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Physiological Basis of <strong>Insomnia</strong> 31 In this study, the EEG sleep characteristics of patients with primary insomnia were reproduced in matched normal sleepers for a week. Sleep patterns were matched by making experimental arousals and awakenings throughout the night in normal sleepers to match the pattern of wake time and arousals seen in the patients with insomnia. Because the EEG sleep produced in the study was similar to that found in patients reporting insomnia, changes in the outcome variables should have reflected the consequences of pure “poor” sleep. Table 2 provides a summary of typical findings for patients with insomnia and compares those findings with the results of this yoke control study. Changes secondary to the poor sleep produced in the yoke control study were clearly different from the symptoms most frequently reported by patients with insomnia. Patients with insomnia typically have difficulty falling asleep both at night and during the MSLT (20–22,24). However, both SL and MSLT data from the yoke control study supported significantly increasing ease of falling asleep as the nights of insomnia increased. Patients with insomnia frequently have elevated body temperature and whole body metabolic rate (6,14,24). Except for an increase in nocturnal metabolic rate probably associated with the experimental sleep disturbance itself (37), the trends in the yoke control study showed lower metabolic rate and decreased body temperature during the day. Patients with insomnia typically report increased stress, anxiety, or depression (1,24). However, in the yoke control study, the state measures of tension and depression decreased significantly during the study. Patients with insomnia typically have elevated MMPI scales, but the MMPI measures were unchanged in this study. Patients with insomnia report increased fatigue and decreased vigor, and similar changes were found in the yoke control study. However, these changes are also found during simple sleep deprivation. Finally, patients with insomnia overestimate their time spent awake during the night. Despite increased awakenings and wake time in the yoke control study, the normal sleepers continued to correctly estimate their wake time during the night. The most parsimonious explanation for the results was that the insomnia sleep pattern resulted only in partial sleep deprivation when imposed on normal sleepers. This interpretation is supported by rebounds of REM and SWS during the recovery night after the 7 nights of yoke insomnia and by decreasing MSLT values. These changes are classic signs of sleep loss. Decreases in vigor and body temperature also suggested simple sleep loss. Because TST in the study was reduced to 6 hours each night for a week, this could easily have resulted in partial sleep deprivation. For example, a study by Rosenthal et al. (38) showed increased sleepiness on the MSLT after just 1 night of 5.6 hours of sleep. The data from the yoke control study support the contention that some patients with insomnia may suffer from mild partial sleep deprivation. As in normal subjects, however, the degree of deficit should be related to the amount of sleep lost and should typically recover after an occasional night of improved sleep. In fact, one could hypothesize that poor sleep in response to hyperarousal is an adaptive
32 Bonnet and Arand response that acts as a homeostatic mechanism to cause partial sleep deprivation and reduce the impact of hyperarousal. Unfortunately, in patients with chronic insomnia, a night of relatively good sleep would remove a portion of the chronic partial sleep deprivation and leave the patient more susceptible to the effect of hyperarousal. This situation leaves patients in the uncomfortable situation of suffering either from hyperarousal or from hyperarousal masked by sleep deprivation. If the poor sleep of patients with insomnia produces only mild sleep loss in matched normal sleepers, how does one explain the consistent secondary symptoms reported by patients with insomnia? As can be seen from Table 2, the secondary symptoms of patients with insomnia appear in normal sleepers who are hyperaroused (35), but not in normal sleepers actually given the poor sleep experienced by patients with insomnia. The major implication of such data is that it is the increased arousal and not the poor sleep per se that is responsible for the symptoms. Is it possible, however, that the development of symptoms in patients with insomnia is actually dependent on poor sleep interacting with personality variables in the patients with insomnia? If this is the case, then one would expect that patients with insomnia who have particularly poor nights of sleep would experience an exacerbation of their insomnia symptoms. In another study (39), it was hypothesized that, if nocturnal sleep parameters produced the daytime dysphoria reported by patients with insomnia, then patients with sleep maintenance insomnia who were kept awake even longer than usual during the night should have had increased dysphoria during the following day. To test this hypothesis, patients with sleep maintenance insomnia were allowed only 80% of their already reduced TST each night for 7 consecutive nights. This sleep reduction was accomplished by waking patients up at the end of each quarter of the night if they accumulated more than 80% of their baseline sleep for that quarter of the night (while holding TIB for the entire night at the baseline level). This paradigm produced very poor sleep (average TST of 4.2 hours on each night for the week). This reduction of TST by experimental awakenings resulted in a significant decrease in daytime MSLT values for these insomnia patients. After 7 nights of 4.2 hours of sleep, MSLT values decreased from 15.6 to 11.1 minutes. Although this reduction was statistically significant, the 11.1-minute value was still within the normal range for the test. In a study in which total sleep was reduced to 5 hours per night in normal young adults (40), MSLT was reduced to 41% of baseline compared to a reduction to 71% of baseline that was found for the patients with insomnia. These results indicated that when the sleep of insomnia patients was experimentally reduced, they displayed some increased sleepiness during the day, in agreement with the expectancy in normal sleepers, but not the increased latency typical in patients with insomnia as their nocturnal sleep worsens. Despite the large reduction in TST, the patients with insomnia did not become pathologically sleepy on the MSLT, and this probably indicated the degree to which their hyperarousal was successful in masking
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
Page 19 and 20: 2 Attarian et al.
Page 21 and 22: 4 Attarian et al. until the 1970s t
Page 23 and 24: 6 Attarian et al. Table 2 Diagnosti
Page 25 and 26: 8 Attarian et al. Duration of Illne
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
Page 35 and 36: 18 Attarian 5. Sutton, D. A., Moldo
Page 37 and 38: 20 Attarian 53. Kageyama, T., Kabut
Page 39 and 40: 22 Attarian
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: 30 Bonnet and Arand chronic caffein
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
Page 59 and 60: 42 Attarian 15 to 40 seconds. PLMs
Page 61 and 62: 44 Fig. 1. Example of a 1-week slee
Page 63 and 64: 46 Fig. 3. One-week printout of an
Page 65 and 66: 48 Attarian Fig. 4. Algorithm. (Use
Page 67 and 68: 50 Attarian 27. Polo-Kantola, P., E
Page 69 and 70: 52 Garcia
Page 71 and 72: 54 Garcia association is known as s
Page 73 and 74: 56 Fig. 1. A sleep log used in chil
Page 75 and 76: 58 Garcia the reality that the tend
Page 77 and 78: 60 Fig. 2. Actigraph recording in a
Page 79 and 80: 62 Garcia neurodevelopmental disabi
Page 81 and 82: 64 Garcia 35. Czeisler, C., kronaue
Page 83 and 84: 66 Garcia
Page 85 and 86: 68 Attarian showed similar degrees
Page 87 and 88: 70 Attarian agitation and hence the
Page 89 and 90: 72 Attarian Affective disorder is s
Page 91 and 92: 74 Attarian and Drug Administration
Page 93 and 94: 76 Fig. 2. Sleep log after treatmen
Page 95 and 96: 78 Attarian 18. Bonnet, M. H. and A
Page 97 and 98: 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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