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Defining Insomnia 7 Table 4 Diagnostic Criteria for Sleep State Misperception A. Complaint of insomnia B. Normal sleep quality and duration C. Normal polysomnography D. The sleep disturbance cannot be attributed to any other medical disorder. E. Other sleep disorders can co-exist. Minimal Criteria: A plus B. Adapted from ref. 9. SLEEP STATE MISPERCEPTION INSOMNIA In this fascinating disorder, complaints of insomnia occur without any objective evidence of sleep disturbance. Patients may report that they have not slept at all in weeks, months, or years. However, on objective sleep studies, they sleep several hours per night (4,11). When results of sleep evaluation are presented, patients with sleep state misperception (SSM) may vehemently insist that the studies are in error because they are convinced that they sleep very little, if at all. Table 4 lists the diagnostic criteria for SSM. Interestingly, none of the nosologies formally embrace the older descriptive clinical characterizations of insomnia in terms of initial, middle, and terminal (late) insomnia. Trouble falling asleep is often referred to as “initial,” early, or sleeponset insomnia. Trouble with frequent or prolonged awakenings is often labeled “middle” or sleep maintenance insomnia. Waking up earlier than desired and being unable to fall back asleep is referred to as “late,” “terminal,” or early morning awakening insomnia. Waking up feeling unrefreshed is commonly referred to as “nonrestorative” sleep. Patients often report some combination of these descriptions, which is generally referred to as “mixed” insomnia. For the purpose of this chapter, although we consider the ICD’s system to provide a more precise definition of the disorder, we use the term primary insomnia because it is the most widely embraced in clinical practice in the United States. We adopt the more descriptive terminology when a more specific characterization of the presenting complaint is required. Classification Based on Duration and Severity Apart from presenting a specific definition of the disorder/disease entity, there is the need to qualify the duration and severity of the defined illness. Typically, duration is framed dichotomously in terms of acute and chronic stages. Severity can be construed in one of two ways. In one case, standards are set for what constitutes significant deviance from population norms with respect to frequency and intensity of presenting symptoms. In the other case, standards are set by “setting the bar” for “pathologic” at a level that is modal for patients who are help-seeking.
8 Attarian et al. Duration of Illness Insomnia lasting less than 1 month is generally considered “acute,” and is often associated with clearly defined precipitants such as stress, acute pain, or substance abuse. Insomnia is characterized as being chronic when symptoms persist unabated for a duration of at least 1 month, and more typically for durations of time that are 6 months or greater. These cutoffs are relatively arbitrary and correspond to traditional medical definitions of what constitutes short and long periods of time. At this time, there are no studies that use risk models to evaluate the natural course of insomnia. Thus, there is no way of definitively defining “chronicity” in terms that are related to when the disorder becomes severe, persistent, and (for want of a better expression) “self-perpetuating.” One clinical cue for differentiating between acute and chronic insomnia resides in the way patients characterize their complaints. When patients stop causally linking their insomnia to its precipitant and instead indicate that their sleep problems seem “to have a life of their own,” this change in presentation may serve to define the “cut point” between the acute and chronic phases of the disorder and suggest when cognitive-behavioral therapy should be indicated. Severity of Illness INTENSITY Although there are no formal diagnostic criteria, most investigators consider 30 or more minutes to fall asleep and/or 30 or more minutes of wakefulness after sleep onset to represent the threshold between normal and abnormal sleep. Recent work by Lichstein and colleagues suggests that this criteria should be set at “more than 30 minutes,” as this definition is better related to the occurrence of complaint in population studies (12). With respect to “how much sleep,” many investigators are reluctant to fix a value for this parameter. Of the investigators who are inclined to set minimums, most specify that the amount of sleep obtained on a regular basis be equal to or less than either 6 or 6.5 hours per night. The reluctance to establish TST parameters is due, in part, to the difficulty in establishing precisely what one considers to be abnormal. Representing what is pathological with a single number is too confounded by factors like age, prior sleep, and the individual’s basal level of sleep need. The lack of an established TST cutoff is also related to the possibility that profound sleep initiation or maintenance problems may occur in the absence of sleep loss. This is an important distinction because it is often assumed that insomnia is synonymous with sleep deprivation. Although it is certainly the case that the daytime symptoms associated with insomnia might be explained, in part, by partial chronic sleep loss, daytime symptoms need not be ascribable only to lack of sleep. For example, it has been shown that patients with insomnia reliably exhibit sleep micro-architectural disturbances such as enhanced high-frequency activity during non-rapid eye movement (NREM) sleep (13–17). This type of activity, which appears to be independent from sleep continuity and architecture parameters, has been shown to be correlated with patient perceptions about sleep quality and quantity (13,18,19).
Page 1 and 2: Clinical Handbook of Insomnia Edite
Page 3 and 4: C URRENT CLINICAL NEUROLOGY Daniel
Page 5 and 6: © 2004 Humana Press Inc. 999 River
Page 8: Series Editor’s Introduction The
Page 11 and 12: x Foreword nervous system hypersomn
Page 14 and 15: Contents Series Editor’s Introduc
Page 16: Contributors HRAYR P. ATTARIAN, MD
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Page 21 and 22: 4 Attarian et al. until the 1970s t
Page 23: 6 Attarian et al. Table 2 Diagnosti
Page 27 and 28: 10 Attarian et al. REFERENCES 1. Ma
Page 29 and 30: 12 Attarian Another study in Austri
Page 31 and 32: 14 Attarian even less well studied.
Page 33 and 34: 16 Attarian communities. A structur
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Page 37 and 38: 20 Attarian 53. Kageyama, T., Kabut
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Page 41 and 42: 24 Bonnet and Arand Table 1 Reporte
Page 43 and 44: 26 Bonnet and Arand On the day spen
Page 45 and 46: 28 Bonnet and Arand SUMMARY These m
Page 47 and 48: 30 Bonnet and Arand chronic caffein
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Page 51 and 52: 34 Bonnet and Arand The Development
Page 53 and 54: 36 Bonnet and Arand ACKNOWLEDGMENT
Page 55 and 56: 38 Bonnet and Arand 45. Bonnet, M.
Page 57 and 58: 40 Attarian Table 1 Types of Insomn
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Page 61 and 62: 44 Fig. 1. Example of a 1-week slee
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58 Garcia the reality that the tend
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60 Fig. 2. Actigraph recording in a
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62 Garcia neurodevelopmental disabi
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64 Garcia 35. Czeisler, C., kronaue
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66 Garcia
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68 Attarian showed similar degrees
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70 Attarian agitation and hence the
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72 Attarian Affective disorder is s
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74 Attarian and Drug Administration
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76 Fig. 2. Sleep log after treatmen
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78 Attarian 18. Bonnet, M. H. and A
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80 Attarian 65. Perlis, M., Aloia,
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82 Attarian was confirmed by resear
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84 Attarian times worrying about th
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86 Attarian insomnia or for other s
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88 Attarian
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90 Duntley tion systems found that
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92 Duntley Case 1 A 36-year-old fem
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94 Fig. 2. The objective amount of
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96 Duntley PROGNOSIS AND COMPLICATI
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98 Duntley
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100 Attarian EPIDEMIOLOGY There are
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102 Attarian CLINICAL MANIFESTATION
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104 Attarian DIAGNOSTIC WORKUP The
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106 Attarian 13. Hauri, P. J. (1998
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108 Plotkin
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110 Plotkin quality of sleep. Ultim
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112 Plotkin of the therapeutic effi
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114 Plotkin months or years. The ef
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116 Plotkin associated somatic disc
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118 Plotkin Table 1 Causes of Secon
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120 Plotkin Table 1 (continued) Lew
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122 Plotkin REFERENCES 1. Foley, D.
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124 Plotkin 48. Marchetti, F., Rome
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126 Plotkin
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128 Karaz Table 1 DSM-IV Diagnoses
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130 Karaz poor. Focusing only on th
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132 Karaz He felt hopeless that his
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134 Karaz Table 4 Diagnostic Criter
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136 Karaz complained of feeling anx
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138 Karaz other physicians avoided
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140 Karaz 17. Attarian, H. P. (2000
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142 Duntley disorders has been conf
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144 Duntley itance. A recent study
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146 Duntley The patient’s primary
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148 Duntley return to sleep. He tos
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150 Duntley Treatment of RLS should
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152 Duntley 34. Cartwright, R. (197
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154 Perlis et al.
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156 Perlis et al. Fig. 1. A schemat
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158 Perlis et al. ditioned arousal
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160 Perlis et al. subjected to empi
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162 Perlis et al. effect), (3) may
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164 Perlis et al. Cognitive Therapy
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166 Perlis et al. Table 2 Cognitive
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168 Perlis et al. Perhaps more impo
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170 Perlis et al. 28. Carskadon, M.
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172 Perlis et al.
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174 Attarian Secondary Insomnias Re
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176 Attarian 50 years of age who sl
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178 Attarian Antidepressants Becaus
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180 Attarian The use of benzodiazep
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182 Attarian to placebo. Zaleplon a
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184 Attarian 3. Wyatt, R. J., Engel
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186 Attarian residual sedation foll
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188 Index Clonidine, 183 CNS arousa
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190 Index Proton pump inhibitors, 1
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Current Clinical Neurology CLINICAL
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