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Sleep State Misperception 91 arousals during the stimulus (19). Patients with SSM have been shown to have elevated levels of physiological arousal as measured by 24-hour metabolic rate, although the increase was less than observed in psychophysioligical insomnia (20). Patients with SSM have demonstrated increased activity on actigraphy during sleep (21). The tendency toward mislabeling sleep as wakefulness in insomnia may reflect elevated levels of CNS arousal, and frequencies that are not normally quantified in standard polysomnography may be important markers for this elevated arousal. In one study, patients with insomnia who have low EEG α frequency activity during sleep were more likely to underestimate total sleep time and overestimate awakenings compared to patients with insomnia who have higher amounts of α frequency EEG activity (22). It has also been demonstrated that increased β/γ activity is correlated with the perception of wakefulness during sleep (23). Another potential cause of SSM is the misperception or mislabeling of another bodily state such as fatigue or depression. For instance, in two recent studies, both nefazodone and fluoxetine alleviated depression and resulted in improvements in subjective sleep quality, although patients given fluoxetine showed significant declines in objective sleep characteristics such as increased number of awakenings and decreased sleep efficiency (24,25). Similarly, no group difference in sleep diary measures of sleep quality was seen between patients given nefazodone or paroxetine, despite the declines in objective sleep measures in the patients given paroxetine (26). Some patients may attribute daytime cognitive difficulties such as trouble concentrating or memory problems to a poor night’s sleep or sleepiness, when sleep is adequate and true sleepiness is not present. Smith and Trinder were able to simulate SSM in 20 healthy volunteers who did not have insomnia by causing microarousals from sleep through the manipulation of the sleep environment. The same individuals did not have any misperception when they were restudied on other nights when the sleep environment was not manipulated to cause the above mentioned arousals. Hence, the researchers postulated that the cause of SSM in insomniacs is due at least partly to the increased number of brief arousals from sleep (27). This sleep misperception as being awake also leads to the perpetuation of the insomnia because of previous sleep being perceived as wake time (13). CLINICAL MANIFESTATIONS Patients with SSM complain of either longstanding insomnia with difficulty initiating or maintaining sleep, nonrestorative sleep, or excessive daytime sleepiness that is not documented by polysomnography and MSLT. The patient must report that the symptoms were present during the testing. Unique to SSM is the tendency for patients to report virtually no sleep for days, weeks, or even years. They often vehemently claim that the essentially normal polysomnographic recordings are in error. Like other forms of insomnia, clinically significant complaints are accompanied by reports of waking dysfunction, such as fatigue that impairs social or occupational function and that the patient believes will improve with treatment.
92 Duntley Case 1 A 36-year-old female presented to the sleep center outpatient clinic for initial evaluation of a lifelong history of insomnia. She stated that as far back as she could remember, which is as young as 4 years old, she had a problem with insomnia. She stated that over the past several years her problem had worsened. There were nights when she did not sleep at all. Most nights she went to bed between 8:30 and 11 PM, and it took her 3–4 hours to actually fall asleep. She reported that she woke up after 45 minutes to 3 hours. The most she slept in a 24-hour period was 3 hours. The next day she would feel severely exhausted. She had tried and failed four different hypnotics. Despite being fatigued, she could not take naps during the day. She did not fall asleep unintentionally during the day in any situation. She denied gasping for air or symptoms of restless legs or any pains, anxieties, or worries at night. She stated that her daughter mentioned that she rarely snored. She denied any morning headaches or dry mouth. She denied cataplexy symptoms and hypnagogic hallucinations, but endorsed rare episodes (three in her entire life) of sleep paralysis. She had no allergies, was not on any medications, and had a past medical history of head banging and rocking sleep disorder as a child and a teenager. She also had a severe febrile illness as an infant. Her family history is significant for delayed sleep phase in her sister. Her social history is significant for considerable amounts of caffeine intake in the form of coffee and chocolate. A review of her systems was negative and her exam was normal. She came in for an overnight polysomnogram (PSG). The PSG revealed 6.8 hours of sleep with 7.9 brief arousals for no apparent reason per hour of sleep. When questioned the next day as to how much she thought she had slept, she mentioned that at best 2 hours. She was set up with an actigraph and asked to fill out concomitantly sleep logs. Figure 1 shows her subjective perception of sleep on the sleep logs. Figure 2 shows the objective amount of sleep she actually got as measured by the actigraph. The results were discussed with the patient and she was reassured. She was accepting of the diagnosis. Unfortunately she was lost to followup. DIFFERENTIAL DIAGNOSIS The presenting symptoms of SSM may be difficult to distinguish from other forms of insomnia. SSM shares many features with psychophysiological insomnia and the underlying pathophysiology may be related. The longstanding, unremitting character of the complaint may resemble idiopathic insomnia. Inadequate sleep hygiene, generalized anxiety disorder, affective disorder, circadian rhythm disorders, and medication use and abuse may co-exist with SSM, but do not explain the
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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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22 Attarian
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24 Bonnet and Arand Table 1 Reporte
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26 Bonnet and Arand On the day spen
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28 Bonnet and Arand SUMMARY These m
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30 Bonnet and Arand chronic caffein
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32 Bonnet and Arand response that a
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34 Bonnet and Arand The Development
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36 Bonnet and Arand ACKNOWLEDGMENT
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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
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: 90 Duntley tion systems found that
Page 111 and 112: 94 Fig. 2. The objective amount of
Page 113 and 114: 96 Duntley PROGNOSIS AND COMPLICATI
Page 115 and 116: 98 Duntley
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.
Page 141 and 142: 124 Plotkin 48. Marchetti, F., Rome
Page 143 and 144: 126 Plotkin
Page 145 and 146: 128 Karaz Table 1 DSM-IV Diagnoses
Page 147 and 148: 130 Karaz poor. Focusing only on th
Page 149 and 150: 132 Karaz He felt hopeless that his
Page 151 and 152: 134 Karaz Table 4 Diagnostic Criter
Page 153 and 154: 136 Karaz complained of feeling anx
Page 155 and 156: 138 Karaz other physicians avoided
Page 157 and 158: 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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