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Psychophysiological <strong>Insomnia</strong> 73 1. A brief psychiatric interview specifically looking for neurovegetative symptoms of affective disorders and/or anxiety permeating daily activities other than sleep. Occasionally, psychological tests such as the MMPI and Profile of Mood States are used, looking for a profile of malaise, guardedness, sensation avoidance, repression, and denial. (The abnormalities on the psychological tests may be either the cause or the result of insomnia.) 2. A general medical evaluation to rule out physical problems, such as other medical or neurologic disorders, medication effects, or substance abuse (10). 3. According to the American Academy of Sleep Medicine practice parameters, polysomnography is not indicated in the routine evaluation of insomnia, except when another sleep disorder is suspected and when insomnia does not respond to appropriate treatment. 4. A sleep log is a graph on which, for 2 to 3 weeks, the patient records bedtime, approximate sleep time, times and duration of awakenings during the sleep period, final awakening time, and naps taken during the day. This record summarizes the patient’s perception of the amount and quality of sleep he or she is getting. 5. Actigraphy is an invaluable tool for evaluating insomnia, especially in patients with unusual complaints, such as “I don’t sleep at all.” It supplements subjective sleep logs. An actigraph is a small, wrist-mounted device that records the activity plotted against time, usually 1 or 2 weeks at a time. There is a close correlation between the rest activity recorded by the actigraph and the wake–sleep pattern as determined by the PSG (41). Certain standardized questionnaires are sometimes used to screen for insomnia and determine its severity (42,43). PREVENTION In early and aggressive treatment of transient insomnia, both with hypnotics and a discussion of good sleep hygiene, addressing the acute stressor may prevent the development of the learned maladaptive associations leading to psychophysiological insomnia (11). PROGNOSIS AND COMPLICATIONS If untreated, psychophysiological insomnia can continue for decades. In some cases, it gradually worsens as a vicious cycle of insomnia develops. Overall quality of life, as measured by the SF-36 Health Status Survey, is greatly impaired by chronic insomnia (44). Complications, as in any serious insomnia, include excessive use of hypnotics, self-treatment with alcohol, treatment of ensuing daytime somnolence by stimulants, and daytime tension with tranquilizers (45). Untreated insomnia is a risk factor for the subsequent development of clinical depression and psychiatric distress (30,46). Other psychological complications include a passive and defeatist attitude (1) and cognitive, particularly memory, impairment (47,48). Chronic insomnia is also associated with an increase in motor vehicle accidents and a decrease in job performance (49). MANAGEMENT There are two main categories of treatment modalities for psychophysiological insomnia: behavioral and pharmacological. The best management strategy is combining hypnotic medication and behavioral methods (50). Although current Food
74 Attarian and Drug Administration guidelines recommend hypnotic medication only for short-term use, studies have shown that the risk of tolerance, addiction, dependence, and rebound insomnia are minimal (51–53). Hypnotics that have clinically proven efficacy include the newer nonbenzodiazepine hypnotics, zolpidem (54,55), zopiclone (56) (not available in the United States), and zaleplon (57,58); the benzodiazepines; and low-dose trazodone. Two studies have shown efficacy of valerian root in the treatment of insomnia, comparable, according to one of the studies, to that of oxazepam (a benzodiazepine) (59,60). Tricyclic antidepressants and antihistamines (including over-the-counter [OTC] sleep aids) are rarely indicated because of a poor side-effect profile and unproven value as hypnotics. There is paucity of data on the efficacy of antidepressants and OTC sleep aids in the treatment of insomnia. Additionally, the risk of serious adverse effects with these medications is well documented (52,61). There is also growing evidence that the benefits of benzodiazepine treatment outweighs the risks in the vast majority of patients. Despite these facts, there has been a significant increase over the past several years in the use of antidepressants and OTC sleep aids in the treatment of insomnia with a concomitant decrease in the use of hypnotics (52). A recent study showed that longterm use of zolpidem is safe, well-tolerated, and effective in the treatment of chronic insomnia (62). Behavioral methods include sleep restriction consolidation, sleep hygiene education, relaxation therapy, and stimulus control therapy (63,64). These behavioral methods are effective in increasing the total sleep time by 13%, reducing SL by 65%, and reducing the wake time after sleep by 48% (65–67). Case 2 A 42-year-old woman referred with the chief complaint of sleep maintenance for approximately 10 years. She is able to initiate sleep, but, a few hours later she wakes up and is unable to return to sleep. Typically, she wakes up in the middle of the night to go to the bathroom, and then is wide awake. She is awake for several hours and lays in bed trying to go back to sleep but tends to worry about issues relating to work, home, and family. Occasionally, she sleeps for brief periods of time throughout the rest of the night. This problem has gradually been worsening over a 10-year period. She stopped drinking caffeine approximately 2–3 years ago, which helped slightly, but did not have a significant impact. She had been taking Tylenol PM for a year or so approximately 4 years ago, which initially helped, but after a while the medication stopped helping her sleep through the night. She has tried not taking Tylenol PM and she said her insomnia became much worse. She most recently has been taking temazepam about once or twice a week when she feels particularly anxious and fears that she will not be able to fall asleep at all. She says this is quite effective and she tends to sleep through most of the night. Although this has been going on for some time, she has just recently sought medical attention because of her recent problems with fatigue and a difficulty
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Clinical Handbook of Insomnia Edite
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C URRENT CLINICAL NEUROLOGY Daniel
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© 2004 Humana Press Inc. 999 River
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Series Editor’s Introduction The
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x Foreword nervous system hypersomn
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Contents Series Editor’s Introduc
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Contributors HRAYR P. ATTARIAN, MD
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2 Attarian et al.
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4 Attarian et al. until the 1970s t
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6 Attarian et al. Table 2 Diagnosti
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8 Attarian et al. Duration of Illne
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10 Attarian et al. REFERENCES 1. Ma
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12 Attarian Another study in Austri
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14 Attarian even less well studied.
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16 Attarian communities. A structur
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18 Attarian 5. Sutton, D. A., Moldo
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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
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
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: 72 Attarian Affective disorder is s
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
Page 101 and 102: 84 Attarian times worrying about th
Page 103 and 104: 86 Attarian insomnia or for other s
Page 105 and 106: 88 Attarian
Page 107 and 108: 90 Duntley tion systems found that
Page 109 and 110: 92 Duntley Case 1 A 36-year-old fem
Page 111 and 112: 94 Fig. 2. The objective amount of
Page 113 and 114: 96 Duntley PROGNOSIS AND COMPLICATI
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Page 117 and 118: 100 Attarian EPIDEMIOLOGY There are
Page 119 and 120: 102 Attarian CLINICAL MANIFESTATION
Page 121 and 122: 104 Attarian DIAGNOSTIC WORKUP The
Page 123 and 124: 106 Attarian 13. Hauri, P. J. (1998
Page 125 and 126: 108 Plotkin
Page 127 and 128: 110 Plotkin quality of sleep. Ultim
Page 129 and 130: 112 Plotkin of the therapeutic effi
Page 131 and 132: 114 Plotkin months or years. The ef
Page 133 and 134: 116 Plotkin associated somatic disc
Page 135 and 136: 118 Plotkin Table 1 Causes of Secon
Page 137 and 138: 120 Plotkin Table 1 (continued) Lew
Page 139 and 140: 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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