Insomnia Insomnia

Recommendations

Info

Cognitive-Behavioral Therapy 155 From: Curent Clinical Neurology: Clinical Handbook of <strong>Insomnia</strong> Edited by: H. P. Attarian © Humana Press Inc., Totowa, NJ 155 13 Cognitive-Behavioral Therapy for <strong>Insomnia</strong> Michael L. Perlis, Michael T. Smith, Carla R. Jungquist, Sara Nowakowski, Henry Orff, and James Soeffing INTRODUCTION This chapter provides an overview of how primary insomnia is assessed and treated using cognitive-behavioral therapy (CBT). Additionally, we provide some upfront information that reviews the CBTs regarding the etiology of chronic insomnia and some follow-up information of the efficacy of CBT for insomnia. The former is provided so that the reader may appreciate the principles on which CBT is founded. The latter is provided so that the reader may appreciate the extent to which CBT for insomnia has been empirically validated. THEORETICAL PERPSECTIVES ON INSOMNIA Behavioral Perspective Since the late 1980s, insomnia has largely been conceptualized from within a behavioral framework. The original model was proposed by Spielman and colleagues and it continues to be the leading theory for both sleep medicine and the subspecialty area of behavioral sleep medicine (1). As illustrated in Fig. 1, the behavioral model posits that insomnia occurs acutely in relation to both predisposing (trait) and precipitating (state) factors and occurs chronically in relation to perpetuating or maintaining factors. Thus, an individual may be prone to insomnia due to trait characteristics, experience acute episodes because of precipitating events, and have chronic insomnia owing to a variety of perpetuating factors. With respect to trait factors, personality characteristics (2,3), physiological arousal (2,3), and genetic predisposition (4) are each thought to contribute to predispose the individual to acute episodes of insomnia. Typical precipitating events (which represent stressors within the larger stress diathesis model of disease) include situational stress (5), acute injury or pain, bereavement, and so on. Perpetuating factors, as the term implies, maintain the chronic form of the disorder even
156 Perlis et al. Fig. 1. A schematic of the differential diagnosis process for the diagnosis of primary insomnia. after the precipitating events have either been stabilized or resolved. Perpetuating factors are any of a variety of compensatory strategies in which the patient engages in an attempt to cope with insomnia symptoms. Typical examples of such factors include excessive daytime napping, extending sleep opportunity, keeping variable sleep–wake schedules, use of alcohol as a hypnotic, spending excessive time awake in bed, diminishing daily activity level due to fatigue, and so on. Central to the behavioral model of chronic insomnia is the role of classical conditioning as the primary maintaining factor. It is hypothesized that, over time, insomnia becomes a conditioned response to the bed and bedroom environment. This process presumably occurs via traditional principles of classical conditioning, resulting from repeated pairings of the bed and bedroom (conditioned stimuli) with states of psychophysiologic hyperarousal (unconditioned stimuli) that are thought to interfere with the normal biological processes of sleep initiation and maintenance. Cognitive Perspective A number of authors have stressed the importance of cognitive factors in primary insomnia (6–8). Given their emphasis on the role of cognition, they and others have developed interventions, which provide for the cognitive component of the more broad-based cognitive-behavioral approach. Within this perspective, two related types of cognitions are thought to be operational: one set is related to the patient’s beliefs about his or her disorder; the other is related to cognitive processes like intrusive thoughts and worry.
Page 1 and 2:
Clinical Handbook of Insomnia Edite
Page 3 and 4:
C URRENT CLINICAL NEUROLOGY Daniel
Page 5 and 6:
© 2004 Humana Press Inc. 999 River
Page 8:
Series Editor’s Introduction The
Page 11 and 12:
x Foreword nervous system hypersomn
Page 14 and 15:
Contents Series Editor’s Introduc
Page 16:
Contributors HRAYR P. ATTARIAN, MD
Page 19 and 20:
2 Attarian et al.
Page 21 and 22:
4 Attarian et al. until the 1970s t
Page 23 and 24:
6 Attarian et al. Table 2 Diagnosti
Page 25 and 26:
8 Attarian et al. Duration of Illne
Page 27 and 28:
10 Attarian et al. REFERENCES 1. Ma
Page 29 and 30:
12 Attarian Another study in Austri
Page 31 and 32:
14 Attarian even less well studied.
Page 33 and 34:
16 Attarian communities. A structur
Page 35 and 36:
18 Attarian 5. Sutton, D. A., Moldo
Page 37 and 38:
20 Attarian 53. Kageyama, T., Kabut
Page 39 and 40:
22 Attarian
Page 41 and 42:
24 Bonnet and Arand Table 1 Reporte
Page 43 and 44:
26 Bonnet and Arand On the day spen
Page 45 and 46:
28 Bonnet and Arand SUMMARY These m
Page 47 and 48:
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 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
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
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: 154 Perlis et al.
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
Page 209: Current Clinical Neurology CLINICAL
show all

Insomnia Insomnia

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?