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Primary Sleep Disorders 147 bedpartners should be interviewed whenever possible. A thorough physical examination should be performed; symptoms elicited during the history may suggest particular systems that require particular emphasis. RLS is a clinical diagnosis based on the four essential clinical features just noted. Polysomnography is not necessary in straightforward cases unless further evaluation for PLMs during sleep is desired. Medical causes should be excluded through careful physical examination and appropriate laboratory evaluation. Nightmares do not require polysomnography unless the history or physical examination leads one to suspect the patient has another contributing sleep disorder. Sleep starts rarely require evaluation beyond a careful history and examination; if features of the history suggest possible seizures, polysomnography with full montage electroencephalogram (EEG) monitoring may be necessary. If OSA or PLMD is suspected, all-night polysomnography is recommended for documentation and determination of severity. If narcolepsy is suspected, then polysomnography followed by MSLT is required for definitive diagnosis. The PSG is a polygraph of EEG findings, eye movements, electromyography readings, oxygen saturation, limb movements, airflow, and chest and abdominal movements taken during sleep, usually for the entire night. An MSLT is a series of four or five opportunities, each separated by a 2-hour interval, to take a 15- to 20-minute nap. The time to the onset of sleep (sleep latency [SL]) is calculated for each nap. The presence or absence of REM sleep is also noted. The mean SL provides a measure of the severity of sleepiness, and the occurrence of REM sleep during the naps is helpful in the diagnosis of narcolepsy. Mean SLs of 5 minutes or less are indicative of pathological sleepiness and SLs of 10 or more are normal. The presence of REM sleep on two or more naps is abnormal and is found in many narcoleptic patients. Nocturnal polysomnography should be performed on the night immediately preceding the MSLT to factor out the impact of sleep deprivation on the mean SL and the patient should be free of any medication effects that may influence sleep. Case 2: OSA Syndrome Presenting with <strong>Insomnia</strong> A 42-year-old man presented with the complaint of approximately a 5year history of insomnia and severe nighttime snoring. Previously, he was a relatively light, but good sleeper. About 5 years ago he started having problems with sleep maintenance insomnia. He also had snoring at night severe enough for his wife to move out of the bedroom in order to be able to sleep. She also had witnessed some pauses in his breathing. He denied falling asleep in sedentary and unusual situations. He denied falling asleep while at work or driving, but he stated that he feels very fatigued and tired. He denied taking daytime naps. He denied uncomfortable sensations in his legs, morning heartburn, or waking up with a bitter taste in his mouth. He denied morning headaches, morning dry mouth, loss of muscle tone in response to emotions, sleep paralysis, or hypnagogic hallucinations. His bedtime was between 10 and 11 PM and it took him about 10–15 minutes to fall asleep, however, after 2 or 3 hours he was awake and could not
148 Duntley return to sleep. He tossed and turned for the rest of the night, sleeping only for 30- to 45-minute intervals at a time until his rise time at 6 or 7 AM. Although he felt restored most of the time, he also had significant fatigue during the day. He had no allergies, was not presently on any medications except vitamins, and did not have a past medical history. There was a family history of snoring and insomnia in one parent and one sibling. He consumed large amounts of caffeine but did not smoke and used alcohol only in social settings. A review of systems was significant for a 25-lb weight gain over the past year. His physical exam was normal. The patient underwent a PSG that revealed reduced sleep efficiency and an RDI of 49.9 breathing events per hour. The lowest oxyhemoglobin saturation was 70%. Following the diagnostic portion of the study, a nasal continuous positive airway pressure (CPAP) trial was initiated. A pressure of 7 cm H 2O was found to be optimal. The patient’s symptoms resolved completely after initiation of CPAP. At the 3-month follow-up visit, he reported consolidated sleep at night and no more daytime fatigue as well as resolution of snoring. PREVENTION Not enough is known about the etiology of narcolepsy, RLS, PLMD, or sleep starts to allow effective prevention. OSA syndrome is amenable to some preventive measures, such as maintenance of lean body weight, avoidance of ethanol and other CNS depressants near bedtime, and avoidance of smoking. Many patients, however, will develop OSA even when known risk factors are not present. Although there is little objective data on prevention of sleep disturbance from nightmares, teaching patients effective methods to deal with emotional stresses and trauma may help minimize sleep disturbance from nightmares. In all patients, teaching good sleep hygiene and treating secondary conditioned insomnia may minimize insomnia symptoms resulting from the primary sleep disorder. Case 3: RLS Presenting with <strong>Insomnia</strong> A 50-year-old woman presented for a 4- to 5-year history of inability to fall asleep. Over the past 4–5 years, she experienced significant trouble falling asleep, mainly due to uncomfortable, indescribable feelings in her legs and sometimes in her arms when she was trying to fall asleep. This discomfort was usually relieved by moving or rubbing her feet. Occasionally, it woke her up from sleep as well. She experienced this about two to three times a week. She also complained of the same discomfort, although less frequently, during the day when sedentary. For example, when she was sitting at her desk at work or when she was riding in a car or an airplane, she often had to get up
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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
Page 113 and 114: 96 Duntley PROGNOSIS AND COMPLICATI
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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
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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: 146 Duntley The patient’s primary
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 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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