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Introduction to Chronic Insomnia:
Classification and Prevalence

Milton K. Erman, MD

 

Primary Psychiatry. 2007;14(5):27-31

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 Pacific Sleep Medicine Services. 

Disclosure: Dr. Erman is a consultant to Cephalon, Mallinckrodt, Neurocrine, sanofi-aventis, and Takeda; is on the speaker’s bureaus of Forest, sanofi-aventis, and Takeda; is on the advisory boards of Cephalon, Neurocrine, sanofi-aventis, and Takeda; has received grant/research support from Arena, Cephalon, Eli Lilly, GlaxoSmithKline, Mallinckrodt, Merck, Organon, Pfizer, Pharmacia, ResMed, sanofi-aventis, Schwarz Pharma, and Takeda; and owns stock in Cephalon, Forest, Merck, Neurocrine, Pfizer, sanofi-aventis, and Sepracor.

 


“In the kingdom of the blind, the one-eyed man is king.” — Desiderius Erasmus (1466-1536)

Despite the dramatic scientific advances in the field of sleep research of the last 50 years, medical students receive little if any teaching about sleep physiology and sleep disorders. In most residency training programs, no instruction is provided to help physicians learn how to diagnose and treat sleep disorders they will see in their practices. As is true for psychiatric disorders, effective treatment of sleep disorders requires the capacity to make the correct diagnosis; this in turn is dependent on an understanding of how various disorders develop and present, how they may progress over the life cycle, and how treatment interventions may affect their course and may lead to remission or resolution of symptoms. I hope that the information presented in this series will help readers open at least one eye to the challenges and opportunities associated with the treatment of sleep disorders!

Introduction

Patients with insomnia have long provided a series of challenges to physicians responsible for their care. The first challenge: Is the insomnia a symptom of another comorbid disorder, medical or psychiatric in origin, or a disorder unto itself? This question does not reflect an abstract heuristic exercise, but must be addressed and answered so appropriate therapy can be given.

The second challenge: What are appropriate therapies for the insomnia complaint, no matter what the origin of the disorder?
 

Primary insomnia is a specific disorder, defined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV)1 as a condition of at least 1 month’s duration, not caused by a medical or psychiatric disorder. In addition, a symptom of insomnia (disturbed sleep initiation or sleep maintenance, or early morning awakening) must be present and must be associated with complaints of daytime dysfunction.1 Although many psychiatric patients may have chronic insomnia symptoms, it is estimated that as few as 10% of the general population suffer from chronic insomnia complaints consistent with these diagnostic criteria.2 

Physicians are often conflicted about proving treatment to patients with insomnia complaints. A list of some justifications supporting insomnia treatment would include: it causes symptomatic distress, it impairs normal functioning, it increases healthcare costs, it is associated with increased risk of comorbid disease, and it is responsive to treatment.

Nosology

Among the classification schemes used to describe insomnia are those included in the International Classification of Sleep Disorders, Second Edition, (ICSD-2),3 the DSM-IV,1 and the World Health Organization’s International Classification of Diseases (ICD-9 and ICD-10).4,5 The ICSD is not as well known or as widely used as the other systems, but is more complete and specific with regard to the definitions of various insomnia disorders. Eleven specific diagnoses are included within the Insomnia Category of the ICSD-2 system, but additional disorders that often present with insomnia complaints are included in other categories (ie, circadian rhythm sleep disorders, sleep related movement disorders, etc.) 

The DSM-IV and ICD classification systems categorize insomnia in a broader fashion, with fewer specific entities. The DSM-IV has a specific category for primary insomnia, a disorder characterized as not being related to or caused by another sleep, mental, medical disorder or affects of a medication.1 Breathing-related sleep disorder is a specific diagnosis, and is recognized as presenting at times with insomnia complaints.5 Circadian rhythm sleep disorder is given a separate category, but restless leg syndrome (RLS) is combined with insomnia of environmental origin and other disturbances in a category of Dyssomnia Not Otherwise Specified. Although there is a specific category for Primary Insomnia, there is no formal category for Secondary Insomnia. Instead, diagnoses reside within the broad Dyssomnia section for categories such as Insomnia Related to Another Mental Disorder, Sleep Disorders Due to a General Medical Condition, Insomnia Type, and Substance-Induced Sleep Disorder, Insomnia Type.

The DSM-IV system divides sleep disorders by presumptive etiology, organic versus nonorganic. Within the nonorganic group, a division is also made on the basis of duration, with “Transient Disorder of Initiating or Maintaining Sleep” given a separate diagnostic code from “Persistent Disorder of Initiating or Maintaining Sleep” (the use of the term Disorder of Initiating or Maintaining Sleep is a holdover from the First Edition of the ICSD, published in 1987).6

Each classification system has advantages and disadvantages. The ICSD has been criticized for being overly detailed and inclusive including descriptions of rare and arcane disorders. In contrast, the DSM-IV and ICD fail to provide diagnostic categories for common causes of insomnia such as RLS. At a practical level, however, most clinicians will need to use a classification such as the ICD for administrative and reimbursement reasons.
 

The 1983 Consensus Conference 

The treatment of insomnia, and regulation of hypnotic medications for the treatment of insomnia, was influenced tremendously over the past 20 plus years by a Consensus Conference held by the National Institutes of Health (NIH) in 1983.7 The title of this conference, “Drugs and Insomnia: The Use of Medications to Promote Sleep,” helps us understand the impact this conference has had on the practice of insomnia treatment.

What led to a consensus conference in medicine in 1983? The absence of a consensus based on scientific evidence, and the lack of adequate scientific evidence to define appropriate treatment. The panel that prepared the Consensus Conference report included psychiatrists, psychopharmacologists, biomedical researchers, epidemiologists, primary care physicians, and public representatives. Among their recommendations, the panel stated “The first obligation of the practitioner is to search for a specific psychiatric or medical disease as the underlying cause. This view considers insomnia as primarily one symptom of a symptom complex, which can be assessed by an appropriate medical history, physical examination, and laboratory procedures.” 

The Conference report did not use the specific terms “primary insomnia” and “secondary insomnia,” but did direct clinicians to search for “a specific psychiatric or medical disease as the underlying cause” of insomnia, implying that insomnia is usually a secondary condition. This may have seemed to be a convenient and rational approach, but it was problematic. The primary and secondary terminology implied cause and effect; for example, depression leads to insomnia, or arthritis leads to insomnia. It would then be rational to assume that treatment of the underlying “cause” would lead to resolution of the secondary symptom; this is an outcome that rarely occurs.

The 1983 conference introduced terminology with regard to the duration of insomnia that has been utilized over the past several decades. Three types of insomnia were specified: transient, short-term, and chronic. Although durations for these various types of insomnia were not given in the document, the description of transient insomnia as being related to minor situational stress and the recommendation that treatment for this condition could be provided for 1–3 nights suggests a duration of <1 week. Short-term insomnia is also not defined with regard to duration; the recommendation that treatment be limited to 3 weeks suggests a duration of action of this disorder of <1 month. Long-term insomnia is also not defined, but since a recommendation that treatment be gradually discontinued after 3–4 months is suggested for this condition, it can be inferred that the duration would be of >1 month and lasting for at least 3–4 months, if not longer. 

Specific treatment recommendations were tied to these conditions and were not based on any scientific evidence or practice parameters. Medications were described as being appropriate for transient insomnia and a combination of medications and behavioral therapies (including sleep hygiene) were deemed appropriate for short-term insomnia. Since this disorder was defined as having a duration of up to 3 weeks, treatment for this long was presumably acceptable. 

The Conference provided specific recommendations with regard to the three types of insomnia. For transient insomnia, the recommendation was for a small dose of a rapidly eliminating hypnotic (unless sustained sedation was desired), with treatment provided for 1–3 nights. For short-term insomnia, the use of sleep hygiene was emphasized, but it was also noted that a benzodiazepines hypnotic, at the smallest effective dose, could be used for a treatment period of “usually not more than 3 weeks.”

For long-term insomnia, the report emphasized the need to treat possible contributory medical and psychiatric conditions. A combined approach using sleep-promoting agents and behavioral therapy was suggested, with a recommendation that medication therapy be provided utilizing a benzodiazepines agent, preferentially on an intermittent basis (ie, 1 night in 3), if possible.

Chronic insomnia proved to be somewhat problematic, since no medications available at that point in time were approved for long-term use. Benzodiazepines were the drugs of choice, with a recommendation for intermittent treatment, such as one night in three. It was also suggested that it would be “wise to discontinue therapy gradually after 3–4 months.”7 

The 2005 State of the Science Conference

The recommendations from the 1983 conference7 influenced clinical practice and regulatory policy over the past 24 years. A 2005 State of the Science conference8 held by the NIH provided more appropriate definitions of insomnia and recommendations for its treatment, and seems to already have influenced regulatory policy. A panel comprised of experts from various disciplines, including psychiatry, psychology, internal medicine, epidemiology, and family medicine, participated in the conference. They addressed questions critical to the current diagnosis and treatment of insomnia, including definition, prevalence, consequences, and appropriate treatment. The specific findings of this State of the Science Conference are referenced in detail in later sections.

Several important changes in perspective were emphasized in the report. Although therapeutic recommendations and product indications in the past had usually focused on short-term treatment, this report noted that, “for millions, the problem is chronic.” Another important change in insomnia nosology endorsed by the panel was that of comorbidity. The report stated that, “Insomnia often is comorbid with other disorders, particularly depression, as well as some cardiovascular, pulmonary, and gastrointestinal disorders.”8

Prevalence

Insomnia is quite prevalent in the general adult population, and even more common in medical and psychiatric patient populations.9 In a survey performed in 1979 by the Gallup Organization,10 95% of a randomly selected sample of adults reported having experienced insomnia at some time in their lives. In another national survey, performed in 1993, ~33% of adults11 in the United States reported having experienced problems with insomnia during the previous year. Findings in the surveys varied based on differences in methodology and populations surveyed. In a recent review of studies reporting insomnia prevalence, Ohayon12 described estimates of prevalence for chronic insomnia ranging from a low of 4.4%13 to a high of 48%.14

Of the 1,000 adults >18 years of age interviewed in the 1991 National Sleep Foundation Survey,15 36% of respondents reported that they experienced a sleep problem, 27% reported occasional insomnia, and 9% reported chronic insomnia. The sleep problems that were reported most frequently by survey respondents were waking up feeling unrefreshed (72%), waking up in the middle of the night (67%), and difficulty getting back to sleep after waking up (57%). In the 2003 Sleep in America Poll,16 in which 1,506 adults between 55–84 years of age were interviewed, 48% had >1 symptoms of insomnia >1 night/week. Reported symptoms of insomnia included frequently waking during the night (33%), waking too early and not being able to get back to sleep (23%), and difficulty falling asleep (18%). Changes in sleep patterns with age precipitate sleep complaints in older adults. 

A 2002 National Sleep Foundation survey16 showed that 58% of respondents experienced symptoms of insomnia at least a few nights a week, with 35% reporting that they experienced at least one symptom of insomnia every night or almost every night over the preceding year. A National Center for Complementary and Alternative Medicine survey assessing insomnia and problems sleeping found that, over a 12 month period, 17.4% of the adult population reported problems with insomnia or trouble sleeping.17 

Insomnia clearly is a common disorder. Is it “worth treating”? Consequences of insomnia will be discussed below, but patients generally define their insomnia as a source of distress and discomfort. For example, in surveys performed in general community populations, Balter and Uhlenhuth18 found that 15% of responders reported that they had had a serious sleep problem during the preceding year.

Another study by Balter and Uhlenhuth19 was performed using a telephone interview of patients who reported that, over the preceding 12 months, they had experienced significant problems with insomnia or had taken medications to promote sleep. Respondents who had taken hypnotics felt that use of these medications had been of benefit for them, and reported that they would be willing to use hypnotics again if the need arose. Prescription hypnotics were reported to have been more effective in the treatment of insomnia than over the counter (OTC) agents. Patients who received prescription hypnotics did not report having experienced negative effects such as rebound insomnia, derealization, or paranoia more frequently than users of OTC agents.

Incidence

Age, gender, and social class influence the incidence of insomnia. Most studies examining insomnia have shown increased prevalence associated with increased age, with a prevalence rate that is relatively stable between 15–44 years of age, but with increases after 45 years of age and continuing increases up to 65 years of age.12 However, the widely held belief that “people don’t sleep as well as they age” is not the explanation of this phenomenon. Although there are clear changes in sleep physiology associated with the aging process, including reductions in the amount of Delta (slow wave) sleep that is recorded and tendencies to greater arousability, comorbid medical problems associated with the aging process play a primary role in the increased rates of insomnia seen. In senior populations, the healthiest individuals (ie, those with greatest levels of physical activity and the fewest health problems) are most likely to report good sleep without complaints of insomnia.20 

In surveys of all age groups, women are typically more likely than men to report problems with disturbed sleep. Women <45 years of age are approximately 1.4 times more likely to report insomnia complaints than men of the same age. In women >45 years of age, the probability of insomnia complaints is increased to 1.7 times that of men the same age.12 Menopausal and perimenopausal symptoms play a clear role in the development of insomnia, although symptomatic treatment for complaints such as hot flashes does not always lead to resolution of insomnia symptoms.

 

 

 

 

 

 

 

 


Social class and marital status also have an impact on sleep. Most studies find an increased risk for insomnia among those who are divorced, separated, or widowed, compared with individuals who are married.13,21 Other studies22-25 suggest that limited years of education, low income, and unemployment may increase insomnia risk.

Levels of stress play a major role in the development and perpetuation of insomnia. Increased stress levels have been demonstrated to be a precipitating factor for development of insomnia. Chronic insomnia patients report that increased stress levels precede and seem to precipitate their insomnia,13,26 and epidemiologic studies show that increased stress levels in the workplace are associated with increased rates of sleep complaints.24 There is an increase in insomnia complaints among shift workers reflective of their circadian rhythm disturbances and the reductions in hours of sleep per week they obtain as a result of their work demands and altered sleep-wake patterns.27,28

Other sleep disorders are associated with disturbances of the circadian rhythms. Two of these, delayed sleep phase syndrome (DSPS) and advanced sleep phase syndrome (ASPS), are frequent causes of insomnia complaints in various patient populations. Patients with DSPS report the inability to go to sleep at a desired “normal” hour (ie, 11pm or midnight), and a similar inability to awaken and function in the morning at a desired “normal” hour (ie, 7 or 8am) (Figure 1). Rather, these individuals report a difficulty feeling sleepy or falling asleep, which may not occur until 3 or 4am, with a similar difficulty in waking (despite obligations such as school or work) until later in the morning, which may not be until 11am or noon. This condition is seen most often in adolescent and young adult populations,29 although it may be seen in individuals of any age. DSPS appears to develop due to combined effects of physiologic predisposition to such circadian delay during young adult life and social factors associated with late night activity.30 

 

 

 

 

 

 

 

 

 


ASPS can be deemed as an exaggeration of the socially adaptive tendency to be an “early bird.” Less common than DSPS, ASPS is seen with increased frequency in older individuals. Patients with ASPS report feeling sleepy at hours earlier than they prefer, often needing to fall asleep in the early evening (Figure 2). Although this may be somewhat inconvenient, the bigger problem for these patients is their tendency to awaken at an early morning hour, with the inability to return to sleep after awakening. As with DSPS, the specific etiology of ASPS is not identified, but may reflect similar trends-—altered physiology favoring a shortened circadian rhythm associated with aging, and absence of alerting activity in the evening hours to delay sleep tendency until a more “normal” later hour.31

Are some people destined to be poor sleepers, no matter how healthy their lifestyle or how limited their levels of stress? This may well be the case; indeed the whole notion that a category of primary insomnia as described in DSM-IV1 is based on the assumption that patients with this condition are free from medical, psychiatric, or drug influences that may cause this condition. Although conditioning factors play a huge role in the development of primary insomnia in many individuals,32,33 there is a possibility of inherited, reduced homeostatic drive to sleep that leaves them predisposed to the development of insomnia.34 PP

 

References

1. Diagnostic and Statistical Manual of Mental DIsorders. 4th ed. Washington, DC: American Psychiatric Association; 1994. 

2. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? JAMA. 1989;262(11):1479-1484.

3. International Classification of Sleep Disorders. Diagnostic and Coding Manual. 2nd ed. Westchester, IL: American Academy of Sleep Medicine; 2005.

4. International Classification of Diseases, Clinical Modification. 4th ed. 9th rev. Salt Lake City, UT: Medicode; 1994.

5. The International Classification of Diseases. 10th ed. Geneva: World Health Organization; 1993.

6. International Classification of Sleep Disorders-Revised. Rochester, MN: American Sleep Disorders Association; 1997.

7. Consensus conference. Drugs and insomnia. The use of medications to promote sleep. JAMA. 1984;251:2410-2414.

8. National Institutes of Health. National Institutes of Health State of the Science Conference statement on Manifestations and Management of Chronic Insomnia in Adults, June 13-15, 2005. Sleep. 2005;28(9):1049-1057.

9. Simon GE, VonKorff M. Prevalence, burden, and treatment of insomnia in primary care. Am J Psychiatry. 1997;154(10):1417-1423.

10. The Gallup Organization. The Gallup Study of Sleeping Habits. Princeton, NJ: Gallup Organization; 1979.

11. Ancoli-Israel S, Roth T. Characteristics of insomnia in the United States: results of the 1991 National Sleep Foundation Survey. I. Sleep. 1999;22(suppl 2):S347-S353. 

12. Ohayon MM. Epidemiology of insomnia: What we know and what we still need to learn. Sleep Med Rev. 2002;6(2):97-111.

13. Ohayon MM, Caulet M, Guilleminault C. How a general population perceives its sleep and how this relates to the complaint of insomnia. Sleep. 1997;20(9):715-723.

14. Quera-Salva MA, Orluc A, Goldenberg F, Guilleminault C. Insomnia and use of hypnotics: Study of a French population. Sleep. 1991;14(5):386-391.

15. Roth T, Ancoli-Israel S. Daytime consequences and correlates of insomnia in the United States: results of the 1991 National Sleep Foundation Survey, 2. Sleep. 1999;22(suppl 2):S354-S358.

16. National Sleep Foundation. 2003 Sleep in America Poll. Available at: http://www.sleepfoundation.org/_content/hottopics/2003SleepPollExecSumm.pdf. Accessed August 23, 2006.

17. Pearson NJ, Johnson LL, Nahin RL. Insomnia, trouble sleeping, and complementary and alternative medicine: Analysis of the 2002 national health interview survey data. Arch Intern Med. 2006;166(16):1775-1182.

18. Balter MB, Uhlenhuth EH. New epidemiologic findings about insomnia and its treatment. J Clin Psychiatry. 1992;53(suppl):34-39.

19. Balter MB, Uhlenhuth EH. The beneficial and adverse effects of hypnotics. J Clin Psychiatry. 1991;52(suppl):16-23. 

20. Hood B, Bruck D, Kennedy G. Determinants of sleep quality in the healthy aged: the role of physical, psychological, circadian and naturalistic light variables. Age Ageing. 2004;33(2):159-165.

21. Hajak G, SINE Study Group, Study of Insomnia in Europe: Epidemiology of severe insomnia and its consequences in Germany. Eur Arch Psychiatry Clin Neurosci. 2001;251(2):49-56.

22. Bixler EO, Vgontzas AN, Lin HM, Vela-Bueno A, Kales A. Insomnia in central Pennsylvania. J Psychosom Res
. 2002;53:589-592.

23. Sutton DA, Moldofsky H, Badley EM. Insomnia and health problems in Canadians. Sleep. 2001;24(6):665-670.

24. Ohayon M. Epidemiological study on insomnia in the general population. Sleep
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25. Li RH, Wing YK, Ho SC, et al. Gender differences in insomnia: A study in the Hong Kong Chinese population. J Psychosom Res. 2002;53:601-609.

26. Ohayon MM, Zulley J, Guilleminault C, Smirne S, Priest RG. How age and daytime activities are related to insomnia in the general population: Consequences for older people. J Am Geriatr Soc. 2001;49(4):360-366.

27. Harma M, Tenkanen L, Sjoblom T, Alikoski T, Heinsalmi P. Combined effects of shift work and life-style on the prevalence of insomnia, sleep deprivation and daytime sleepiness. Scand J Work Environ Health. 1998;24(4):300-307. 

28. Tachibana H, Izumi T, Honda S, et al. A study of the impact of occupational and domestic factors on insomnia among industrial workers of a manufacturing company in Japan. Occup Med (Lond). 1996;46(3):221-227.

29. Thorpy MJ, Korman E, Spielman AJ, Glovinsky PB. Delayed sleep phase syndrome in adolescents. J Adolesc Health Care. 1988;9(1):22-27. 

30. Wyatt JK. Delayed sleep phase syndrome: pathophysiology and treatment options. Sleep. 2004;27(6):1195-1203.

31. Avidan AY. Sleep in the geriatric patient population. Semin Neurol. 2005;25(1):52-63.

32. Spielman AJ, Saskin P, Thorpy MJ. Treatment of chronic insomnia by restriction of time in bed. Sleep. 1987;10(1):45-56.

33. Spielman AJ, Caruso LS, Glovinsky PB. A behavioral perspective on insomnia treatment. Psychiatr Clin North Am. 1987;10(4):541-53.

34. Pigeon WR, Perlis ML. Sleep homeostasis in primary insomnia. Sleep Med Rev. 2006;10(4):247-254.