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Medical and Neurological Causes 117 residual cognitive dulling, lingering hypnotic effects, or uncomfortable side effects. There may be a role for medications that have antidepressant or anxiolytic characteristics, especially in the early stages following cancer diagnosis. Chronic treatment may be better achieved by nonpharmacologic interventions (54,55) such as cognitive therapy, relaxation therapy, biofeedback, and behavioral approaches to improve sleep quality. Degenerative conditions of the CNS alter the chemical and structural substrates that regulate sleep; most of these produce fragmented sleep, with or without daytime hypersomnia. Disrupted sleep patterns are common in Alzheimer’s Dementia (56), and the difficulties produced by perceptual impairment may aggravate nocturnal behaviors and confusion (57,58), characterized as a “sundown” syndrome. Cholinergic agonists or cholinesterase inhibitors utilized to treat Alzheimer’s Dementia may aggravate difficulties with sleep initiation, by augmenting cholinergic tone in the basal forebrain and cerebral cortex, favoring the maintenance of wakefulness. Parkinson’s disease (PD) may disrupt sleep by way of tremor, dystonia, or periodic nocturnal movements, whereas the dopamine agonist medications used for treatment of PD may also cause insomnia, dystonia, or dyskinesia. Thus, inadequate symptomatic treatment at night or the side effects of treatment may cause sleep disruption by similar mechanisms. The dopamine agonists tend to enhance dreaming, and many patients report increased nightmares in association with bedtime doses of levodopa and pergolide. These medications may also cause increased motor activity during dreams. Lewy body dementia has a high incidence of REM behavior disorder and sleep fragmentation (58a). The EEG in progressive supranuclear palsy has been observed to include more elemental changes in sleep architecture, with decreased total sleep time, decreased sleep spindles, and diminished REM sleep (59,60). Multiple systems atrophy also produces considerable sleep disruption, with increased arousal and diminished slow wave sleep (61). Huntington’s chorea has been associated with decreased sleep efficiency, and sleep may become dramatically fragmented as behavioral symptoms increase. Fatal Familial Insomnia is a rare prion-associated spongeform encephalopathy with rapid progression through fulminant insomnia to dementia and death over the course of months (62). Insomnia is also commonly seen in association with Creutzfeldt-Jakob disease (63,64), especially when the thalamic degeneration is disproportionately observed. Neuropathy and radiculopathy are associated with chronic pain, fasciculations, and muscle spasms that cause impaired sleep initiation/maintenance, and periodic limb movements of sleep are augmented in peripheral nerve disorders, further exacerbating difficulties with sleep maintenance. Muscular dystrophy and inflammatory myopathies can cause insomnia by similar mechanisms, in addition to their effects on ventilatory and pharyngeal musculature that lead to hypoventilation and frequent aspiration. Most of the medications used to treat the symptoms of neuropathy are sedating for the majority of people who take them, but the anticonvulsants carbamazepine and lamotrigine have been reported to cause insomnia. Myelopathy can also cause pain, muscle spasms, spasticity, constipation,
118 Plotkin Table 1 Causes of Secondary Insomnia Skin conditions Allergic, infectious, or inflammatory dermatitis Burns Herpes zoster reactivation (shingles) Lacerations Swelling Edema Diaphoresis Dressings, bandages, or splints Oral corticosteroid medications Sleep-disordered breathing due to pathology in the nasopharynx, oropharynx, and larynx Nasal polyps Excessive oropharyngeal adipose tissue Oropharyngeal or nasopharyngeal mass lesion Macroglossia Uvular hypertrophy Retrognathia Pharyngeal muscle weakness Neck anatomy (short, broad, restricted in motion, anterior adipose deposition) Cervical mass lesions Hyoid pathology Cervical spine degeneration Other conditions affecting the pharyngeal and laryngeal tree Postnasal drip Chronic/recurrent sinusitis Allergic, infectious, or inflammatory pharyngitis Sleep-related laryngospasm, choking, or repetitive swallowing Bruxism Pulmonary disorders Asthma Chronic obstructive pulmonary disease Restrictive/interstitial pulmonary disease Bronchitis Pneumonia/pneumonitis Pleuritis Pulmonary neoplasia Hypoxia Chest wall pain Cough Bronchodilator medications, methylxanthines derivatives, inhaled steroids Cardiovascular diseases Nocturnal angina Ppalpitations, tachycardia, arrythmia Paroxysmal dyspnea Orthopnea 118
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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.
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40 Attarian Table 1 Types of Insomn
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42 Attarian 15 to 40 seconds. PLMs
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44 Fig. 1. Example of a 1-week slee
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46 Fig. 3. One-week printout of an
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48 Attarian Fig. 4. Algorithm. (Use
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50 Attarian 27. Polo-Kantola, P., E
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52 Garcia
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54 Garcia association is known as s
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56 Fig. 1. A sleep log used in chil
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58 Garcia the reality that the tend
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60 Fig. 2. Actigraph recording in a
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62 Garcia neurodevelopmental disabi
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64 Garcia 35. Czeisler, C., kronaue
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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 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: 116 Plotkin associated somatic disc
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
Page 159 and 160: 142 Duntley disorders has been conf
Page 161 and 162: 144 Duntley itance. A recent study
Page 163 and 164: 146 Duntley The patient’s primary
Page 165 and 166: 148 Duntley return to sleep. He tos
Page 167 and 168: 150 Duntley Treatment of RLS should
Page 169 and 170: 152 Duntley 34. Cartwright, R. (197
Page 171 and 172: 154 Perlis et al.
Page 173 and 174: 156 Perlis et al. Fig. 1. A schemat
Page 175 and 176: 158 Perlis et al. ditioned arousal
Page 177 and 178: 160 Perlis et al. subjected to empi
Page 179 and 180: 162 Perlis et al. effect), (3) may
Page 181 and 182: 164 Perlis et al. Cognitive Therapy
Page 183 and 184: 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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