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Idiopathic Insomnia 81 From: Current Clinical Neurology: Clinical Handbook of Insomnia Edited by: H. P. Attarian © Humana Press Inc., Totowa, NJ 81 7 Idiopathic Insomnia You know I can’t sleep, I can’t stop my brain You know it’s three weeks, I’m going insane. You know I’d give you everything I’ve got for a little peace of mind. —The Beatles (I’m so tired) Hrayr P. Attarian DEFINITION The International Classification of Sleep Disorders (ICSD) defines idiopathic insomnia, or childhood-onset, insomnia as a lifelong inability to get adequate amounts of sleep. This is presumably due to an abnormality in the neurological control of the sleep– wake system (1). However, not everyone agrees that this disorder is a separate and unique type of insomnia. For example, the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) regards the apparent neurological predisposition toward insomnia described here as a component of a broader entity named primary insomnia that includes idiopathic insomnia, psychophysiological insomnia, and sleep state misperception (SSM) (2,3). HISTORICAL NOTE The Association of Sleep Disorders Centers (now the American Academy of Sleep Disorders) developed and published Sleep Nosology in 1979. In that publication, a new category entitled “childhood-onset insomnia” was presented. It was described as “sleep-onset and sleep maintenance insomnia, resulting in daytime symptoms of inadequate sleep, that is characterized by a distinctive history of (unexplained) development before puberty, and persistence into adulthood.” It was postulated that this new entity represented “a CNS [central nervous system] shift or dysfunction of the sleep-arousal equilibrium” (4). The existence of this disorder
82 Attarian was confirmed by research done in the 1980s. It was also documented that this is a distinct form of insomnia by showing that childhood-onset insomnia was different from adult-onset insomnia on polysomnographic grounds (5) and that it could be distinguished from other types of insomnia in a cluster analysis (6). EPIDEMIOLOGY Idiopathic insomnia is rarely seen in its pure form. Chronic and serious insomnia over a lifetime almost always leads to other factors such as maladaptive behaviors; poor sleep hygiene, and emotional disturbances that further complicate the picture (7). A predisposition toward poor sleep exists in many insomniacs. However, in its pure form, idiopathic insomnia represents less than 5% of all insomniacs (8). Evidence shows that idiopathic insomnia often, but not always, has familial patterns of inheritance (1). ETIOLOGY Idiopathic insomnia may be due to some dysfunction in the brain’s sleep–wake center. It may represent either hyperactivity in the wake center or hypoactivity in the sleep center (5,9). Another, and more commonly accepted theory, is that patients with idiopathic insomnia are just simply organically hyperaroused (10). PATHOGENESIS AND PATHOPHYSIOLOGY Sleep–wake centers include the sleep-promoting center present in the anterior hypothalamus, the raphe nuclei, and medial forebrain area, and the wake-promoting center in the ascending reticular-activating system including the posterior hypothalamus (7,9). Whether a person is awake or asleep depends on the neurophysiological balance between the reticular-activating system and the sleep-inducing maintenance systems (11). Idiopathic insomnia presumably is due to a shift of this balance toward arousal. Either hyperactivity in the arousal system or hypoactivity in the sleep system may cause idiopathic insomnia (9). Patients suffering from idiopathic insomnia may have a neurochemical, neuroanatomical, or neurophysiological dysfunction or lesions interfering with normal sleep (11). Idiopathic insomniacs are often hyperaroused during wakefulness on questionnaires, auditoryevoked potentials, and electroencephalogram (EEG) (12). Physiological hyperarousal in many systems (cardiac, core temperature, corticosteroids, etc.) is not confined to patients with idiopathic insomnia but is frequently found in all primary insomniacs (10). Despite animal data showing the creation of insomniac animals with medial forebrain and the medial preoptic area (13), no direct human evidence for structural neuropathology exists (14). Difficult birth and prematurity are likely risk factors for the development of idiopathic insomnia (1). CLINICAL MANIFESTATIONS Idiopathic insomnia is a chronic and serious inability to initiate and maintain sleep that can often be observed as early as the first few weeks of life. Parents often
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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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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
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Page 101 and 102: 84 Attarian times worrying about th
Page 103 and 104: 86 Attarian insomnia or for other s
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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.
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
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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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