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Cognitive-Behavioral Therapy 167 issues related to comorbid psychiatric and medical disorders, and the simultaneous use of sedative hypnotics. Treatment Compliance The single most important complicating factor is poor treatment compliance. At the beginning of treatment, the clinician should proactively address the fact that the prescriptions may seem counterintuitive and that adhering to the treatment will be difficult. Providing the patient with a complete and thoughtful rationale for each aspect of the treatment, managing the patient’s expectations, and encouraging an active self-management approach are essential. Providing the rationale for treatment is likely to gain patient compliance in at least two ways. First, the effort to explain therapy is less imperative, thereby making the patient an active partner in the treatment process and making him or her less resistant or reactive to the prescriptions. Second, a fluid, interesting, and compelling explanation will support and enhance the patient’s perception of the clinician as a competent authority. With respect to expectation, the patient should not anticipate that the results will be immediate. In fact, the patient should be cautioned that his or her sleep problem is likely to briefly “get worse before it gets better.” Sometimes an appeal to the research literature, demonstrating that treatment gains are maintained and often continue to improve in the long-term, may help maintain the patient’s motivation despite the short-term difficulty adjusting to the procedures. With respect to “active self-management,” it is important to remember that the treatment alternative is medication and that this requires very little in the way of lifestyle change. Thus, the clinician must spend a considerable amount of time working with the patient to “make and stay with the investment.” Comorbity of Mental and Medical Disorders Many patients with chronic insomnia report mild or subthreshold levels of depressive symptoms. When depressive symptoms become severe, they may interfere with the patient’s ability and motivation to successfully follow the recommended protocol. If medical factors become exacerbated, expectations for clinical gains need to be tempered until stabilization occurs. Throughout the course of treatment, both medical and psychiatric factors should be monitored and consideration should be given for further evaluation and intervention. CBT and Sedative Hypnotics Not yet addressed is the possibility of using sedative hypnotics acutely, along with CBT for insomnia (i.e., dual or combined therapy). This is a promising and underinvestigated area of inquiry. Initial studies were mixed (46–48), but promising work continues (49). The benefit of combined therapy is a more rapid reduction of symptoms. The risk of combining pharmacotherapy with behavioral treatment, however, is that once patients start using medications, they may be less inclined to adopt or tolerate behavioral interventions. Work is ongoing to determine the most effective way to combine these two strategies to capitalize on the immediate reduction in symptoms afforded by sedative hypnotics and the long-term efficacy of CBT (50).
168 Perlis et al. Perhaps more important than the issue of combined therapy to the practice of CBT for insomnia is that many of the patients referred for CBT have been taking sedative hypnotics for years and are very apprehensive about discontinuing treatment. Often, the initial phases of treatment involve collaboration with the referring physician to assist the patient in the weaning process. Use of sleep diaries to provide feedback about sleep continuity during the withdrawal process and education about rebound insomnia and the medication itself are important for this kind of intervention. It should be noted that the chronic use of sedative hypnotics often leaves the patient with as poor a sleep continuity profile as if no medications at all were being used. This is difficult for the patient to appreciate because of the rebound insomnia that occurs during the withdrawal period. As noted previously in this chapter, the natural assumption during the withdrawal from medication is, “This is how I will sleep without medications from now on.” In combination with a careful weaning process, sleep diaries may serve as the “hard data” to demonstrate to the patient that this assumption is not true. THE EFFICACY OF CBT There are a variety of studies that attest to the efficacy of behavioral treatments for primary insomnia. These studies have been reviewed in two meta-analyses (51,52). Results from the two quantitative reviews are as follows: 32–41% global improvement in sleep following behavioral treatment where SL was reduced by 39.5–43% (effect sizes: 0.87–0.88), number of intermittent awakenings was reduced by 30–73% (effect sizes: 0.53–0.63), duration of intermittent awakenings was reduced by 46% (effect size: 0.65) and TST increased by 8–9.4% (effect size: 0.42). In actual minutes, pre–post measures revealed that patients fell asleep 24–28 minutes sooner, had 0.5–1.2 fewer awakenings and obtained about 30–32 more minutes of sleep a night. Comparative data showed that SRT or SCT yielded the greatest improvement, followed by multicomponent therapies. Treatment gains were maintained or enhanced over follow-up periods ranging from 3 weeks to 3 years. In addition to these data, there is a study by Morin and colleagues that suggests that behavior therapy yields, during acute treatment, comparable results to pharmacotherapy for insomnia and that behavior therapy has better long-term efficacy (51). A recent study by our group (53) confirms this finding in a comparative metaanalytic study and extends it by demonstrating that during acute treatment behavior, therapy yields results comparable to those of pharmacotherapy and may provide superior results for sleep-onset problems. REFERENCES 1. Spielman, A., Caruso, L., and Glovinsky, P. (1987) A behavioral perspective on insomnia treatment. Psychiatr. Clin. North Am. 10, 541–553. 2. Stepanski, E. J. (2000) Behavioral therapy for insomnia. In: Principles and Practice of Sleep Medicine (Kryger, M. H., Roth, T. G., and Dement, W. C., eds.), W. B. Saunders Company, Philadelphia, PA, pp. 647–656.
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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
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90 Duntley tion systems found that
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92 Duntley Case 1 A 36-year-old fem
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94 Fig. 2. The objective amount of
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96 Duntley PROGNOSIS AND COMPLICATI
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98 Duntley
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100 Attarian EPIDEMIOLOGY There are
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102 Attarian CLINICAL MANIFESTATION
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104 Attarian DIAGNOSTIC WORKUP The
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106 Attarian 13. Hauri, P. J. (1998
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108 Plotkin
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110 Plotkin quality of sleep. Ultim
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112 Plotkin of the therapeutic effi
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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 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: 166 Perlis et al. Table 2 Cognitive
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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