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EDITORIAL COMMENT |
Ecole de Psychologie Université Laval Quebec G1K 7P4 Canada
Insomnia is a highly prevalent complaint in the general population, as well as in primary care and specialty clinics. It is often associated with functional impairments, reduced quality of life, and significant health care costs (1). Surprisingly, insomnia is often unrecognized and may remain untreated for extended periods. The article by Rosa and Bonnet in this issue (2) reports some intriguing data about the relationship (or lack thereof) between subjective reports of insomnia and electroencephalogram (EEG) sleep. The main finding is that retrospective and global reports of insomnia are related only modestly to EEG sleep impairments recorded in the laboratory. A related, although paradoxical finding, is the observation of objective daytime impairments, despite the absence of laboratory-based evidence of sleep disturbances. These puzzling findings highlight the complex nature of insomnia and raise important implications for the assessment, diagnosis, and treatment of insomnia.
Insomnia is a complex, heterogeneous condition that can be symptomatic of an underlying medical, psychiatric, or substance abuse disorder. Or, it can be a syndrome in itself, in which case the diagnosis of primary insomnia is often made by default (3). What makes this condition particularly challenging to evaluate and treat is that some people complain of insomnia but do not show any objective evidence of poor sleep, although others report and show objective evidence of impaired sleep, and still others may experience sleep disruptions, but are not concerned and do not complain about it (4). These discrepancies between subjective and objective measurements of sleep, which are present in both poor and good sleepers, typically involve an overestimation of the time spent awake and an underestimation of time spent asleep during the nocturnal period (5–8). Although the most common explanation to account for this lack of concordance is that insomniacs misperceive or even exaggerate their sleep difficulties, several other clinical and methodological factors must be considered as well.
The first issue requiring clarification is that the degree of discrepancy between a subjective complaint of insomnia and objective measures of EEG sleep usually falls along a continuum, including at one end, cases of pure sleep state misperception (ie, subjective complaint of insomnia without any objective finding) and, at the other end, cases of pure or true insomnia (ie, subjective complaint fully corroborated by objective findings). Most individuals will fall between those two extremes when estimating sleep parameters but, naturally, because self-defined poor sleepers spend more time awake, there is also more room for error in this subgroup than in good sleepers. The proportion of cases with pure sleep state misperception is relatively low among treatment-seeking insomniacs (6) and some longitudinal evidence suggests that this condition may actually be a prodromal phase to a more psychophysiologically based insomnia (9).
A second issue is that insomnia is more than a physiological phenomenon. There is an important psychological component as well, involving a conditioned response in which the stimuli that typically are associated with sleep (eg, bedtime rituals, bedroom environment) become associated with the fear of not sleeping, performance anxiety, and with the frustration of sleeplessness. For this reason, sleep is not the same in the laboratory as it is usually at home (10, 11). Otherwise good sleepers usually sleep worst in the laboratory than at home and insomniacs actually sleep better in the lab because the discriminative cues keeping them awake at home are no longer present in the laboratory. Because of these effects, it is often necessary to conduct several consecutive recording nights, and discard the data from the first adaptation night, to obtain ecologically valid data.
Another important consideration is that current scoring criteria for sleep do not take into account behavioral and phenomenological features of sleep. Polysomnography is the accepted "gold standard" to measure sleep, and even if the criteria used to distinguish wakefulness from sleep are objective and operational, they may not be sensitive enough to subtle EEG changes (eg, micro-arousals, alpha-delta sleep, beta activity) that often characterized insomnia. Recent research using power spectral analysis and evoked potentials has uncovered such subtle, yet objective, EEG impairments in the sleep of individuals complaining of chronic insomnia (12–13).
An important implication of the article by Rosa and Bonnet (4) is that clinicians should never rely exclusively on a screening questionnaire or on global assessment to make the diagnosis of insomnia. Given the heterogeneity of insomnia complaints, and the fine distinctions between the symptom and the syndrome of insomnia, a sound assessment should always involve a face-to-face, multifocused, clinical evaluation. This would include a detailed history of the nature, duration, course, and severity of the sleep problem, as well as the presence of medical, psychological, behavioral, and environmental contributing factors. Whenever feasible, the initial insomnia complaint should be validated with prospective, daily sleep diaries. Although sleep diary data may not reflect absolute values from EEG measures, it is more likely to yield a valid sample of a patient’s typical sleep at home compared with that of 1 or 2 nights of recording in the sleep laboratory. Polysomnography is usually not indicated for the routine assessment of insomnia, unless there is evidence/symptoms of other sleep disorders (14). It is also important to realize that psychological factors (anxiety, depression) may alter perception of sleep and time estimation (8), and assessment of these factors should always be part of the evaluation of insomnia.
Another implication is the need to refine our current diagnostic criteria of insomnia (ie, difficulties initiating and/or maintaining sleep, or nonrestorative sleep, associated with impairments of daytime functioning or marked distress for more than 1 month). Although clinical studies often rely on a number of operational (although arbitrary) criteria such as a sleep latency and/or time awake after sleep onset greater than 30 minutes per night, with a corresponding sleep efficiency smaller than 80% to 85%, there are no standard quantitative criteria to diagnose insomnia. Also, there is extensive variability across studies as to whether the selected criteria are based on a global and retrospective evaluation, on daily and prospective sleep diary estimates or, on polysomnographic recordings. Standardized and operationally defined criteria are particularly important for research purposes, although such criteria may not need to be as stringent in clinical practice. For instance, when a patient complains of sleeping for only 5 hours per night, it makes little practical difference whether polysomnography reveals that total sleep time is actually 4, 5, or 6 hours. The most central feature of insomnia remains the subjective perception of inadequate sleep duration or quality; its clinical significance should be judged by its impact on daytime functioning, quality of life, mood, and energy.
There are implications for treatment as well. First, the danger in assuming that all subjective complaints of insomnia are unsubstantiated by objective evidence is that insomnia may continue to be undertreated. Just as it is inappropriate to initiate treatment without a careful evaluation and accurate diagnosis, it would be equally unwise to ignore insomnia complaints. Because chronic insomnia is an important risk factor for major depression (15), and for several other significant morbidity, early recognition and treatment of this condition is warranted clinically. Because most practitioners will not have access to laboratory data when treating insomnia patients, it is more sensible to treat the subjective complaint. Significant advances have been made in the management of insomnia (16, 17), and interventions such as sleep education and cognitive-behavior therapy have proven effective and important components of treatment. Even pure cases of sleep state misperception deserve clinical attention and may benefit from cognitive therapy aimed at correcting time estimations.
ACKNOWLEDGMENTS
This article was supported, in part, by a grant from the National Institute of Mental Health (MH55469).
REFERENCES
This article has been cited by other articles:
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  J. Savard, S. Simard, H. Ivers, and C. M. Morin Randomized Study on the Efficacy of Cognitive-Behavioral Therapy for Insomnia Secondary to Breast Cancer, Part I: Sleep and Psychological Effects J. Clin. Oncol., September 1, 2005; 23(25): 6083 - 6096. [Abstract] [Full Text] [PDF]
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 D. W. Levine, M. E. Dailey, B. Rockhill, D. Tipping, M. J. Naughton, and S. A. Shumaker Validation of the Women's Health Initiative Insomnia Rating Scale in a Multicenter Controlled Clinical Trial Psychosom Med, January 1, 2005; 67(1): 98 - 104. [Abstract] [Full Text] [PDF]
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J. Savard, L. Laroche, S. Simard, H. Ivers, and C. M. Morin Chronic Insomnia and Immune Functioning Psychosom Med, March 1, 2003; 65(2): 211 - 221. [Abstract] [Full Text] [PDF]
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