Insomnia Insomnia

Recommendations

Info

Primary Sleep Disorders 143 architecture, with fragmented nocturnal sleep being a basic manifestation of this dysregulation. Sleep paralysis and hypnogogic hallucinations can be unpleasant enough to result in anxiety about sleeping. The stimulants and antidepressants used to treat excessive daytime sleepiness and cataplexy can further contribute to difficulty sleeping. The anxiety resulting from a nightmare may result in awakenings and difficulty returning to sleep. With sleep starts, an awakening coincides with the abnormal motor activity; when repetitive, this can result in difficulty falling asleep or returning to sleep after awakening in the night. In the primary sleep disorders, many patients do not develop a complaint of insomnia despite demonstrable sleep fragmentation, suggesting individual differences in susceptibility. Psychophysiological insomnia has been shown to have a familial tendency (18), and genetic predisposition likely plays a role in the development of an insomnia complaint in the primary sleep disorders. Additionally, poor sleep hygiene often develops, leading to further difficulty sleeping. For instance, in RLS, patients often report that they get their best sleep late in the morning, leading to a tendency to sleep in late when possible, leading to further difficulties initiating sleep. In any of the disorders, the perception of difficulty sleeping can lead to anxiety directed toward sleep and therefore a secondary component of psychophysiological insomnia. PATHOGENESIS AND PATHOPHYSIOLOGY In OSA, repetitive complete or partial occlusions of the upper airway result in repetitive arousals during sleep. Pharyngeal patency is maintained by a balance of outward forces created by actively contracting pharyngeal muscles such as the genioglossus that are phasically active during inspiration, and negative intraluminal forces created during inspiration (19). In OSA, this patency is compromised through a narrowing of the upper airway through either anatomical means such as hypertrophied tonsils, or dynamic means such as reduction of the phasic inspiratory contractions. This leads to an increased effort of breathing and hypoxemia, resulting in arousals or awakenings, associated with a surge in sympathetic nervous system activity. Because most arousals and awakenings in OSA are brief, patients are usually unaware of the frequency of awakenings. Some awakenings may be long enough for the patient to recall, leading to an insomnia complaint. Apneas are sometimes associated with a sensation of choking, not breathing, dyspnea, or tachycardia. This can lead to a fear of sleep that can sometimes reach phobic levels. The total number of apneic and hypopneic episodes per hour of sleep is called either the apnea-hypopnea index (AHI) or the respiratory disturbance index (RDI), although many laboratories include events such as respiration effort-related arousals or snore arousals in the RDI. An AHI score of 5 or higher is enough to establish the diagnosis of OSA syndrome. The pathophysiology of RLS remains unclear. Most cases are idiopathic, but a significant percentage are hereditary, with an autosomal-dominant pattern of inher-
144 Duntley itance. A recent study established the presence of a susceptibility locus on chromosome 12q (20). RLS may also be associated with a variety of medical conditions, including neuropathy (21), uremia (22), and iron deficiency (23). Medications such as lithium or antidepressants may precipitate or worsen RLS symptoms (24–26), as may withdrawal from medications such as benzodiazepines or anticonvulsants. Sleep-onset insomnia is induced by the need to move the legs and the accompanying paresthesias. Sleep maintenance difficulties may occur if symptoms are present during nocturnal awakenings. Additionally, most patients with RLS have PLMs while sleeping that may be associated with sleep maintenance difficulties. Although many patients with PLMs during sleep complain of insomnia and daytime sleepiness (11), the relationship between the leg movements and symptoms remains unclear. Mendelson found no correlation between PLM arousal index and subjective complaint of disturbed sleep, subjective measurements of awakening refreshed or Multiple Sleep Latency Test (MSLT) values (27). In a randomized, controlled clinical trial, pramipexole normalized the PLM index in RLS patients without a corresponding improvement in sleep architecture (28). Although a dysregulation of rapid eye movement (REM) sleep is the most clinically salient feature of narcolepsy, this disorder is also characterized by a dysregulation of other aspects of sleep architecture including sleep continuity. Recent evidence suggests this dysregulation is secondary to a deficiency in hypocretin mechanisms. Narcolepsy in dogs was recently shown to be secondary to mutations in the hypocretin-2 receptor gene (29) and hypocretin knockout mice exhibit features characteristic of narcolepsy including episodes of atonia resembling cataplexy and disrupted sleep (30). Most patients with narcolepsy have undetectable cerebrospinal fluid hypocretin (31) and histology on six human narcolepsy brains revealed a generalized absence of hypocretin (31). Systemic administration of hypocretin-1 in narcoleptic dogs resulted in improvement in sleep architecture (33). Nightmares may be triggered by emotionally charged experiences, and when recurrent are felt to reflect unresolved daytime emotional conflicts (34). Nightmares may also be caused by a variety of medications including β-blockers, dopaminergic agents, and some antidepressants (35–37). Nightmares are also a prominent feature of other sleep disorders such as REM sleep behavior disorder. Ethanol withdrawal can cause nightmares so unpleasant that some patients report a resumption of drinking to prevent them (38). The end result is an awakening in which anxietyarousing dream content is recalled, resulting in prolongation of the awakening. It is unclear if sleep starts are a primary motor disorder or if an abnormality in the sensory system or abnormal central nervous system (CNS) imagery provokes the motor response as a secondary phenomenon. CLINICAL MANIFESTATIONS Patients usually have accompanying symptoms that distinguish their sleep disorder and the resulting insomnia from other etiologies of insomnia. Patients with OSA typically have a combination of nocturnal and daytime symptoms that raise
Page 1 and 2:
Clinical Handbook of Insomnia Edite
Page 3 and 4:
C URRENT CLINICAL NEUROLOGY Daniel
Page 5 and 6:
© 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 and 58:
40 Attarian Table 1 Types of Insomn
Page 59 and 60:
42 Attarian 15 to 40 seconds. PLMs
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
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
Page 115 and 116: 98 Duntley
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
Page 143 and 144: 126 Plotkin
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: 142 Duntley disorders has been conf
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 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
Page 209: Current Clinical Neurology CLINICAL
show all

Insomnia Insomnia

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?