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Differential Diagnosis of Insomnia 41 idiopathic insomnia, psychological functioning is remarkably intact. In severe cases, daytime functioning may be severely disrupted, and affected patients may be unable to hold a job. During childhood and adolescence, idiopathic insomnia is often associated with dyslexia and hyperactivity. In many cases, diffuse, nonspecific abnormalities are seen on an electroencephalogram (EEG) (4,5). There is no direct human evidence for structural neuropathology. Although idiopathic insomnia appears in childhood, not all childhood insomnia is idiopathic (6). Sleep State Misperception Insomnia In this fascinating disorder, complaints of insomnia occur without any objective evidence of sleep disturbance. Patients may report that they have not slept at all in weeks, months, or years. However, on objective sleep studies, they sleep several hours per night (7). When results of sleep evaluation are presented, patients with sleep state misperception (SSM) may vehemently insist that the studies are in error because they are convinced that they sleep very little, if at all. Poor Sleep Hygiene In some patients, insomnia is the result of lifestyle. In others, poor sleep hygiene develops as a result of chronic insomnia. For example, in the latter case, patients may begin to drink more coffee to remain awake during the day and more alcohol to fall asleep at night. They may stay in bed for extended periods in an attempt to get more sleep. However, such ploys only serve to perpetuate the insomnia (5). Fatal Familial Insomnia This hereditary condition, with autosomal-dominant transmission, is characterized clinically by progressive insomnia, dysautonomia, dysphagia, dysarthria, diplopia changes in circadian rhythm of hormone secretion, motor signs, myoclonus, and slight to moderate deterioration of cognition. The usual age of onset is between 35 and 60 years, and the course of the illness is between 7 and 32 months. In this condition, an abnormal prion protein (PrPsc) is present in the brain, and there is mutation of gene coding for PrPsc. The fatal nature of this illness is due to neurological degenerative changes, not to the insomnia itself (8, 9). Restless Legs Syndrome and Periodic Limb Movement Disorder These familial, common, and related conditions are found in varying degrees in up to 10% of the population (10). The prevalence of periodic limb movement disorder (PLMD) is 3.9% and restless legs syndrome (RLS) is 5.5% (11). The four cardinal symptoms of RLS are a desire to move the legs, accompanying paresthesias that are characterized as uncomfortable or indescribable, motor restlessness, and worsening of symptoms at night and at rest (12). Symptoms of RLS may worsen with administration of antidepressants (13,14) and during pregnancy (15). Periodic limb movements (PLMs) occur in 80% of patients with RLS (16). They are repetitive, stereotyped movements recurring at 5- to 90-second intervals lasting usually
42 Attarian 15 to 40 seconds. PLMs are not considered abnormal unless they lead to severe sleep disturbance or excessive daytime sleepiness, or both, in which case they form a separate intrinsic sleep disorder, PLMD (10). RLS can be easily differentiated from primary insomnias by history due to the characteristic symptoms with which it presents. Insomnia as a result of PLMD may require the aid of a polysomnogram (PSG; see later) to make the correct diagnosis. Other Sleep Disorders Occasionally, insomnia is the presenting complaint in obstructive sleep apnea (OSA) syndrome. In a group of older adults with insomnia, a respiratory disturbance index (RDI) of at least 15 per hour was found in 29% of patients (17). In another study of a large group of patients with insomnia, RDI of at least 30 per hour was found in 2.3% of patients vs 1.3% of controls (18). The presence of excessive daytime sleepiness, snoring, and observed apneas raises the possibility of OSA syndrome. In circadian rhythm abnormalities, patients sleep well but not at socially acceptable times (5). Those with the advanced sleep-phase syndrome have excessive sleepiness in the evening and undesired early morning awakening. Those with the delayed sleep-phase syndrome have sleep-onset insomnia, excessive daytime sleepiness (particularly in the morning), or both. Other circadian rhythm abnormalities presenting with a variety of insomnia symptoms include irregular sleep– wake cycle, non-24-hour sleep–wake syndrome and sleep disturbances in blind individuals, and those resulting from social circumstances: jet lag and shift-work sleep disorder (19). Having patients fill out sleep diaries or sleep logs during a 1- or 2-week period when they are free of social restrictions of their bedtime and wake time (going to bed whenever they are sleepy and getting up on their own without an alarm) helps make the diagnosis of circadian rhythm abnormalities. Occasionally, narcolepsy presents as insomnia because 50% of patients with narcolepsy have disrupted sleep at night (20,21). Again, excessive daytime sleepiness and ancillary symptomatology (sleep paralysis, hypnic hallucinations, and cataplexy) differentiate insomnia resulting from narcolepsy from the primary insomnias. Neurologic and Medical Conditions Conditions that can cause insomnia, among other symptoms, include neurodegenerative diseases (22), pain, allergies (23), gastroesophageal reflux (24), and asthma (25). All of these can be easily differentiated from primary insomnias by history and physical exam. Menopause-Related Insomnia There is a high level of sleep disturbance occurring in about 42% of middle-aged women (26). Although cross-sectional analyses indicate that sleep disturbance may be independent of menopausal status, transition into postmenopausal status is associated with deleterious changes in sleep among women not receiving hormone replacement therapy (26,27).
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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
Page 8: Series Editor’s Introduction The
Page 11 and 12: x Foreword nervous system hypersomn
Page 14 and 15: Contents Series Editor’s Introduc
Page 16: Contributors HRAYR P. ATTARIAN, MD
Page 19 and 20: 2 Attarian et al.
Page 21 and 22: 4 Attarian et al. until the 1970s t
Page 23 and 24: 6 Attarian et al. Table 2 Diagnosti
Page 25 and 26: 8 Attarian et al. Duration of Illne
Page 27 and 28: 10 Attarian et al. REFERENCES 1. Ma
Page 29 and 30: 12 Attarian Another study in Austri
Page 31 and 32: 14 Attarian even less well studied.
Page 33 and 34: 16 Attarian communities. A structur
Page 35 and 36: 18 Attarian 5. Sutton, D. A., Moldo
Page 37 and 38: 20 Attarian 53. Kageyama, T., Kabut
Page 39 and 40: 22 Attarian
Page 41 and 42: 24 Bonnet and Arand Table 1 Reporte
Page 43 and 44: 26 Bonnet and Arand On the day spen
Page 45 and 46: 28 Bonnet and Arand SUMMARY These m
Page 47 and 48: 30 Bonnet and Arand chronic caffein
Page 49 and 50: 32 Bonnet and Arand response that a
Page 51 and 52: 34 Bonnet and Arand The Development
Page 53 and 54: 36 Bonnet and Arand ACKNOWLEDGMENT
Page 55 and 56: 38 Bonnet and Arand 45. Bonnet, M.
Page 57: 40 Attarian Table 1 Types of Insomn
Page 61 and 62: 44 Fig. 1. Example of a 1-week slee
Page 63 and 64: 46 Fig. 3. One-week printout of an
Page 65 and 66: 48 Attarian Fig. 4. Algorithm. (Use
Page 67 and 68: 50 Attarian 27. Polo-Kantola, P., E
Page 69 and 70: 52 Garcia
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
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Page 89 and 90: 72 Attarian Affective disorder is s
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Page 97 and 98: 80 Attarian 65. Perlis, M., Aloia,
Page 99 and 100: 82 Attarian was confirmed by resear
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Page 107 and 108: 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
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130 Karaz poor. Focusing only on th
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132 Karaz He felt hopeless that his
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134 Karaz Table 4 Diagnostic Criter
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136 Karaz complained of feeling anx
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138 Karaz other physicians avoided
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140 Karaz 17. Attarian, H. P. (2000
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142 Duntley disorders has been conf
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144 Duntley itance. A recent study
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146 Duntley The patient’s primary
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148 Duntley return to sleep. He tos
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150 Duntley Treatment of RLS should
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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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