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Medical and Neurological Causes 115 function may produce a hypotonic (overfilled) bladder that requires intermittent catheterization to avoid overflow incontinence, or a hypertonic bladder that produces discomfort and the urge to void with the smallest amount of urine volume. Once the cause of urological dysfunction has been identified and appropriately addressed, the use of hypnotic medications tend to be benign, and the pharmacology of different medications can be chosen for the most practical solution. Tricyclic antidepressant medications tend to cause urinary retention and increase urinary hesitancy, and would not be an ideal choice. Chronic renal disease commonly causes insomnia (24), worsened by electrolyte fluctuations caused by hemodialysis and the high incidence of periodic limb movement disorder (PLMD). The rheumatoid disorders, and musculoskeletal discomfort in general, are highly associated with chronic sleep disruption. Rheumatoid arthritis (25,26), ankylosing spondylitis (27), systemic lupus erythematosis (28), vasculitis, polymyalgia rheumatica, and fibromyalgia (29) can produce sleep disruption, which may become a very debilitating aspect of the disease, complicating functional recovery. Daytime pain is reported to be worse following unrefreshing sleep (30). The pain certainly is a profound trigger of sleep disturbance, as are the effects of glucocorticoid medications (31) commonly used to treat the rheumatoid diseases. The electroencephalogram (EEG) during non-rapid eye movement (NREM) sleep may include considerable alpha range activity, even in deep sleep (the “alpha-delta” sleep pattern), but alpha intrusion is not specific to the rheumatoid disorders. The same pattern may be seen in chronic fatigue syndrome (32), with its cardinal symptoms of idiopathic fatigue, headache, arthralgia, myalgia, and insomnia (33). Osteoarthritis may become more symptomatic as the morning approaches, after a night of relative immobility, and may result in early awakening. Degenerative change of the spine, scoliosis, and scleroderma may cause impaired ventilation, which causes frequent arousals and impaired sleep. Various endocrine disturbances cause insomnia, because of either the activating effects of the hormones or the somatic discomfort produced by their imbalances. Insomnia is more prevalent in hyperthyroidism, in association with a globally activated behavioral state, and sleep studies have shown an overall increase in the percentage of deep sleep (34) once difficulties with sleep initiation are overcome. The return to a serological and clinical euthyroid state may not guarantee the resolution of insomnia. Hypothyroidism more commonly causes fatigue and lethargy, and PSG has shown an associated decrease in deep sleep. Adrenal dysfunction causing catacholamine secretion will cause sympathetic activation and insomnia, and excessive glucocorticoid levels also cause insomnia (5,31). It has been suggested that elevated glucocorticoid levels may alter the production of endogenous γaminobutyric acid (GABA)-related steroid production (35), causing some of the observed insomnia. Disruption of the hypothalamic–pituitary–adrenal axis has been found in association with chronic insomnia, although it is not clear whether the disruption of hormonal secretion is cause or effect of insomnia (36,37). There is considerable clinical reporting of insomnia during menses (38), with or without
116 Plotkin associated somatic discomfort, and during menopause (39). Insomnia is reported in up to one-third of patients with diabetes mellitus (40). Treatment of sleep disruption in endocrine disturbance may be complicated by hormonal fluctuations and potential medical complications of therapy, and may require multiple modalities, spanning the pharmacological, behavioral, and alternative therapeutic realms. Pregnancy may induce changes in sleep, which are observed to be most profound in the first and third trimesters (41). The insomnia seen in the first trimester of pregnancy may be related to hormone fluctuations, whereas the insomnia associated with the third trimester is typically caused by physical discomfort including a firm, enlarged abdomen, urinary frequency, backache, hip ache, and fetal movements (42). One study found that insomnia was reported more frequently in multiparous (vs nulliparous) women (43). Changes in sleep architecture have been shown to include increased waking after sleep onset (WASO) and lower sleep efficiency, along with decreased percentage of REM sleep (44). Sleep problems during pregnancy are frequently followed by postpartum sleep disruption caused by a polyphasic sleeper (the neonate), and the incidence of maternal insomnia and depression has been shown to increase when an infant has significant sleep problems (45). Treatment of insomnia during pregnancy and breastfeeding provides a therapeutic challenge. Concerns must include the health of the developing child, to whom some amount of medication is inevitably transferred, potentially affecting the developing CNS (46). In most cases of pregnancy and lactation, it is best to apply conservative behavioral and environmental treatment measures (47). In severe cases of insomnia, pharmacological options can be used with the recognition that most have an unknown effect on human fetal development, and some actually are contraindicated. In one study (48), benzodiazepines were shown to account for the greatest number of psychotropic medication exposures during pregnancy. They were mostly utilized to treat anxiety and insomnia, and no clustering of fetal malformation was observed in the population studied. Cancer may produce insomnia due to pernicious effects on systemic physiology, painful tissue changes, therapeutic efforts, or the anxiety and depression accompanying the diagnosis. Insomnia has been found to occur in more than half (53%) of the patients with newly diagnosed lung cancer, and was felt to be a severe symptom in more than one-quarter (49). Insomnia occurred in 19% of women with breast cancer, and was of chronic character 95% of the time (50). Insomnia has been examined in a variety of cancer types (51), and has been found to occur in about one-third of cases, along with reports of fatigue, leg restlessness, and excessive sleepiness. The fatigue associated with cancer treatment may in part be due to insomnia (52). The claudication associated with hematologic disorders such as sickle cell anemia causes severe intermittent sleep disruption (53), made worse by occult sleep-disordered breathing and PLMD. Treatment should take into consideration the anticipated duration of the underlying disease, and any potential medical issues that could complicate pharmacotherapy. Insomnia therapy should be directed to preserve the quality of daytime function, improving sleep with a minimum of
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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
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
Page 105 and 106: 88 Attarian
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 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: 114 Plotkin months or years. The ef
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 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
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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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