have contributed to the onset of sleep problems (ie, family/work conicts, job stresses, acute medical conditions).
Introduction
This column provides information on how and why insomnia develops, as well as on its treatment, focusing primarily on behavioral interventions. The origins of chronic insomnia are usually much more complex, with contributions from predisposing, precipitating, and perpetuating factors. Most insomnia can be related, at least in part, to comorbid medical and psychiatric conditions, which may play a role in any of these three contributory realms. Behavioral treatments for insomnia can be very effective for many patients, but there are substantial challenges to clinicians desiring to use these treatments. Clinicians must be educated in how to use behavioral treatment modalities, and must be able to identify which patients are most likely to benet from their use. Patients must be motivated to accept these treatments, especially since they may not experience immediate relief. Both patients and clinicians must be able to recognize that the appropriate use of behavioral modalities typically requires multiple sessions for teaching/training in their use, with further sessions necessary to assess the response that has been generated and to reinforce the importance of continuing to implement cognitive-behavioral interventions that have been identied. Sleep hygiene is a critical element of importance for all patients, including those receiving hypnotic medications. Core elements of sleep hygiene, such as efforts to reduce levels of arousal/activation during the hours before bedtime, paying attention to the sleep environment, and reducing use of alcohol and caffeine in the hours before bedtime will benet all patients and will help to strengthen the effects of other treatment approaches, both behavioral and pharmacologic.
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Models of Insomnia
Many models to explain the development and persistence of insomnia have been proposed. For example, insomnia has been proposed to be a disorder of hyperarousal. These patients maintain a state of excessive arousal (out of context with their need for arousal in their sleep or relaxation environment) that interferes with their capacity to sleep. Other etiologic theories are based on models of inadequate sleep drive, or cognitively driven excessive arousal that interferes with the capacity to fall asleep or stay asleep. A practical model for understanding how insomnia may develop and why it may persist as a chronic condition was rst elucidated by Spielman and colleagues.2 Spielmans model, commonly referred to as the 3-P model (Figure),2-4 incorporates the impact of various traits (predisposing factors) and life stresses (precipitating factors) in the development of insomnia. It also recognizes that chronic insomnia is maintained (unintentionally) by maladaptive coping strategies (perpetuating factors). Thus, a person may be prone to insomnia due to trait characteristics, may experience a trenchant or short-term insomnia as a consequence of precipitating stresses, and may develop a persistent and chronic insomnia as a consequence of pathologic coping strategies and poor sleep hygiene.
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depression, anxiety disorders, bipolar disorder, obsessive-compulsive disorder, or psychotic disorders may interact with the personality traits of these patients to increase anxiety and concern about sleep.5,6 Social factors may also be contributory to this process. Parental demands, care-giving for a spouse or parent, or arousal related to a bed-partners sleep tendencies, schedule, or habits may all contribute to increased risk of developing insomnia. Biological components may also play a role in precipitation of insomnia. The model of hyperarousal mentioned above could be a precipitating component of insomnia. It has also been speculated that some patients may be congenitally or constitutionally poor sleepers, on the basis of reduced homeostatic (intrinsic) sleep drive. Patients with idiopathic insomnia report such a history, complaining of onset of insomnia in infancy or childhood without other cause.7
Therapeutics
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Understanding how insomnia develops may provide opportunities to treat insomnia at early stages and prevent progression to chronic insomnia. For example, using the Spielman model,2-4 if physicians and therapists recognize that premorbid traits predisposing to development of insomnia exist, they may be more aggressive in treating stress and instructing patients on avoidance of key stressors capable of provoking insomnia. If stressors are neutralized or insomnia symptoms are quickly and effectively treated, patients may revert to their pre-morbid, non-insomniac state. If interventions are not made until perpetuating elements have developed, the insomnia condition is more likely to become chronic. Understanding how insomnia develops is also important when insomnia has become established as a chronic condition. Identication of elements that have contributed to the development of insomnia, and educating the patient about the roles that behavior and conditioning have played in this process, should help physicians and patients understand that behavioral therapies combined with pharmacologic interventions are useful treatment options.
Behavioral Treatments
Various behavioral therapies have demonstrated efcacy in the treatment of chronic insomnia.9 Research supports the hypothesis that non-pharmacologic therapies can be very effective in the treatment of insomnia, and an effort should be made to include behavioral therapies in the treatment of every patient with insomnia. Although implementation of some of the formal and involved therapies discussed below may not always be practical, a patients history should always be reviewed to nd elements of sleep hygiene that may be responsive to treatment. Numerous specic behavioral therapies have been described in the past, including sleep restriction, relaxation therapies, and stimulus control therapy. Some of the elements from these specic therapies may also be incorporated in a more global approach to the treatment of insomnia using cognitive-behavioral therapy (CBT). Sleep restriction therapy was initially described by Spielman and colleagues10 and is based on an assumption that sleep deprivation will promote a stronger drive to fall and remain asleep. Although this relationship is demonstrated in basic animal and human sleep research, insomnia patients often deny that their sleep is driven in any way by sleep deprivation, remarking that, No matter how long I stay awake I cannot fall asleep. Operationally, sleep restriction involves an initial limitation of time in bed to an amount close to the number of hours that the insomnia patient reports having slept. This restriction is based on assumption that most insomnia patients underestimate the amount of sleep that they have obtained. If they are limited to the 5 hours, for example, which they report they have been receiving, their sleep will be restricted. As a consequence, it is expected that sleep drive will be increased, leading to improved sleep efciency during the limited number of hours in bed. As the patient reports that sleep continuity and efciency has improvedmanifested as fewer awakenings and less time awake during the limited time in beda gradual and progressive lengthening of time in bed is allowed. This technique requires a compliant patient, careful record keeping and record analysis by patient and therapist, and recognition that at least several weeks will be required before signicant changes will be observed by the patient. Stimulus control therapy (SCT), originally described by Bootzin and colleagues,11 has become so widely utilized in the behavioral treatment of insomnia that many practitioners do not appreciate that it denes a specic and universal approach to the treatment of insomnia. SCT consists of a series of ve instructions given to patients to strengthen their capacity to fall asleep at night and to improve their capacity to sleep on a regular basis in their own bedroom. Although it is helpful for many patients, some of its components, such as getting up from bed and going to another room if unable to sleep, may increase levels of arousal and make it extremely hard for patients to be able to return to sleep when they return to their bedroom. As with all behavioral modalities, it requires consistent application over an extended period of time to have signicant benet.
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CBT, demonstrated to be effective in the treatment of depression, has also demonstrated efcacy in multiple research studies as a treatment for insomnia.12-14 Typically, CBT attempts to address maladaptive behaviors and thought patterns that plague insomniac patients. These disturbances develop over long periods of time, become an entrenched part of the insomniacs thought and behavior patterns, and exacerbate insomnia severity. These disturbances tend to develop no matter how the insomnia originally developed, and include behavioral and cognitive elements that interfere with the patients ability to relax and fall asleep. Examples of maladaptive behaviors include irregular sleep-wake patterns, frequent daytime naps, clock watching, and going to bed at too early an hour. Among maladaptive thought patterns are trying too hard to fall asleep (which provokes greater arousal), pathologic anxiety generated by the immediate inability to fall asleep, and excessive worry about sleep loss and its possible next day consequences. CBT includes various techniques to alter dysfunctional sleep cognitions, beliefs, attitudes, and expectations. Treatment targets include unrealistic expectations (I must get 8 hours of sleep every night or I will not be able to function), faulty causal attributions (My insomnia is something I was born with and is beyond my control), and pathologic anxiety about consequences of insomnia (My insomnia is causing my poor health). CBT is designed to interrupt the self-fullling nature of these beliefs and behaviors, and provides patients with coping skills to prevent or minimize recurrence of sleep disturbances after treatment. Among strategies used are instructions to maintain realistic expectations about the amount of sleep you will be able to attain, to never try to sleep, to try to minimize the importance of sleep, and to not catastrophize during or after a poor night of sleep.10
References
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1. BrainyQuote. W. C. Fields Quotes. Available at: www.brainyquote.com/quotes/authors/w/w_c_elds.html. Accessed June 4, 2007. 2. Spielman AJ, Caruso LS, Glovinsky PB. A behavioral perspective on insomnia treatment. Psychiatr Clin North Am. 1987;10(4):541-553. 3. Glovinsky PB, Spielman AJ. How did I get insomnia? In: Glovinsky PB, Spielman AJ. The Insomnia Answer: A Personalized Program for Identifying and Overcoming the Three Types of Insomnia. New York, NY: Berkley Publishing Group; 2006:51-82. 4. Perlis ML, Smith M, Pigeon. Etiology an pathophysiology of insomnia. In: Kryger MH, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 4th ed. Philadelphia, PA; Elsevier Science; 2005:714-725. 5. Stein M, Mellman T. Anxiety disorders. In: Kryger MH, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 4th ed. Chapt. 111. Philadelphia, PA; Elsevier Science; 2005:1297-1310. 6. Benka R. Mood disorders. In: Kryger MH, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 4th ed. Chapt. 112. Philadelphia, PA: Elsevier Science; 2005:1311-1326. 7. International Classication of Sleep Disorders. Diagnostic and Coding Manual. 2nd ed. Westchester, IL: American Academy of Sleep Medicine; 2005. 8. Gillin C, Drummond S, Clark C, Moore P. Medication and substance abuse. In: Kryger MH, Roth T, Dement W, eds. Principles and Practice of Sleep Medicine. 4th ed. Philadelphia, PA: Elsevier Science; 2005:1345-1358. 9. Morin C, Espie C. Insomnia: A Clinical Guide to Assessment and Treatment. New York, NY: Springer; 2004. 10. Spielman AJ, Saskin P, Thorpy MJ. Treatment of chronic insomnia by restriction of time in bed. Sleep. 1987;10(1):45-56. 11. Bootzin RR, Epstein D, Wood JM. Stimulus control instructions. In: Hauri P, ed. Case Studies in Insomnia. New York, NY: Plenum Press; 1991:19-28. 12. Backhaus J, Hohagen F, Voderholzer U, Riemann D. Long-term effectiveness of a short-term cognitive-behavioral group treatment for primary insomnia. Eur Arch Psychiatry Clin Neurosci. 2001;251(1):35-41. 13. Jacobs GD, Benson H, Friedman R. Perceived benets in behavioral-medicine insomnia program: a clinical report. Am J Med. 1996;100(2):212-216. 14. Edinger JD, Wohlgemuth WK, Radtke RA, Marsh GR, Quillian RE. Cognitive behavioral therapy for treatment of chronic primary insomnia: a randomized controlled trial. JAMA. 2001;285(14):1856-1864.
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