Insomnia Insomnia

Recommendations

Info

<strong>Insomnia</strong> in Children and Adolescents 57 Some children with asthma suffer from insomnia. Children with asthma have more frequent arousals and earlier final wake times (18). Sleep-onset insomnia is rarely the problem. Most asthma attacks in children occur in the last two-thirds of the night (19). This coincides with the poorest lung function occurring during the 24-hour cycle. Peak flow is 50% of waking maximum and oxygen saturations may fall 10% (20,21). The nocturnal arousals associated with asthma have been found to have consequences for school performance. Increases in daytime sleepiness as measured using the epworth sleepiness scale, variable attention in school, and increased daydreaming as measured by neuropsychological tests. These tests measure both errors of commission that correlate with hyperactivity and omission that correlate with distractibility (22). Finally, although bruxism is not a cause of sleeplessness, it may be a symptom. Children who grind their teeth as a self-calming mechanism do so less when time in bed is decreased (23). INSOMNIA IN THE SCHOOL-AGED CHILD School age includes the ages between 5 years and adolescence. The incidence of sleep disorders decreases in school-age children (24). Fears and anxieties both at sleep onset and in the middle of the sleep period are the most common complaint in this age group. Often, these are short-term anxieties manifesting as insomnia. This is often termed adjustment sleep disorder. In other cases, anxieties may be a manifestation of more lasting emotional, psychological, or psychiatric disorders such as depression and posttraumatic stress disorder (25). One must be aware that insomnia also may be a symptom of child sexual abuse (26). <strong>Insomnia</strong> is commonly reported in children with attention deficit hyperactivity disorder (ADHD). Parents commonly report that these children have difficulty falling asleep, are restless sleepers, and awaken early (27,28). Additionally, treatment for ADHD with stimulant medications may worsen sleep (29). SLEEP DISORDERS IN ADOLESCENCE Adolescence sees the emergence of circadian rhythm disorders. Even teens without a circadian rhythm disorder have a tendency toward later sleep onset, increased total sleep requirement, and an increase in daytime sleepiness when compared to preadolescents (30,31). Adolescents are predisposed to a delayed sleep onset. This is caused by a change in their biological clock. In reference to biological clocks, the term period refers to the length of the circadian cycle and is approximately, but not exactly, 24 hours. In the general population, the circadian period is approximately 24.5 hours, explaining why it is easier to stay up later than go to bed earlier for most people. In adolescence, the period becomes prolonged. In some teens, it may exceed 25 hours (30,31). The biological phenomenon of delayed sleep phase driven by the adolescent circadian clock has been separated from the social pressures on teens to stay up later. Work by Carskadon et al. has emphasized that the tendency is biological and not merely a preference or effect of social pressures (31). This emphasizes
58 Garcia the reality that the tendency toward delayed sleep-phase syndrome seen in teens is biologically driven by the circadian system. The treatment of circadian rhythm disorders in children and adolescents can be discussed in three groups: chronotherapy, phototherapy, and pharmacotherapy. A review of the sleep log helps to set the context for discussion of chronotherapy or sleep–wake scheduling. A common method of chronotherapy is known as sleepphase advancement (32–34). Taking into account the youth’s social expectations and requirements, a reasonable wake time is agreed upon. The agreed upon earlier wake time drives the sleep-onset time earlier. There is often a 3- to 5-day delay as the sleep phase advances. The teen may be advised that during this time, he or she may feel tired. It is emphasized that over the next 2 to 3 months, strict wake and bedtimes must be adhered to 7 days a week. Once a more appropriate sleep phase has been established, relaxing the schedule once or twice a week may be allowed if it does not throw the teen back into a delayed sleep phase. Alternatively, some physicians prefer to delay the sleep onset and wake time by several hours each day until the sleep-onset and wake times have been delayed to a phase consistent with the teen’s social expectations. This form of chronotherapy is known as sleep-phase delay. For example, the teen falling asleep at 3 AM and waking at noon is asked to delay sleep onset until 6 AM. The wake time is proportionately delayed until 3 PM. On the second day, sleep onset is at 9 AM and wake time is at 6 PM. The sleep-onset time is delayed 3 hours each day until sleep onset is at 9 PM and wake time is at 6 AM. Thereafter, the sleep phase is fixed again for several months. One may choose to emphasize the nature of the relationship at this point. The physician is often seen as a coach. This places responsibility and control in the hands of adolescent. Phototherapy is the second fundamental treatment in children with circadian rhythm disorders (35–37). The goal is to decrease the evening light and increase exposure to waking bright light. It is important that the teen’s exposure to bright light, including television and computer monitors is eliminated after 9 PM. In the morning, early morning bright light exposure with a light box or ambient light is effective in resetting the biological clock. Generally, 10,000 lux is necessary. Precautions should be taken to avoid exposure to ultraviolet spectrum (38) light. Use of light therapy should be avoided in patients with a history of bipolar disease as it can trigger mania. It should be emphasized that the patient need not look directly at thea light box; the direction of gaze may deviate 15°. It is recognized that children often have difficulty using a light box and integrating the light box into their morning routine is often a challenge. Some children choose to put the light box on the breakfast table or where they do their homework in the morning. Medication therapy is mentioned last because it is rarely effective without simultaneously using sleep–wake scheduling and/or phototherapy. Two groups of medication have been described. The first is the sleep-inducing medications including the benzodiazepines and zolpidem. These medications are most effective when there is a pre-existing sleep debt. The second is melatonin. Melatonin has been shown to advance the sleep phase in some patients with delayed sleep-phase syndrome (39–
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: 56 Fig. 1. A sleep log used in chil
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 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

Create successful ePaper yourself

Delete template?

Save as template?