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Physiological Basis of Insomnia 23 INTRODUCTION Physiological Basis of Insomnia Michael H. Bonnet and Donna L. Arand Patients with insomnia often have symptoms that include tension, anxiety, depression, fatigue, and irritability (1–4). Frequently, insomnia begins in conjunction with significant stress (5). As a result, many investigators hypothesized that insomnia is the result of internalization of emotions producing emotional arousal. More recently, it has been hypothesized that insomnia can develop entirely from physiological activation, as in phase-shift insomnia or in individuals predisposed to physiological activation. Several studies have found significantly increased physiological activation in patients with insomnia. Table 1 summarizes the psychological changes in insomnia patients. For example, Monroe (6) reported increased rectal temperature, heart rate, basal skin resistance, and phasic vasoconstrictions 30 minutes prior to and during sleep in patients with insomnia as compared to normal sleepers. Other studies have shown that patients with sleep-onset insomnia had increased frontalis (7) and mentalis electromyogram (EMG) (8,9), increased heart rate (10,11), increased finger temperature, and more β and less α frequencies in the electroencephalogram (EEG) (8,9). However, significantly elevated body temperature has not been reported in all studies of poor sleepers (12,13). Poor sleepers have increased secretion of corticosteroids and adrenaline (12,14) compared with good sleepers in most, but not all, studies (15). The inconsistent results in some of these physiological activation studies may indicate that physiological activation is not a major factor in all patients (16) or that wide variability and small sample sizes may make it difficult to show clear physiological differences. It might be that lack of control of daytime activity in the studies obscured differences. It is also possible that the involved physiological system(s) differs from patient to patient and that more global measures, such as whole body oxygen use or heart rate variability, would more consistently show differences. From: Current Clinical Neurology: Clinical Handbook of Insomnia Edited by: H. P. Attarian © Humana Press Inc., Totowa, NJ 23 3
24 Bonnet and Arand Table 1 Reported Physiological Changes in Insomnia Patients Physiological variable Studies (ref. no.) Increased body temperature 6 Increased heart rate 6,10,11,26 Increased sympathetic nervous system activity 11 Decreased parasympathetic nervous system activity 11 Increased EMG 7–9 Increased EEG β 8,9 Decreased EEG α 8,9 Increased corticosteroids 12,14 Increased adrenaline Increased V 14 · O2 24,25 Increased skin resistance 6 Increased phasic vasoconstrictions 6 Increased daytime sleep latency 20, 21, 24 EMG, electromyogram; EEG, electroencephalogram. Other research has examined daytime function in patients with insomnia to verify subjectively reported deficits in performance, mood, and alertness. The cumulative partial sleep deprivation that should arise from chronic insomnia should produce daytime sleepiness or increased susceptibility to acute sleep loss in patients with insomnia, but studies have consistently found that these patients are not sleepier than normal controls on the Multiple Sleep Latency Test (MSLT) (13,17,18) or after sleep loss (19). These individuals may actually have longer MSLT latencies (20,21). Studies have found that patients with insomnia made more errors on a line-tracing task (22), produced fewer responses in a word category test (13), and performed worse on the Romberg (balance) test (23). However, such deficits may have reflected that elevated arousal reduces steadiness or blocks higher order associates. Studies that compared daytime performance of insomnia patients to performance of normal controls have generally not found differences on tests that are sensitive to sleep loss (18,23). Based on these results and on patient reports that they are fatigued or “washed out” during the day, it has been hypothesized that standard sleep and sleeploss tests are confounded in that they “simultaneously measure sleep need and hyperarousal, which is interfering with sleep onset” (p. 59) (20). This concept is supported by studies (18,20,22) that reported significant negative correlations between total sleep at night and MSLT values the next day. With this background in mind, we planned a series of experiments to define more general measures of physiological activity in patients with psychophysiological insomnia and to differentiate causal factors in the production of both poor nocturnal sleep and compromised daytime function. This chapter reviews our work to define metabolic and cardiac changes in patients with insomnia and the relationship of such physiological changes to poor sleep and the report of insomnia.
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: 22 Attarian
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 and 50: 32 Bonnet and Arand response that a
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
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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
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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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