Insomnia Insomnia

Recommendations

Info

<strong>Insomnia</strong> in Psychiatric Disorders 129 Table 2 Diagnostic Criteria for a Major Depressive Episode In the same 2 weeks, the patient has had five or more of the following symptoms, which are a definite change from usual functioning. Either depressed mood or decreased interest or pleasure must be one of the five. • Depressed mood for almost all day nearly every day • Markedly decreased interests for almost all day nearly every day. • Appetite and or weight increased or decreased for almost all day nearly every day. • Decreased or increased sleep for almost all day nearly every day. • Patient agitated or retarded for almost all day nearly every day. • Fatigue or loss of energy for almost all day nearly every day. • Patient feels worthless or inappropriately guilty for almost all day nearly every day. • Trouble thinking or concentrating for almost all day nearly every day. • Repeated thoughts about death (other than the fear of dying), suicide (with or without a plan), or has made a suicide attempt. These symptoms cause clinically important distress or impair work, social, or personal functioning This disorder is not directly caused by a general medical condition or the use of substances, including prescription medications. Unless the symptoms are severe (defined as severely impaired functioning, severe preoccupation with worthlessness, ideas of suicide, delusions, or hallucinations, or psychomotor retardation), the episode has not begun within 2 months of the loss of a loved one. Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorder, Fourth Edition, Text Revision. Copyright © 2000 American Psychiatric Association absence of depression symptoms in the initial evaluation of insomnia should not rule out the risk of major depression in future visits. Patients with insomnia and no depression at intake were at approximately 40-fold higher risk of developing new episodes of major depression in comparison to individuals with no insomnia (6). There is another group of insomnia patients who have major depression, yet their sole complaint is insomnia. The psychiatric literature described individuals with “Alexithymia” (patients without words to express their feeling state). These individuals are more likely to have “masked depression.” They are particularly commonly seen in the primary care setting. Patients with masked depression substitute somatic complaints such as insomnia for the traditional core symptoms of depressed mood or loss of pleasure. Therefore, it is important to focus on the objective component of the mental status. The general demeanor and posture of patients with depression may appear to be slowed. They may walk slowly, holding their heads down and lacking spontaneity. Patients with depression may respond to questions with long pauses and short answers (7). Their facial expressions may be blunted and their eye contact may be
130 Karaz poor. Focusing only on the contents of the patient’s complaints may result in overlooking depression and in turn a poor treatment outcome. Severe insomnia is an independent risk factor for suicide during the first 2 years of an episode of major depression (8). Treatment of Depression/<strong>Insomnia</strong> Symptoms Selective serotonin reuptake inhibitors (SSRIs) like fluoxetine, paroxetine, sertraline, and fluvoxamine are commonly used for treatment of depression. SSRI antidepressants decrease total sleep time (TST), increase number of arousals, suppress REM sleep, and increase the number of phasic REMs. Despite their arousing effect on the sleep electroencephalogram (EEG), SSRI antidepressants improve subjective sleep quality in subjects with major depression and primary insomnia (9). On the other hand, insomnia is the most common residual symptom among patients who have otherwise been successfully treated with fluoxetine for depression. This phenomenon may be unique to the newer antidepressant medications like fluoxetine (8). Tricyclic antidepressants play a role in treatment of depression/anxiety symptoms. Tricyclic antidepressants decrease REM sleep and increase REM latency. EEG measures of sleep continuity may improve with tricyclic antidepressants (8). The tertiary amine tricyclic antidepressants (e.g., Amitriptyline and Imipramine) have a more sedating effect than the secondary amine tricyclics like Desipramine and Nortriptyline. The secondary amines group has fewer adverse effects. Some clinicians believe that depressed patients with marked insomnia and anxiety obtain some immediate relief from the sedating antidepressants before the full antidepressant effect takes place, which might increase the likelihood of compliance during the acute phase of treatment (10). One drawback of the tricyclic antidepressants is the risk of fatal effects if an overdose is ingested. Patients were randomly assigned to an initial prescription of the SSRI fluoxetine or the tricyclic Imipramine. The rate of improvement in insomnia was identical in both groups (11). Serotonin receptor modulators like Trazodone and Nefazodone increase sleep continuity. However, Trazodone decreases REM sleep and may cause daytime sedation, whereas Nefazodone increases REM and has minimal daytime sedation (12). Monoamine oxidase inhibitors (MAOIs), antidepressants like Tranylcypromine (Parnate) and Phenelzine (Nardil), still have a role in the treatment of depression. However, because of the necessity to regulate the diet and to continuously evaluate the concomitant medications, MAOIs are not used as a first line of treatment (10). Benzodiazepines like Lorazepam, Clonazepam, and Alprazolam are sedating, induce sleep, and have anti-anxiety and muscle relaxant effects. Newer medications like Zolpidem act selectively on the ω1 benzodiazepine receptors and have a sedative effect without anxiolytic, anticonvulsant, and muscle relaxant effects. They do not cause rebound effects or withdrawal when discontinued (12). A doubleblind study by Smith and co-workers found that patients taking fluoxetine for
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: 128 Karaz Table 1 DSM-IV Diagnoses
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
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?