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Pharmacological Treatment 181 Table 2 Nonbenzodiazepine Hypnotics Drug T 1/2 half life Onset of action Peak plasma conc Active metabolites Zolpidem 1.5–2.4 hours 30 minutes 1.5 hours No Zaleplon 1 hours 30 minutes 1 hour No Zopiclone 5–6 hours 30 minutes 2 hours No not with altered renal function. Schlich et al. as early as 1991, studied 107 patients with insomnia, about 60% of whom were over 60 years of age. The subjects were given 10 mg of zolpidem on a nightly basis for 6 months. An improvement in all efficacy parameters—time taken to fall asleep, total amount of nocturnal sleep, and number of nocturnal awakenings—was reported by the investigator and the patients; the improvement was evident from the first evaluation day and was maintained throughout the trial. Improvement was also maintained during the washout period with a lack of rebound insomnia. There was no sign of withdrawal symptoms and tolerance to zolpidem did not develop over the 6-month treatment period. Adverse events were mild and infrequent, and tended to resolve with a dose reduction (41). The following year, Maarek and colleagues reported the results of their open-label zolpidem trial. They enrolled 96 subjects who received 10–20 mg of zolpidem a night for 6 to 12 months. Again, improvement in all sleep parameters was noted in 90% of subjects with no rebound and withdrawal effects on discontinuation (42). Saletu-Zyhlarz et al., in a single-blind, placebo-controlled crossover study, compared 10 mg of zolpidem to placebo. Fifteen adult patients diagnosed with nonorganic insomnia were enrolled. Objective and subjective sleep and awakening quality measures were investigated in 3 subsequent nights in the sleep laboratory. There was a significant lengthening of the total sleep period and total sleep time, an improvement in sleep efficiency and a shortening of SLs after zolpidem as compared with placebo. Zolpidem also increased the length of stage 4 and stage 3 + 4 non-REM sleep as compared with placebo (43).These are some of the important studies looking at zolpidem; there are others in the medical literature that have produced results, concordant with the above. Zaleplon also is an effective and safe hypnotic (44). The onset of action is approximately 30 minutes, and the duration of action is about 4 hours. Peak zaleplon serum concentrations occur in about 1 hour, and its elimination half-life is also about 1 hour. Similar to zolpidem, its dose needs to be adjusted with altered hepatic function but not with renal impairment. The Zaleplon Clinical Study Group looked at the efficacy and safety of three doses of zaleplon, a novel compared with those of placebo in outpatients with insomnia in this 4-week study, using 10 mg of zolpidem as active control. Post-sleep questionnaires were used to determine treatment effects on the patient’s perception of sleep, development of tolerance during therapy, or rebound insomnia or withdrawal on discontinuation of therapy. SL was significantly shorter throughout the 4 weeks of study with any dose of zaleplon compared
182 Attarian to placebo. Zaleplon also had significant effects on sleep duration, number of awakenings, and sleep quality compared to placebo. No pharmacological tolerance developed with zaleplon and there were no indications of rebound insomnia or withdrawal symptoms after treatment discontinuation. There was no significant difference in the frequency of adverse events with active treatment compared to placebo. These results show that zaleplon provides effective treatment of insomnia with a favorable safety profile (45). A similar study was done to look at its efficacy and safety in the elderly (>65 years) population. Again, zaleplon proved to be a safe and effective treatment for insomnia in the elderly with no significant adverse effects of rebound insomnia (46). Because of its short half-life, there is no residual sedation when zaleplon is administered in the middle of the night; hence, it is the ideal medication for sleep maintenance insomnia. Walsh et al. assessed residual sedation after 10 mg of zaleplon in a randomized, double-blind, placebo- and active drug-controlled cross-over study with 30 mg of flurazepam (as an active control). The drug (zaleplon, flurazepam, or placebo) was taken during a nocturnal awakening in patients with sleep maintenance insomnia. Twenty-two healthy sleep maintenance insomniacs were enrolled and received zaleplon, flurazepam, or placebo after an experimental awakening 3.5 hours after bedtime on 2 consecutive nights. Residual sedation was measured with SL testing (5 and 6.5 hour postdrug), and other psychometric tests. Zaleplon did not differ from placebo on any measure of residual sedation; flurazepam showed significant sedation on all measures (47). A related medication, zopiclone (not available in the United States), has also been shown in several studies to be as effective as benzodiazepines in relieving symptoms of insomnia and as safe as the other “Z” medications (35). It can also be helpful in shift-work insomnia. In a recent study, 29 shift workers suffering from insomnia were included and treated with zopiclone (7.5 mg/day) or placebo according to a random, double-blind protocol. Patients completed a sleep diary and a wrist actigraph was used to evaluate episodes of rest and activity. A self-administered subjective sleep questionnaire was filled out just after awakening. Zopicone was found to increase the duration of sleep significantly over the baseline duration after the first and second night on duty. Subjective estimation of sleep was better in patients taking zopiclone who exhibited a smaller number of shorter awakening episodes (48). Another method of use of hypnotics have come into favor in recent years that maximizes benefits for chronic insomniacs and minimizes tolerance or dependence. Several studies, mainly with zolpidem, have shown that non-nightly, discontinuous use with stimulus control therapy (SCT) has shown to be both effective and safe in chronic use (49). In 2002, Hajak et al. published their data on discontinuous, nonnightly hypnotic therapy in the treatment of chronic insomnia. In a prospective, observational open study in 550 primary care settings throughout Germany, 2690 patients with chronic insomnia were treated with zolpidem according to an “asneeded” administration treatment schedule (up to five tablets per week chosen by the patient), in addition to the optional use of SCT, during drug-free nights. After
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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
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116 Plotkin associated somatic disc
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118 Plotkin Table 1 Causes of Secon
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120 Plotkin Table 1 (continued) Lew
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122 Plotkin REFERENCES 1. Foley, D.
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124 Plotkin 48. Marchetti, F., Rome
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126 Plotkin
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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 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: 180 Attarian The use of benzodiazep
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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