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Cognitive-Behavioral Therapy 161 and irritation over the fact that they are awake. The combination of these instructions re-establishes the bed and bedroom as strong cues for sleep, and entrains the circadian sleep–wake cycle to the desired phase. Sleep Restriction SRT is recommended for both sleep initiation and sleep maintenance problems. SRT requires patients to limit the amount of time in bed (TIB) to an amount equal to their average TST. In order to accomplish this, the clinician works with the patient to establish a fixed wake time and decrease sleep opportunity by limiting the subject’s TIB to an amount that equals his or her average TST as ascertained by baseline sleep diary measures. Once a target amount of TIB is set, the patient’s bedtime is delayed to later in the night so that the TIB and average TST are the same. Initially, this intervention results in a reduction in TST, such that the patient gets less total sleep than he or she is accustomed to. This controlled form of sleep loss usually corresponds to a decrease in SL and WASO time. Thus, during the acute phase of treatment, the patient gets less sleep, but sleeps in a more consolidated fashion (i.e., he or she fall asleeps more quickly and stays asleep for longer periods of time). The increase in consolidated sleep is formally represented as sleep efficiency (TST/TIB). The patient’s sleep efficiency is monitored on a weekly basis. If the patient’s average weekly sleep efficiency reaches 85–90% (depending on age), then sleep opportunity is incrementally increased by 15 minutes. The increase in sleep opportunity is accomplished by having the patient retire 15 minutes earlier for the next week of treatment. The upward titration process is usually continued for about 4 weeks, thus allowing for an increase of about 1 hour in sleep opportunity. When the patient does not reach the 85–90% benchmark, some clinicians reduce the total sleep opportunity to the previous “set point,” others maintain the subject’s total sleep opportunity until adequate sleep efficiency is observed, whereas still others combine these approaches. With respect to the last possibility, the clinician may maintain the subject’s total sleep opportunity for 2–3 weeks and then downwardly titrate the TIB when there is clear evidence that the patient cannot sustain his or her clinical gains. SRT is thought to be effective for two reasons. First, it prevents the patient from coping with his or her insomnia by extending sleep opportunity. This strategy, although increasing the opportunity to get more sleep, produces a form of sleep that is shallow and fragmented. Second, the initial sleep loss that occurs with SRT is thought to increase the “pressure for sleep,” which in turn produces quicker SLs, less WASO, and more efficient sleep. Three points merit further comment. First, total TIB is manipulated by phase delaying the patient’s sleep period. This, along with keeping a fixed wake time, results in sleep restriction. It is plausible, however, that total TIB could be altered by having the subject wake up at an earlier time. This approach is not adopted because fixing “wake up time” at an early hour (1) does not capitalize on the fact that extending wakefulness is easier to tolerate than curtailing sleep, (2) delays the initial increase in time awake before sleep for 24 hours (and thus delays the clinical
162 Perlis et al. effect), (3) may reinforce the tendency for EMAs, and (4) undermines the opportunity to pair “sleep” with the bed/bedroom. Second, it should be noted that SRT has some paradoxical aspects. One paradox is that patients who report being unable to sleep are in essence being told to sleep less. The other paradox occurs over the course of treatment. With therapy, patients find that it is difficult to stay awake until the prescribed hour. This, if not paradoxical, is at least ironic for the patient who initially presents with sleep-onset difficulties. Finally, it should be noted that SRT may be contraindicated in patients with histories of mania or seizure disorder because it may aggravate these conditions. Adjunctive Interventions Sleep Hygiene Education Sleep hygiene education is recommended, along with SRT and SCT, for both sleep initiation and maintenance problems. It may also have some value as a means toward increasing TST. Sleep hygiene education addresses a variety of behaviors that may influence sleep quality and quantity. The intervention most often involves providing the patient with a handout and then reviewing the items and the rationales for them. Table 1 contains a set of sleep hygiene instructions. It should be noted that in this formulation, several aspects of other therapies are adopted. For example, items 1, 2, 12, 13, and 15 are traditionally considered part of SCT and/or SRT. Sleep hygiene education is most helpful when tailored to a behavioral analysis of the patient’s sleep–wake behaviors. The tailoring process allows the clinician the opportunity to (1) demonstrate the extent to which he or she comprehends the patient’s individual circumstances (by knowing which items do and do not apply), (2) suggest modifications, and (3) show the patient the rules, which are in many ways too “absolutistic.” Consider the following two examples: • The admonishment to avoid caffeinated products may be, in general, too simply construed. Caffeinated beverages may be used to combat daytime fatigue (especially during acute therapy) and, if the withdrawal is timed correctly, may actually enhance the subject’s ability to fall asleep. • The prohibition against napping may not be practical. Elderly subjects or subjects with extreme work performance demands may indeed need to compensate for sleep loss. A more considerate approach to napping may entail taking into account the time of the nap, the duration of the nap, and how nocturnal sleep is handled on days when subjects nap. Napping earlier in the day will allow for more homeostatic pressure for nocturnal sleep. Limiting the duration of the nap will allow for less of a discharge of the homeostat and enhance the subjects sensation of feeling rested from the nap (by avoiding awakening from slow wave sleep). Going to bed later, when one naps during the day, may minimize the effects of the nap on nocturnal sleep. Finally, it can be argued that the most important aspect of sleep hygiene education derives not so much from the “tips” provided, but from allowing the clinician the opportunity to demonstrate his or her knowledge. A thoughtful and elaborate review may enhance the patient’s confidence in the therapist and in the treatment regimen. Such enhanced confidence may lead to greater adherence or compliance with the more difficult aspects of therapy.
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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
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 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: 160 Perlis et al. subjected to empi
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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