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Primary Sleep Disorders 141 DEFINITION From: Current Clinical Neurology: Clinical Handbook of Insomnia Edited by: H. P. Attarian © Humana Press Inc., Totowa, NJ 141 12 Insomnia in Primary Sleep Disorders Stephen Duntley Insomnia is defined in the International Classification of Sleep Disorders as “difficulty in initiating and/or maintaining sleep” (1). In primary insomnia, the term insomnia constitutes a diagnostic entity. In other disorders it is considered a symptom and not a primary diagnosis. Insomnia is frequently a component of the symptom complexes of other primary sleep disorders, and is listed among the diagnostic criteria for the following dyssomnias: obstructive sleep apnea (OSA) syndrome, central sleep apnea syndrome, central alveolar hypoventilation syndrome, periodic limb movement disorder (PLMD), and restless legs syndrome (RLS). Disrupted sleep is among the diagnostic criteria for narcolepsy. The complaint of insomnia can also accompany parasomnias, and is listed among the diagnostic criteria for sleep starts and nightmares (1). As in other forms of insomnia, in order to be considered a clinically significant problem, the complaint of sleep disturbance must be associated with adverse daytime consequences such as fatigue, decreased concentration, or irritability. HISTORICAL PERSPECTIVES In what is likely the first report of RLS in the medical literature, Thomas Willis, an English physician, described a patient in the late 1600s for whom sleep was impossible because of restlessness in the arms and legs, which were compared to a person being tortured on the rack. There were subsequently sporadic reports of patients with similar symptoms, but the syndrome was not described in detail until the 1940s. A thorough description of the phenomenon of PLMs during sleep awaited development and clinical application of polysomnography, with typical features being described by Lugaresi and colleagues in 1966 (2). Insomnia associated with OSA was first described by Guilleminault and colleagues in 1973 (3). Since these initial reports, the common association between insomnia and these other sleep
142 Duntley disorders has been confirmed, although the clinical significance of this relationship continues to be defined. EPIDEMIOLOGY The epidemiology of insomnia in sleep disorders is dependent on the epidemiology of the primary sleep disorder itself. One community-based population study found about 2% of women and 4% of men have OSA syndrome (4). A recent university-based study of patients with sleep-disordered breathing found that of 231 patients sampled, 116 complained of clinically significant insomnia (5). Among postmenopausal women complaining of insomnia, 83% were noted to have upper airway resistance syndrome (UARS) or OSA syndrome (6). Insomnia complaints in patients with OSA syndrome, like insomnia complaints in general, may be more frequent among women than men (7). Central sleep apnea syndrome is less common than OSA, but patients appear to be less likely to report daytime hypersomnolence and more likely to complain of insomnia (8). RLS is common, with a recent population-based study revealing bedtime symptoms in 10–15% of individuals (9). Difficulty falling asleep was reported by 84.7% of patients and 86% reported frequent awakenings with difficulty falling back asleep because of symptoms (10). PLMD increases with age, being uncommon before 30 years of age, seen in 5% of individuals between 30 and 50 years of age, and in about 44% of individuals aged 65 and older (11). One multicenter study found PLMD to be the primary diagnosis in 17% of patients complaining of insomnia (12). Narcolepsy has a prevalence of about 0.05% (13). Fragmented sleep is found in up to 90% of patients with narcolepsy (14) and tends to be relatively mild initially, increasing in severity over time (15). Nightmares with a frequency of once a week or greater are seen in 4% of the adult population in Austria (16). One study in France found that 18.3% of insomnia patients were diagnosed as having nightmares (17). Occasional sleep starts are a nearly universal phenomenon. Sleep starts may rarely become repetitive at sleep onset resulting in sleep-onset insomnia. ETIOLOGY The cause of insomnia varies according to the primary sleep disorder, and may result from the sleep-onset and maintenance difficulties inherent in the disorder itself or from secondary symptoms of the disorder. For instance, in OSA syndrome, the termination of the apnea is associated with an arousal or awakening that may be perceived and remembered by the patient. OSA syndrome is also associated with other symptoms, such as nocturia and dry mouth, which can contribute to the development of an insomnia complaint. In RLS, the dysesthesias and need to move the legs prevents sleep onset, and may prevent returning to sleep after awakenings in the middle of the night. In PLMD, limb movements are associated with arousals or awakenings that may lead to the perception of difficulty initiating or maintaining sleep. In narcolepsy, the neurochemical defect leads to dysregulation of sleep
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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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66 Garcia
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68 Attarian showed similar degrees
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70 Attarian agitation and hence the
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72 Attarian Affective disorder is s
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74 Attarian and Drug Administration
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76 Fig. 2. Sleep log after treatmen
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78 Attarian 18. Bonnet, M. H. and A
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80 Attarian 65. Perlis, M., Aloia,
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82 Attarian was confirmed by resear
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84 Attarian times worrying about th
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86 Attarian insomnia or for other s
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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
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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: 140 Karaz 17. Attarian, H. P. (2000
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
Page 185 and 186: 168 Perlis et al. Perhaps more impo
Page 187 and 188: 170 Perlis et al. 28. Carskadon, M.
Page 189 and 190: 172 Perlis et al.
Page 191 and 192: 174 Attarian Secondary Insomnias Re
Page 193 and 194: 176 Attarian 50 years of age who sl
Page 195 and 196: 178 Attarian Antidepressants Becaus
Page 197 and 198: 180 Attarian The use of benzodiazep
Page 199 and 200: 182 Attarian to placebo. Zaleplon a
Page 201 and 202: 184 Attarian 3. Wyatt, R. J., Engel
Page 203 and 204: 186 Attarian residual sedation foll
Page 205 and 206: 188 Index Clonidine, 183 CNS arousa
Page 207 and 208: 190 Index Proton pump inhibitors, 1
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Current Clinical Neurology CLINICAL
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