Insomnia Insomnia

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Idiopathic <strong>Insomnia</strong> 83 report that these patients slept much less, or required less sleep, than their siblings when they were infants. Sleep latency is long. Sleep is riddled with many awakenings and may show sleep-stage abnormalities, such as rapid eye movement (REM) sleep with few eye movements or ill-formed sleep spindles during stage 2 sleep (5). Paradoxically, idiopathic insomniacs may show fewer body movements per unit of sleep than do normal sleepers (14). The spectrum of severity of insomnia in this condition varies from mild (essentially a light sleeper) to severe and incapacitating, as the presumed underlying neurological abnormality varies from mild to severe (14). Daytime features typically include decreased attention and vigilance, low levels of energy and concentration, and a deterioration of mood commonly described as grim and subdued, rather than obviously depressed or anxious. In mild or moderate idiopathic insomnia, psychological functioning is remarkably intact. In severe cases, daytime functioning may be severely disrupted and affected patients may be unable to hold a job. During childhood and adolescence, idiopathic insomnia is often associated with soft neurological signs (i.e., as dyslexia or hyperactivity). Many cases show diffuse nonspecific abnormalities on the EEG (1). The ICSD’s diagnostic criteria for idiopathic insomnia are (1) a complaint of insomnia combined with a complaint of decreased functioning during wakefulness; (2) long-standing insomnia, typically beginning in early childhood or soon after birth; (3) relentless insomnia during periods of both poor and good emotional adjustment; (4) one or more of the following polysomnography: increased sleep latency, reduced sleep efficiency, and increased number and duration of awakenings often a reversed first-night effect (best sleep on the first night); (5) the diagnosis cannot be made if medical or psychiatric disease or stress can explain the early Case 1 Mr. T. is a 53-year-old man with lifelong history of insomnia. Mr. T. stated that his mother told him that he had trouble sleeping even during his infancy. He stated that as far back as he could remember he has had insomnia. Around age 10 or 11 he started having some anxiety associated with his inability to sleep. He stated that when he has a decent night’s sleep for several nights in a row, he really does not feel depressed and anxious; but not getting a good night’s sleep creates anxiety over the inability to sleep, which then becomes reinforced when he does not sleep easily the following night. For reasons unknown, he did not seek medical attention for his problem until about 1 year ago when he mentioned it to his primary care physician. He was tried on Xanax, Ambien, Trazodone, Remeron, and over-the-counter Tylenol PM. Few medications had any impact on his sleep. Even with medication, he had only one good night every 2–3 weeks, during which he would sleep 6–7 solid hours. Most of the time, Mr. T. goes to bed between 11 PM and midnight feeling sleepy and tired, but when he lays down he is awake for at least 1 hour, some-
84 Attarian times worrying about the day’s events or sometimes just laying there. He then manages to fall asleep, only to wake up several times in the middle of the night, staying awake each time for 30–40 minutes. His total awake time in the middle of the night, he reports, is about 2 hours. He wakes up between 8 and 8:30 AM feeling fatigued and not restored. Despite his fatigue, he is not sleepy during the day, does not fall asleep unintentionally, and does not take naps. He has no other sleep complaints, and he does not have any family history of insomnia. Physical exam is normal. onset of this insomnia; and (6) other sleep disorders causing insomnia can occur simultaneously (e.g., adjustment sleep disorder). Minimal criteria: 1, 2, and 5 (1). DIFFERENTIAL DIAGNOSIS Not all insomnia in childhood is idiopathic or childhood-onset insomnia. Although the complaints of insomnia are seen in up to 41% of children (15), as mentioned previously, idiopathic insomnia in its pure form is rarely seen. Idiopathic insomnia is diagnosed when insomnia predates the development of the other complicating factors (emotional problems, ill adaptive associations, or poor sleep hygiene) and when the imbalance of the sleep–wake system plays a paramount role (1). Idiopathic insomnia should be differentiated from other common childhood insomnias such as sleep-onset association disorder and limit-setting sleep disorder. In the former, habits, objects, or conditions become associated with the transition to sleep and need to be re-established throughout the night to permit return to sleep after normal awakenings, otherwise periods of waking are prolonged (16). The latter is a disorder of childhood characterized by normal sleep ability and deliberate attempts to remain awake at bedtime and, sometimes, after nighttime awakenings using a variety of requests, demands, and stalling tactics (stories, drinks, bathroom trips, blanket adjustments, television) (16). A careful history of the child’s bedtime behavior enables one to distinguish these disorders from idiopathic insomnia. Idiopathic insomnia is differentiated from short sleepers by the accompanying fatigue and daytime performance impairment, whereas short sleepers feel and function well during waking hours. Idiopathic insomnia is difficult to distinguish from psychophysiological insomnia, which is also accompanied by an innate predisposition toward poor sleep. In idiopathic insomnia, the presumed sleep–wake imbalance is enough to cause the insomnia by itself; in psychophysiological insomnia, the inherent sleep–wake disturbance is weaker, needing the addition of the stress of maladaptive conditioning to trigger the insomnia (1). Psychologically, most patients with idiopathic insomnia are remarkably healthy, given their chronic lack of sleep (1). However, as in other primary insomnias, patients with idiopathic insomnia tend to be emotional repressors (7). Although the insomnia is persistent, relentless, and almost unvaried through both poor and good
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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
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 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: 82 Attarian was confirmed by resear
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
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
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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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