Insomnia: Assessment and Management in Primary Care
Am Fam Physician. 1999 Jun 1;59(11):3029-3038.
Patients with insomnia may experience one or more of the following problems: difficulty falling asleep, difficulty maintaining sleep, waking up too early in the morning and nonrefreshing sleep. In addition, daytime consequences such as fatigue, lack of energy, difficulty concentrating and irritability are often present. Approximately 10 percent of adults experience persistent insomnia, although most patients do not mention it during routine office visits. Asking sleep-related questions during the general review of systems and asking patients with sleep complaints to keep a sleep diary are helpful approaches in detecting insomnia. Behavior and pharmacologic therapies are used in treating insomnia. Behavior approaches take a few weeks to improve sleep but continue to provide relief even after training sessions have ended. Hypnotic medications are safe and effective in inducing, maintaining and consolidating sleep. Effective treatment of insomnia may improve the quality of life for many patients.
Up to one third of patients seen in the primary care setting experience occasional difficulties in sleeping, and up to 10 percent of patients have chronic sleep problems. Although insomnia is rarely the chief reason for an office visit, its detection may be enhanced by incorporating sleep-related questions into the general review of patient systems.
This article offers up-to-date information on insomnia and highlights the key role of the primary care physician in its recognition and management. Behavior approaches, such as relaxation therapy, sleep restriction therapy and stimulus control therapy, are described, in addition to pharmacologic treatments such as hypnotic medications, antidepressants and other medications.
Definition and Prevalence
Insomnia is an experience of inadequate or poor-quality sleep characterized by one or more of the following problems: difficulty falling asleep, difficulty maintaining sleep, waking up too early in the morning and sleep that is not refreshing. Insomnia also involves daytime consequences such as fatigue, lack of energy, difficulty concentrating and irritability.
Periods of sleep difficulty lasting between one night and a few weeks are referred to as acute insomnia. Chronic insomnia refers to sleep difficulty occurring at least three nights per week for one month or more.
From 30 to 40 percent of adults indicate some level of insomnia within any given year, and about 10 to 15 percent indicate that the insomnia is chronic, severe, or both.1 The prevalence of insomnia increases with age and is more common in women.1,2
Types of Insomnia
Acute insomnia is often caused by an emotional or physical discomfort. Some examples of common discomforts include significant life stress, acute illness and environmental disturbances such as noise, light and temperature.3 Sleeping at a time that is inconsistent with the daily biologic rhythm, such as occurs in persons with jet lag, also may cause acute insomnia.4
Chronic insomnia may be caused by many different factors acting singly or in combination and often occurs in conjunction with other health problems. In other cases, sleep disturbance is the major or sole complaint and involves abnormal sleep-wake regulation or physiology during sleep. Since treatment of underlying conditions is crucial in the management of insomnia, identifying specific associations is important.
Insomnia and Psychiatric, Medical and Neurologic Disorders. Although psychiatric disorders are a common cause of chronic insomnia, they account for less than 50 percent of cases. Mood and anxiety disorders are the most common psychiatric diagnoses associated with insomnia.5,6 Insomnia may also be associated with a wide variety of medical and neurologic disorders.7,8 Factors that cause problems throughout the day, such as pain, immobility, difficulty breathing, dementia and hormone changes associated with pregnancy, perimenopause and menopause may also cause insomnia. Many medical disorders worsen at night, either from sleep per se, the circadian influence (e.g., asthma) or recumbency (e.g., gastroesophageal reflux).
Insomnia and Medication/Substance Use. A variety of prescription and nonprescription drugs, and drugs of abuse (e.g., heroin, cocaine, other stimulants) cause increased wakefulness and poor-quality sleep.9,10 The likelihood of any given drug contributing to insomnia is unpredictable and may be related to such factors as dosage, lipid solubility and individual patient differences. Some drugs that are commonly associated with insomnia are stimulating antidepressants, steroids, decongestants, beta blockers, caffeine, alcohol, nicotine and illicit drugs.
Insomnia and Specific Sleep Disorders. Insomnia may be associated with specific sleep disorders, including restless legs syndrome, periodic limb movement disorder, sleep apnea and circadian rhythm sleep disorders.
Restless Legs Syndrome. Restless legs syndrome is characterized by unpleasant sensations in the legs or feet that are temporarily relieved by moving the limbs. Symptoms increase in the evening, especially when a person is lying down and remaining still. The dysesthesias cause difficulty falling asleep and are often accompanied by periodic limb movements.
Periodic Limb Movement Disorder. Periodic limb movement disorder is characterized by bilateral repeated, rhythmic, small-amplitude jerking or twitching movements in the lower extremities and, less frequently, in the arms. These movements occur every 20 to 90 seconds and can lead to arousals, which are usually not perceived by the patient. Rather, the patient reports that sleep is not refreshing. Characteristically, the bed partner is more likely to report the movement problem. This condition and restless legs syndrome are more common in older patients.11
Obstructive Sleep Apnea. Obstructive sleep apnea is most commonly associated with snoring, daytime sleepiness and obesity but occasionally presents with insomnia.12 Circadian Rhythm Sleep Disorders. Circadian rhythm sleep disorders are characterized by an inability to sleep because of a mismatch between the circadian sleep rhythm and the desired or required sleep schedule (Table 1).
TABLE 1 Features of Selected Circadian Rhythm Sleep Disorders
Features of Selected Circadian Rhythm Sleep Disorders
Delayed sleep phase syndrome
Difficulty falling asleep at the desired time
Difficulty waking at the desired time
Advanced sleep phase syndrome
Difficulty staying awake in the evening
Waking too early
Problems related to shift work
Difficulty getting enough sleep during available sleep times
Primary Insomnia. When other causes of insomnia are ruled out or treated, any remaining difficulty with sleep may be classified as primary insomnia. Factors such as chronic stress, hyperarousal, poor sleep habits and behavior conditioning may contribute to primary insomnia.13
The primary consequences of acute insomnia are sleepiness, negative mood and impairment of performance. The severity of these consequences is related to the amount of sleep lost on one or more nights.
Patients with chronic insomnia frequently complain of fatigue, mood changes (e.g., depression, irritability), difficulty concentrating and impaired daytime functioning. Because insomnia has a variety of causes, the consequences may not be uniform. For example, when objectively assessed, the level of daytime sleepiness may be elevated in patients with periodic limb movement disorder14 and rheumatoid arthritis15 but not in patients with primary insomnia.16
Recognition and Assessment
A brief sleep history incorporated into the routine review of systems can be helpful in detecting patients with insomnia. Direct inquiry is important because more than one half of patients who believe that they have chronic insomnia have never discussed the problem with a physician. Examples of appropriate questions are shown in Table 2. Several of these questions will be helpful in determining the diagnosis, which is important in treatment selection.
TABLE 2 Suggested Questions About Sleep and Sleepiness
Suggested Questions About Sleep and Sleepiness
How has the patient been sleeping recently?
When did the problem begin? (To differentiate between acute and chronic insomnia)
Does the patient have a psychiatric or medical condition that may cause insomnia? (May relate to an underlying condition that should be treated first)
Is the sleep environment conducive to sleep? (Noise, interruptions, temperature, light)
Does the patient report “creeping, crawling or uncomfortable feelings” in the legs that are relieved by moving the legs? (May relate to restless legs syndrome)
Does the bed partner report that the patient's legs or arms jerk during sleep? (May relate to periodic limb movements in sleep)
Does the patient snore loudly, gasp, choke or stop breathing during sleep? (May relate to obstructive sleep apnea)
Is the patient a shift worker? What are the work hours? Is the patient an adolescent? (May relate to circadian sleep disorders/sleep deprivation)
What are the bedtimes and rise times on weekdays and weekends? (May relate to poor sleep hygiene)
Does the patient use caffeine, tobacco or alcohol? Does the patient take over-the-counter or prescription medications (such as stimulating antidepressants, steroids, decongestants, beta blockers)? (May relate to substance-induced insomnia)
What daytime consequences does the patient report? (Daytime consequences may be significant)
Does the patient report dozing off or having difficulty staying awake during routine tasks, especially while driving? (This is a serious problem that should be dealt with promptly)
It is helpful for patients to keep a sleep diary for one to two weeks. Sleep diaries usually record bedtime, total sleep time, time until sleep onset, number of awakenings, use of sleep medications, time out of bed in the morning and a rating of quality of sleep and daytime symptoms. The sleep diary provides a night-to-night account of the patient's sleep schedule and perception of sleep. Moreover, it may serve as a baseline for assessment of treatment effects. Completing the diary each morning and using estimates rather than exact times should minimize the likelihood that the process itself will be disruptive to sleep. Figure 1 shows a sample sleep diary.
Assessment should include questions that address both sleep and daytime functioning, since sleep needs vary markedly from person to person. For example, one patient who sleeps six hours may feel totally unrefreshed, while another who sleeps six hours might have no sleep-related complaints during the day.
Although the ability to maintain sleep decreases with age, the need for sleep does not change significantly. A patient who complains of not sleeping “a full eight hours” but whose sleep is otherwise restorative is within the bounds of normal behavior, and reassurance may be all that is needed. However, a patient who complains of severe insomnia or excessive daytime sleepiness should be evaluated, regardless of age.20
The cause of acute insomnia (no one episode lasts longer than several weeks) is often related to a single specific event. The need for treatment is usually determined by the severity of the daytime sequelae, the duration of the episode and the degree to which episodes become predictable. Even brief episodes of acute insomnia may warrant treatment because persons who are typically good sleepers can and do become significantly sleepy after a loss of just a few hours of sleep on one or more nights.21 In addition, untreated acute insomnia may develop into chronic insomnia.22
When the insomnia persists beyond one or two nights or becomes predictable, treatment should be considered. Pharmacologic treatment usually predominates—especially short-acting hypnotics. Adjunctive sleep hygiene measures may also be useful (Table 3). The goal of treatment is to improve the patient's sleep, but it may not be possible to achieve normal sleep every night.
TABLE 3 General Sleep Hygiene Measures
General Sleep Hygiene Measures
Sleep hygiene measures may help promote sleep. Sleep hygiene measures relate to health practices and environmental influences on sleep:
Wake up at the same time each day.
Discontinue caffeine intake four to six hours before bedtime and minimize total daily use. Caffeine is a stimulant and may disrupt sleep.
Avoid nicotine, especially near bedtime and on night awakenings. It is also a stimulant.
Avoid the use of alcohol in the late evening to facilitate sleep onset. Alcohol can cause awakening later in the night.
Avoid heavy meals too close to bedtime, since this may interfere with sleep. A light snack may be sleep-inducing.
Regular exercise in the late afternoon may deepen sleep. Vigorous exercise within three to four hours of bedtime may interfere with sleep.
Minimize noise, light and excessive temperatures during the sleep period.
Move the alarm clock away from the bed if it is a source of distraction.
Chronic insomnia may be a significant therapeutic challenge. Since chronic insomnia is often multifactorial in etiology, a patient may need multiple treatment modalities. If an underlying medical or psychiatric condition is identified, this condition should be treated first. In some patients, the mechanisms that maintain the insomnia are more important than the precipitating factors.
If chronic insomnia appears to be primary or persists after treatment of an underlying condition, two general treatment approaches are available: behavior and pharmacologic. Usually pharmacologic treatment provides rapid symptom relief, but controlled studies of long-term treatment have not been conducted. A few weeks of therapy are necessary before sleep improves with behavior approaches, but the relief continues after training sessions have been completed.23 To date, all treatments should be viewed as providing symptomatic relief, since no treatment has been shown to improve overall health or rates of survival.
Behavior interventions seek to change maladaptive sleep habits, reduce autonomic arousal and alter dysfunctional beliefs and attitudes, which are presumed to maintain insomnia. These therapies have been shown to produce reliable and durable improvements in patients with chronic primary insomnia.24 At times, the various behavior treatments are compatible and may be combined, although it is not clear whether increased therapeutic benefit results.
Relaxation Therapy. Relaxation therapy is based on observations that patients with insomnia often display high levels of physiologic, cognitive and/or emotional arousal, both at night and during the daytime. Of several relaxation methods, none has been shown to be more efficacious than the others. Progressive muscle relaxation, autogenic training and electromyographic biofeedback seek to reduce somatic arousal (e.g., muscle tension), whereas attention-focusing procedures such as imagery training and meditation are intended to lower presleep cognitive arousal (e.g., intrusive thoughts, racing mind).
Abdominal breathing may be used as a component of various relaxation techniques, or it may be used alone. Relaxation therapy is useful for both sleep-onset and sleep-maintenance insomnia. These techniques require regular practice with a trained professional over a period of several weeks.
Sleep Restriction Therapy. Poor sleepers often increase their time in bed in an effort to provide more opportunity for sleep, a strategy that is more likely to result in fragmented and poor-quality sleep. Sleep restriction therapy25 consists of curtailing the amount of time spent in bed to increase the percentage of time spent asleep. This improves the patient's sleep efficiency (time asleep/time in bed). For example, a person who reports staying in bed for eight hours but sleeping an average of five hours per night would initially be told to decrease the time spent in bed to five hours. The allowable time in bed per night is increased 15 to 30 minutes as sleep efficiency improves. Adjustments are made over a period of weeks until an optimal sleep duration is achieved. Typically, it is best to alter the bedtime and to keep the rising time constant in order to maintain a regular sleep-wake rhythm. By creating a mild state of sleep deprivation, this therapy promotes more rapid sleep onset and more efficient sleep. To minimize daytime sleepiness, time in bed should not be reduced to less than five hours per night. Sleep restriction therapy is modified in older adults by allowing a short afternoon nap.23
Stimulus Control Therapy. Stimulus control therapy26 is based on the premise that insomnia is a conditioned response to temporal (bedtime) and environmental (bed/bedroom) cues usually associated with sleep. The main objective of stimulus control therapy is to reassociate the bed and bedroom with the rapid onset of sleep. Stimulus control instructions involve going to bed only when sleepy; using the bed and bedroom only for sleep; getting out of bed and going into another room when unable to fall asleep or return to sleep easily and returning to bed only when sleepy again; maintaining a regular morning rising time regardless of duration of sleep the previous night; and avoiding daytime naps. Clinical trials have documented the efficacy of stimulus control therapy for both sleep onset and sleep-maintenance insomnia.27,28
Cognitive Therapy. Cognitive therapy involves identifying dysfunctional beliefs and attitudes about sleep and replacing them with more adaptive substitutes. For example, patients who believe that sleeping eight hours per night is absolutely necessary to function during the day are asked to question the evidence and their own experience to see if this is true for them. Patients who are convinced that insomnia is destroying their ability to enjoy life are encouraged to develop more adaptive coping skills and to cease viewing themselves as victims. These attitudinal changes often help minimize the anticipatory anxiety and arousal that interfere with sleep.
Hypnotic Medications. The primary indication for hypnotic medication is short-term management of insomnia—either as the sole treatment modality or as adjunctive therapy until the underlying problem is controlled. The most common medications used to promote sleep are benzodiazepine receptor agonists. These compounds have been shown to be effective in inducing, maintaining and consolidating sleep, compared with placebo.29 Patients report significant relief of both nighttime and daytime symptoms.30 Differences between the compounds' ability to induce and maintain sleep are based on rate of absorption and elimination and are minor. The most common side effects of these medications are anterograde amnesia and, for long-acting drugs, residual daytime drowsiness. Currently an estimated 10 to 15 percent of patients who use hypnotic medications use them regularly for more than one year,31 although little safety or efficacy data are available to guide their use beyond two to three months. While selected patients may benefit from chronic use of these medications, there are no clear indications showing which patients might benefit from chronic therapy.
Dosage, pharmacokinetic properties (absorption rate, distribution, elimination half-life) and risk-benefit ratio are the key factors in selecting the most appropriate medication. Dosage is the single best predictor of the risk of side effects. It affects both the peak amount of a drug in the body as well as the duration of action of the medication. Once an effective dosage is established, increasing the dosage rarely leads to increased efficacy but does increase the frequency of side effects.
Elimination half-life varies considerably among hypnotic medications and is the best predictor of next-day residual effects. In patients who need to be alert because of occupational or societal demands, short-acting medications are preferred. However, patients with insomnia and high levels of daytime anxiety may benefit more from long-acting medications. It is important to remember that, with age, the volume of distribution increases and the rate of metabolism slows for most of these medications. These actions lead to higher drug concentrations and a longer duration of action. Hypnotic medications are contraindicated in pregnant women, patients with untreated obstructive sleep apnea, patients with a history of substance abuse and patients who might need to awaken and function during their normal sleep period. Finally, patients with hepatic, renal or pulmonary disease must be monitored more carefully than otherwise healthy patients with insomnia.
It is very common for sedating antidepressants to be prescribed for insomnia, often in low dosages, but little scientific evidence supports the efficacy or safety of this approach in the treatment of most types of insomnia. When prescribed for patients with major depression, sedating antidepressants improve subjective and objective measures of insomnia,32 and sleep symptoms often improve more quickly than other symptoms of depression. When administered concurrently with “alerting” antidepressants, low dosages of sedating antidepressants such as trazodone again improve insomnia.33 However, in non-depressed patients, the data to recommend use of antidepressants are minimal.34
Antidepressants have a range of adverse effects including anticholinergic effects, cardiac toxicity, orthostatic hypotension and sexual dysfunction (selective serotonin reuptake inhibitors [SSRIs]). Tricyclic antidepressants and SSRIs can exacerbate restless legs syndrome and periodic limb movement disorder in some patients. The lethal dosage/effective dosage ratio for tricyclic antidepressants is smaller than that for benzodiazepines.
With little scientific evidence to support the efficacy and safety of antidepressants in the treatment of insomnia, the clearest indications for their use are in patients with insomnia that is associated with psychiatric disorders or patients who have a previous history of substance abuse.
Antihistamines. Drugs that antagonize central histamine H1 receptors have sedative effects. The most common antihistamines used for treatment of insomnia are diphenhydramine and hydroxyzine; most over-the-counter sleep aids include an antihistamine. Few recent studies have assessed the efficacy of antihistamines in the treatment of insomnia, but older studies demonstrated subjective and objective improvements during short-term treatment.35 The long-term efficacy of antihistamines in the management of insomnia has not been demonstrated. Adverse effects associated with antihistamines include daytime sedation, cognitive impairment and anticholinergic effects. Tolerance and discontinuation effects have been noted.31
Melatonin. Melatonin has several physiologic actions, including a phase-shifting effect on circadian rhythms, increased sleepiness when administered during daytime hours and vasoconstriction. Its mechanisms of action are unknown but may involve interaction with melatonin receptors in the suprachiasmatic nucleus. The role of melatonin in treating any sleep-related disorder remains to be defined.36 Clinical studies in patients with insomnia have provided inconsistent results.
Other Drugs. Barbiturates and a number of older nonbenzodiazepine, nonbarbiturate drugs such as chloral hydrate, methyprylon and meprobamate are still available. These drugs are not recommended for the treatment of insomnia because of a narrow therapeutic ratio, rapid development of tolerance, systemic toxicity, potential for abuse and the possibility of severe clinical complications on withdrawal.
Finally, a variety of herbal preparations (e.g., valerian root, herbal teas), so-called nutritional substances (e.g., l-tryptophan) and over-the-counter drugs are promoted, especially in the lay press, for the treatment of insomnia. In general, little scientific evidence supports the efficacy or safety of these products.
Sleep disturbance is a reliable predictor of psychologic ill health, physical ill health, or both. Thus a report of disturbed sleep signals the need for further evaluation. Physicians should inquire about sleep during periodic patient assessments. Insomnia is often associated with psychiatric or medical illness, sometimes as the primary or initial symptom of a problem. Effective treatments for insomnia are available. In some patients, improvement in sleep leads to an improved quality of life.
Logistical support for the Working Group was provided with the assistance of the American Sleep Disorders Association through an unrestricted educational grant from Wyeth-Ayerst Laboratories.
Members of the National Heart, Lung, and Blood Institute Working Group on Insomnia include: James K. Walsh, Ph.D. (chair); Ruth M. Benca, M.D., Ph.D.; Michael Bonnet, Ph.D.; Daniel J. Buysse, M.D.; Jim Ricca, M.D., M.P.H.; Peter J. Hauri, Ph.D.; Charles Morin, Ph.D.; Thomas Roth, Ph.D.; Richard D. Simon, Jr., M.D.; James Kiley, Ph.D.; Andrew Monjan, Ph.D., M.P.H.; and Susan Rogus, R.N., M.S.
1. Mellinger GD, Balter MB, Uhlenhuth EH. Insomnia and its treatment. Prevalence and correlates. Arch Gen Psychiatry. 1985;42:225–32.
2. Foley DJ, Monjan AA, Brown SL, Simonsick EM, Wallace RB, Blazer DG. Sleep complaints among elderly persons: an epidemiologic study of three communities. Sleep. 1995;18:425–32.
3. Roehrs T, Zorick F, Roth T. Transient and short-term insomnia. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine. 2d ed. Philadelphia: Saunders, 1994:486–93.
4. Nicholson AN, Pascoe PA, Spencer MB, Stone BM, Roehrs T, Roth T. Sleep after transmeridian flights. Lancet. 1986;2(8517):1205–8.
5. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? JAMA. 1989;262:1479–84.
6. Breslau N, Roth T, Rosenthal L, Andreski P. Sleep disturbance and psychiatric disorders: a longitudinal epidemiological study of young adults. Biol Psychiatry. 1996;39:411–8.
7. Gislason T, Almqvist M. Somatic diseases and sleep complaints. An epidemiological study of 3,201 Swedish men. Acta Med Scand. 1987;221:475–81.
8. Klink ME, Quan SF, Kaltenborn WT, Lebowitz MD. Risk factors associated with complaints of insomnia in a general adult population. Influence of previous complaints of insomnia. Arch Intern Med. 1992;152:1634–7.
9. Buysse DJ. Drugs affecting sleep, sleepiness and performance. In: Monk TH, ed. Sleep, sleepiness and performance. New York: Wiley, 1991:249–306.
10. Obermeyer WH, Benca RM. Effects of drugs on sleep. Neurol Clin. 1996;14:827–40.
11. Hening WA, Walters AS, Chokroverty S. Motor functions and dysfunctions of sleep. In: Chokroverty S, ed. Sleep disorders medicine: basic science, technical considerations, and clinical aspects. Boston: Butterworth-Heinemann, 1994: 255–94.
12. Buysse DJ, Reynolds CF 3d, Hauri PJ, Roth T, Stepanski EJ, Thorpy MJ, et al. Diagnostic concordance for DSM-IV sleep disorders: a report from the APA/NIMH DSM-IV field trial. Am J Psychiatry. 1994;151:1351–60.
13. Bonnet MH, Arand DL. Hyperarousal and insomnia. Sleep Medicine Reviews. 1997;1(2):97–108.
14. Doghramji K, Browman CP, Gaddy JR, Walsh JK. Triazolam diminishes daytime sleepiness and sleep fragmentation in patients with periodic leg movements in sleep. J Clin Psychopharmacol. 1991;11:284–90.
15. Walsh JK, Muehlbach MJ, Lauter SA, Hilliker NA, Schweitzer PK. Effects of triazolam on sleep, daytime sleepiness, and morning stiffness in patients with rheumatoid arthritis. J Rheumatol. 1996;23:245–52.
16. Bonnet MH, Arand DL. 24-hour metabolic rate in insomniacs and matched normal sleepers. Sleep. 1995;18:581–8.
17. Kuppermann M, Lubeck DP, Mazonson PD, Patrick DL, Stewart AL, Buesching DP, et al. Sleep problems and their correlates in a working population. J Gen Intern Med. 1995;10:25–32.
18. Simon GE, VonKorff M. Prevalence, burden, and treatment of insomnia in primary care. Am J Psychiatry. 1997;154:1417–23.
19. Üstün TB, Privett M, Lecrubier Y, et al. Form, frequency and burden of sleep problems in general health care: A report from the WHO collaborative study on psychological problems in general health care. Eur Psychiatry. 1996;11(suppl l):5S–10S.
20. National Institutes of Health Consensus Development Statement. The treatment of sleep disorders of older people. March 26–28, 1990. Sleep. 1991;14:169–77.
21. Carskadon MA, Dement WC. Nocturnal determinants of daytime sleepiness. Sleep. 1982;5(suppl 2):S73–81.
22. Angst J, Vollrath M, Koch R, Dobler-Mikola A. The Zurich Study. VII. Insomnia: symptoms, classification and prevalence. Eur Arch Psychiatry Neurol Sci. 1989;238:285–93.
23. Morin CM. Insomnia: psychological assessment and management. New York: Guilford, 1993.
24. Morin CM, Culbert JP, Schwartz SM. Nonpharma-cological interventions for insomnia: a meta-analysis of treatment efficacy. Am J Psychiatry. 1994;151:1172–80.
25. Spielman AJ, Saskin P, Thorpy MJ. Treatment of chronic insomnia by restriction of time in bed. Sleep. 1987;10:45–56.
26. Bootzin RR, Epstein D, Wood JM. Stimulus control instructions. In: Hauri P, ed. Case studies in insomnia. New York: Plenum, 1991:19–28.
27. Espie CA, Lindsay WR, Brooks DN, Hood EM, Turvey T. A controlled comparative investigation of psychological treatments for chronic sleep-onset insomnia. Behav Res Ther. 1989;27:79–88.
28. Lacks P, Bertelson AD, Sugerman J, Kunkel J. The treatment of sleep-maintenance insomnia with stimulus-control techniques. Behav Res Ther. 1983;21:291–5.
29. Nowell PD, Mazumdar S, Buysse DJ, Dew MA, Reynolds CF 3d, Kupfer DJ. Benzodiazepines and zolpidem for chronic insomnia: a meta-analysis of treatment efficacy. JAMA. 1997;278:2170–7.
30. Balter MB, Uhlenhuth EH. The beneficial and adverse effects of hypnotics. J Clin Psychiatry. 1991;52 (suppl):16–23.
31. Balter MB, Uhlenhuth EH. New epidemiologic findings about insomnia and its treatment. J Clin Psychiatry. 1992;53(suppl):34–9.
32. Sharpley AL, Cowen PJ. Effect of pharmacologic treatments on the sleep of depressed patients. Biol Psychiatry. 1995;37:85–98.
33. Nierenberg AA, Adler LA, Peselow E, Zornberg G, Rosenthal M. Trazodone for antidepressant-associated insomnia. Am J Psychiatry. 1994;151:1069–72.
34. Walsh JK, Erman M, Erwin CW, Jamieson A, Mahowald M, Regestein Q, et al. Subjective hypnotic efficacy of trazodone and zolpidem in DSMIII-R primary insomnia. Human Psychopharmacology. 1998;13:191–8.
35. Roth T, Roehrs T, Koshorek G, Sicklesteel J, Zorick F. Sedative effects of antihistamines. J Allergy Clin Immunol. 1987;80:94–8.
36. Roth T, Richardson G. Commentary: is melatonin administration an effective hypnotic? J Biol Rhythms. 1997;12:666–9.
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