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Cognitive-Behavioral Therapy 159 Objective Assessment In current clinical practice, the diagnosis of primary insomnia does not require an in-laboratory, polysomnographic study to substantiate the diagnosis. This is true for three reasons. First, there is enough of a general correspondence between the subjective complaint and objective measures so that polysomnographic assessment is not required to verify the sleep continuity disturbance. Second, traditional polysomnography does not reveal, or allow for the quantification of, the underlying sleep pathophysiologies that presumably give rise to the patient’s complaints. Third, and most pragmatically, third-party payers will not reimburse for sleep studies on patients with likely primary insomnia. However, sleep studies are indicated if the patient demonstrates symptoms consistent with other intrinsic sleep disorders and/ or fails to respond to treatment. When assessed with polysomnography, patients with primary insomnia reliably exhibit increased SL, increased FNAs, increased WASO time, and decreased TST relative to good sleeper controls. Polysomnographic findings, however, do not correspond in a one-to-one fashion to patient perceptions of sleep continuity. Patients with insomnia routinely report more severe sleep disturbance than is evident on traditional polysomnographic measures (28–30). Some have argued that this discrepancy might be explained by the findings that patients with primary insomnia show a greater degree of psychopathology, including tendencies to somatize internal conflicts and exaggerate symptoms (31–33). Others have argued that the subjective–objective discrepancy findings reflect a cardinal feature of the disorder, that is, the persistence of sensory and information processing into NREM sleep. The continuance of such processes into polysomnographic-defined sleep are thought to be the basis for patient difficulties distinguishing between wakefulness and sleep (3). The extent to which one or both of these factors contributes to the discrepancies between subjective and objective measures of sleep in insomnia continues to be a matter of ongoing debate. (For additional information on these issues, please see the following section on the cognitive-behavioral perspective on insomnia.) When polysomnography is not feasible, the use of alternative, less costly objective devices can be particularly helpful when the clinician suspects a high degree of SSM. SSM is a term (as well as disorder) used to describe the common finding among patients with insomnia that there is a discrepancy between a patient’s subjective impression of sleep parameters and what is measured via objective recording methods. At the level of self-report, extreme values (gathered retrospectively or prospectively) may suggest that this is a component of the disorder (e.g., SLs >2 hours, WASO >2 hours, or a TST of ≤4 hours). In the absence of a polysomnographic study, actigraphs may be used to obtain corroborating prospective data. Actigraphs are wristwatch-like devices that utilize sophisticated movement detectors to estimate the traditional sleep continuity parameters (e.g., SL, WASO, FNA, and TST). This information may, in turn, be compared to the selfreport data to assess the degree to which SSM is occurring. The extent to which subjective–objective discrepancies can be resolved using actigraphy has not been
160 Perlis et al. subjected to empirical validation. In our clinical practice, however, we have found that actigraphy can be used to assess for SSM. COGNITIVE-BEHAVIORAL TREATMENT The most common CBTs for primary insomnia are sleep hygiene education, stimulus control therapy (SCT), sleep restriction therapy (SRT), relaxation training, and cognitive therapy. (For a detailed explanation of each of these therapies see ref. 6.) Of all the available psychological treatments, SCT is the most well-validated and is considered the “gold standard” for the behavioral treatment of insomnia. In practice, most behavioral sleep medicine clinicians adopt a multicomponent approach that usually contains SCT, SRT, and sleep hygiene therapy. Therapeutic Regimen The CBT of insomnia generally requires 4 to 8 weeks time with once-a-week, face-to-face meetings with the clinical provider. Sessions range from 30 to 90 minutes depending on the stage of treatment and the degree of patient compliance. Intake sessions are usually 60 to 90 minutes in duration. During this session, the clinical history is obtained and the patient is instructed in the use of sleep diaries. No intervention is provided during the first week. This time frame is used to collect the baseline sleep–wake data that will guide treatment for the balance of therapy. The primary interventions (SCT and SRT) are deployed over the course of the next one to two 60-minute sessions. Once these treatments are delivered, the patient enters into a phase of treatment where TST is upwardly titrated over the course of the next two to five visits. These follow-up sessions require about 30 minutes, unless additional interventions are being integrated into the treatment program or extra effort is required to gain patient compliance. Adjunctive treatments include cognitive therapy, relaxation training, and relapse prevention. First-Line Interventions Stimulus Control Therapy SCT is recommended for both sleep initiation and sleep maintenance problems. SCT is generally considered the first-line behavioral treatment for chronic primary insomnia because it has the most research support (34). SCT instructions limit the amount of time patients spend awake in the bed/bedroom, and are designed to decondition pre-sleep arousal and re-associate the bed/bedroom environment with rapid, well-consolidated sleep. Typical instructions include (1) maintaining a fixed wake time 7 days a week, irrespective of how much sleep one gets during the night; (2) avoiding any behavior in the bed or bedroom other than sleep or sexual activity; (3) sleeping only in the bedroom; (4) leaving the bedroom when awake for approximately 15 to 20 minutes; (5) returning to the bedroom only when sleepy. Some clinicians, in an effort to prevent “clock-watching” behavior, encourage patients to leave the bedroom as soon as they feel “clearly awake” or experience annoyance
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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
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 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: 158 Perlis et al. ditioned arousal
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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