Insomnia Insomnia

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Sleep Hygiene 103 Case 2 A 26-year-old psychology student presented to the sleep medicine center’s clinic for initial evaluation of recent sleep-onset initiation insomnia. In the past, she had only rare problems falling and staying asleep. About 6–7 months prior to coming to the center, the problem became persistent. Currently, she goes to bed exhausted, sleepy, around midnight or 1 AM but is still unable to fall asleep. She lays in bed anywhere from 30 minutes to 3–4 hours tossing and turning, but does not leave the bed or the bedroom. She usually gets up at 7 AM with an alarm and on weekends, when she doesn’t have to go to work, she sleeps into late morning and sometimes, until early afternoon. During the day, she takes a 45- to 90-minute nap. She also uses her bedroom during the day to study, eat, watch television, read, and sometimes works late into the night shortly before retiring. She does not abuse caffeine and uses alcohol only socially. She does not abuse recreational drugs and does not smoke. She denies cataplexy, hypnagogic hallucinations, snoring, choking spells, falling asleep unintentionally during the day, or symptoms of restless legs. The only symptom she states that she has experienced is rare periods of sleep paralysis, maybe two to three times in her life time. She has a past medical history of attention deficit hyperactivity disorder. She is taking Dexedrine and Ambien when needed. Her exam is normal and her Beck’s Depression Inventory score is 6 (not depressed). DIFFERENTIAL DIAGNOSIS The differential diagnosis of poor sleep hygiene insomnia includes three main categories of disorders. The other extrinsic sleep disorders are environmental sleep disorder; adjustment sleep disorder; sleep-onset association disorder; nocturnal eating or drinking syndrome; limit-setting sleep disorder; food allergy insomnia; insufficient sleep syndrome; altitude insomnia; the hypnotic-, stimulant-, and alcohol-dependent insomnias; and toxin-induced sleep disorder (1). Sometimes, it is hard to differentiate individual disorders from each other because of significant overlap among them. The second main category is the primary insomnias, which include psychophysiological insomnia, childhood-onset, or idiopathic insomnia, and sleep state misperception insomnia (1). Any of these may co-exist with poor sleep hygiene and may cause or be exacerbated by it. The third category is the secondary insomnias, including insomnia due to other sleep disorders such as obstructive sleep apnea, restless legs syndrome, periodic limb movement syndrome, and even narcolepsy. <strong>Insomnia</strong> can be caused by a variety of neurological, psychiatric, and other medical illnesses. Degenerative neurological illnesses, anxiety disorders, asthma, and so on, are some examples. When the symptoms of the underlying disorder are prominent, secondary insomnias are usually suspected and diagnostic testing appropriate to the circumstance may elucidate the underlying cause of the insomnia.
104 Attarian DIAGNOSTIC WORKUP The diagnosis of inadequate sleep hygiene is best made through careful and detailed history of the patient’s daily sleep-related habits (13). These include bedtime, rise time, time spent in bed awake, different nonsleep-related activities in which the patient engages in the bed and the bedroom including watching TV, reading, and so on, timing of exercise, activities engaged in prior to bedtime and while awake at night, amount and timing of caffeine or alcohol ingestion, and daytime napping. In short, the diagnosis should try to identify any activity that is not compatible with sleep. A useful diagnostic tool is a detailed sleep questionnaire completed by the patient and the bedpartner (14,15). As in most primary insomnias, sleep diaries are essential tools in identifying sleep problems and charting their evolution and response to treatment. In a paper published in 1998, Blake and Gomez introduced a simple but useful questionnaire by which to measure compliance with sleep hygiene education (16). As in most insomnias, a thorough psychiatric and medical evaluation, including a physical exam, should be done to rule out medical or psychiatric causes of the insomnia. Per ASDA (now AASM) guidelines, polysomnography is not indicated in routine evaluation of insomnia, except when the diagnosis is uncertain and a primary sleep disorder is suspected, and when insomnia does not respond to appropriate behavioral and pharmacological treatments (17). PROGNOSIS AND COMPLICATIONS As in most extrinsic sleep disorders, once the underlying cause is removed, the symptoms resolve completely. The sooner treatment is started, the more complete the resolution of symptoms, and the better the prognosis. If poor sleep hygiene is allowed to continue, psychophysiological insomnia may result in susceptible individuals. Some recent publications find a high correlation between poor sleep hygiene, especially among younger drivers and high accident rates (18,19). PREVENTION Education is the cornerstone for the prevention of poor sleep hygiene insomnia. Almost everyone engages in poor sleep hygiene at various times. There is also a large number of external sleep disruptors such as noise, ambient light, and so on, outside of one’s control. Although it is extremely important to educate people about sleep hygiene, these rules do not strictly apply to everyone. A short daily nap is part of the lifestyles of some cultures and does not necessarily constitute poor sleep hygiene if it does not result in symptoms of insomnia or sleep disturbances. Similarly, a cup of coffee or a drink with dinner or even reading in bed may not negatively impact some people’s sleep. However, either because of their predisposition or because of the additive effect of different factors, some people may develop significant insomnia.
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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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Page 71 and 72: 54 Garcia association is known as s
Page 73 and 74: 56 Fig. 1. A sleep log used in chil
Page 75 and 76: 58 Garcia the reality that the tend
Page 77 and 78: 60 Fig. 2. Actigraph recording in a
Page 79 and 80: 62 Garcia neurodevelopmental disabi
Page 81 and 82: 64 Garcia 35. Czeisler, C., kronaue
Page 83 and 84: 66 Garcia
Page 85 and 86: 68 Attarian showed similar degrees
Page 87 and 88: 70 Attarian agitation and hence the
Page 89 and 90: 72 Attarian Affective disorder is s
Page 91 and 92: 74 Attarian and Drug Administration
Page 93 and 94: 76 Fig. 2. Sleep log after treatmen
Page 95 and 96: 78 Attarian 18. Bonnet, M. H. and A
Page 97 and 98: 80 Attarian 65. Perlis, M., Aloia,
Page 99 and 100: 82 Attarian was confirmed by resear
Page 101 and 102: 84 Attarian times worrying about th
Page 103 and 104: 86 Attarian insomnia or for other s
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Page 107 and 108: 90 Duntley tion systems found that
Page 109 and 110: 92 Duntley Case 1 A 36-year-old fem
Page 111 and 112: 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: 102 Attarian CLINICAL MANIFESTATION
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 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
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154 Perlis et al.
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156 Perlis et al. Fig. 1. A schemat
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158 Perlis et al. ditioned arousal
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160 Perlis et al. subjected to empi
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162 Perlis et al. effect), (3) may
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164 Perlis et al. Cognitive Therapy
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166 Perlis et al. Table 2 Cognitive
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168 Perlis et al. Perhaps more impo
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170 Perlis et al. 28. Carskadon, M.
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172 Perlis et al.
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174 Attarian Secondary Insomnias Re
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176 Attarian 50 years of age who sl
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178 Attarian Antidepressants Becaus
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180 Attarian The use of benzodiazep
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182 Attarian to placebo. Zaleplon a
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184 Attarian 3. Wyatt, R. J., Engel
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186 Attarian residual sedation foll
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188 Index Clonidine, 183 CNS arousa
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190 Index Proton pump inhibitors, 1
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Current Clinical Neurology CLINICAL
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