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Physiological Basis of Insomnia 33 their sleep tendency. Of equal interest, patients did not report significant decreases in their sleep quality or show changes in personality or physiological parameters consistent with more severe insomnia when their wake time during the night was increased by 2 hours. One conclusion from such data is that the reports of poor sleep quality and daytime dysphoria from patients with insomnia are not directly related to their EEG sleep, but rather to their level of arousal (41). In support of these results, Chambers and Kim (42) reported a significant negative correlation between state anxiety at bedtime and reports of feeling rested on the next day for patients with insomnia despite the fact that neither anxiety nor reports of feeling rested were significantly correlated with sleep values. Level of Arousal and the Perception of Sleep Insomnia patients commonly overestimate how long it takes to fall asleep at night and underestimate their TST. Is such misperception related to personality or to underlying physiology? We decided to look at several physiological manipulations to determine if they produced changes in the perception of sleep onset (43). Patients with insomnia subjectively estimate that it takes much longer to fall asleep than EEG measures indicate (44). One means of examining this phenomenon is to divide the subjective estimate of SL by the EEG estimate to derive a unitless indicator of degree of estimation difference. For example, sleep deprivation or the use of benzodiazepines decreases the level of arousal and was hypothesized to decrease this subjective to objective ratio of SLs. Conversely, administration of caffeine, which increases arousal level, or sleep during the daytime, when level of arousal is higher, should increase the ratio. Specifically, results from several studies (43) indicated that the ratio of subjective to objective SL decreased when subjects were given triazolam or diazepam to decrease level of arousal, and the decreases tended to be dose related. Similarly, the ratio of subjective to objective SL decreased during sleep deprivation; again, the decreases were related to the amount of sleep lost. In two tests of increased arousal, the ratios of subjective to objective SLs increased after an initial night of caffeine consumption and were greater during sleep periods that began midday than in sleep periods that began later in the evening. These data supported the contention that the perception of falling asleep was related to the level of physiological arousal at sleep onset. The consistency of the findings with six different experimental manipulations supports the argument that estimates of SL may also be dependent on level of physiological arousal. These data support the idea that subjectively reported poor sleep or insomnia is a physiological phenomenon that can be controlled by varying the level of arousal. The point is that poor sleep, whether it is acute or chronic, is a physiological (as opposed to a psychological) event that is amenable to physiological exploration and modification.
34 Bonnet and Arand The Development of Insomnia It is well known that the incidence of insomnia increases with age. This increase could be associated with increasing sympathetic nervous system dominance that is also associated with age or with cognitive or behavioral changes. Unfortunately, very little empirical work has examined how insomnia starts or develops. One theory holds that individuals placed in a situation of temporary stress develop poor sleep hygiene or inappropriate conditioned responses to their sleep environment. Then, the poor hygiene or inappropriate responses continue to produce poor sleep after the period of stress passes. If this is true, one way to understand the development of insomnia would be to take normal young adults, expose them to a temporary stress, and evaluate the insomnia produced. We specifically followed this methodology in a recent study of 50 normal sleepers exposed to a series of stressful experiences, including first night in a sleep laboratory, 3-hour phase advance of sleep time, 6-hour advance of sleep time, and sleep following administration of 400 mg of caffeine 30 minutes prior to bedtime (45,46). It was found that there was both wide variability and remarkable consistency in the responses seen. The variability was in the between-subject response to the situational stress—some subjects continued to have nearly normal nights of sleep even after a 6-hour phase advance of bedtime or caffeine ingestion, whereas other individuals had poor sleep following all of the stresses. This study involved so many participants that it was possible to form “extreme” groups—in this case the 25% of the population that slept best on the first night in the laboratory (super sleepers) and the 25% who had the worst sleep on that night (situational insomnia [SI]). Significant correlations were found between sleep efficiency on the first night and on the other stress nights in the complete data set and also by comparing sleep values in the extreme groups. Subjects who had poor sleep on their laboratory adaptation night (and were therefore called the SI group) also had increased MSLT on the day that followed. They had normal sleep on the baseline night that followed, but then had significantly worse sleep on the phase-advance nights and after caffeine administration. Their sleep was so bad after the 6-hour phase advance (about 4.5 hours compared with about 7 hours for the super sleepers) that their MSLTs were significantly reduced on the day that followed. The SI group also had very poor sleep after caffeine administration but surprisingly, the MSLTs after caffeine administration were significantly increased. The super sleep group did not have any significant changes in MSLT throughout the study. The implication is that the SI group was not only more sensitive to all of the stresses in terms of the production of poor sleep, but also was more sensitive to the arousing effect of caffeine. This study also examined other differences between the SI and good sleeping groups (see Table 2). No significant differences were found on the MMPI or mood measures. Whole body metabolic rate was nonsignificantly increased in the SI group. The SI group was found to have increased heart rate, increased LFP and
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 and 48: 30 Bonnet and Arand chronic caffein
Page 49: 32 Bonnet and Arand response that a
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,
Page 99 and 100: 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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