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<strong>Insomnia</strong> in Children and Adolescents 61 INSOMNIA IN CHILDREN WITH DEVELOPMENTAL DISABILITIES <strong>Insomnia</strong> is seen commonly in children with developmental disabilities (44). One study of 214 children ages 1–18 with severe mental retardation found that 86% exhibited difficulties with sleep (45). Sleep disorders in children with disabilities stress a sometimes already burdened family system. One study found that in children with disabilities without a sleep disorder, 21% of parents had daytime sleepiness. Of parents with children with disabilities and a sleep disorder, 64% of the parents complained of daytime sleepiness (46). Sleep disorders impact daytime behaviors in children with developmental disabilities. Irritability and mood lability are also increased (47,48). The aberrant behavior checklist, used to quantify difficult behaviors in children with disabilities, was found to be increased when difficulties with sleep were identified (49). There is an increase in self-injurious behavior in children found to have difficulties with sleep. Interestingly, worsening mental handicap does not predict increased incidence of sleep disorders. Some syndromes are associated with an increased incidence of sleep difficulties including autism, Prader-Willi, Angelman, Smith-Magenis, Sanfilippo, Rett syndrome, and cerebral palsy. Of children with autism, 63–72% are identified as having sleep difficulties (50–52). These problems are often severe. Sleep problems include prolonged sleep latencies (the length of time between going to bed and going to sleep), prolonged periods of nocturnal wakefulness, shortened total sleep time, and early morning waking. Children with autism are more likely to suffer from sleep disorders than other children with developmental delays, with the most common problem being early waking (53). Of children with Sanfilippo syndrome, 78% have problems with sleep; 46% of which are severe enough to warrant medication management (54). Of children with Smith-Magenis syndrome, 59% suffer from sleep problems (55). Treatment begins with the same basic principles used in children without developmental disabilities. For example, one study found that the gradual extinction technique described for sleep-onset association disorder resulted in quick and lasting reductions in sleep disorder symptoms in children with developmental disabilities (56). Sleep–wake scheduling, or chronotherapy, has been found to be effective in children with developmental disabilities. In this case, the wake time is fixed. The nap time is minimized. Using a sleep log (see Fig. 1 for an example of a sleep log) the individual’s average sleep requirement is determined. The bedtime is then approximated and increased or decreased until a 90% sleep efficiency is achieved (57). A combination of sleep–wake scheduling and phototherapy was effective in one study (58). Finally, medication management is often required in this population. The benzodiazepines may not be effective in this population. (59). Some authors have recommended choral hydrate (60). Melatonin has been used effectively in a population of blind children with developmental disabilities (59,61,62). Melatonin has been used in sleep disorders associated with
62 Garcia neurodevelopmental disabilities including Rett syndrome (63), tuberous sclerosis, (64), autism (65), and Asperger syndrome (51). Again, the reservations previously discussed in the treatment of circadian rhythm disorders apply here. Many sleepinducing medications have been used, but in general, the literature is incomplete in measuring which medications are most effective. Further research is necessary. Case 3 Erin is a 5-year-old girl with autism. Her sleep-onset time and wake times are variable. Her sleep-onset time ranges from 9 PM to 1 AM. Her wake time ranges from 4 AM to 9:30 AM. Additionally, she has difficulty maintaining her sleep. Several times a week she will be fully alert for 1 to 2 hours between 1 AM and 3 AM. Her daytime behavior deteriorates when she has nights of shorter total sleep time. She has no history of snoring. She takes a 1- to 2-hour afternoon nap when cared for by her grandmother 3 days a week. Intervention for Erin involved sleep–wake scheduling and medication management. Her afternoon nap was gradually eliminated over a 3-week period. A regular wake time of 7 AM was initiated. Several weeks after the regular wake time was established, her middle-of-the-night arousals decreased to once every 2 or 3 weeks. It became clear that although most nights she was asleep by 10 PM, once or twice a week she continued to be awake after midnight. Her parents had already tried over-the-counter melatonin without much success. Doxepin (10 mg/1 mL) 2 mL (20 mg) was given when she was not asleep by 10:30 PM. This helped to further regularize her sleep phase. CONCLUSIONS A developmental approach to the diagnosis of youth with insomnia makes this difficult issue more approachable. Treatment is driven by the diagnosis. Careful patient- and family-specific treatments provide enormous benefits. Childhood treatment leads to the prevention of lifelong insomnia. Treatment of the child with a neurodevelopmental diagnosis provides relief to the family as well as the child. REFERENCES 1. Ragins, N. and Schachter, S. (1957) A study of sleep behavior in two-year-old children. J. Am. Acad. Child Psychiatry 10, 464–480. 2. Bax, M. (1980) Sleep disturbance in the young child. Br. Med. J. 280, 1177–1179. 3. Bernal, J. (1973) Night waking in infancy during the first 14 months. Dev. Med. Child Neurol. 15, 760–769. 4. Blurton Jones, N., Ferreira, M. C., Farquar, M., and Macdonald, B. L. (1978) The association between perinatal factors and later night waking. Dev. Med. Child Neurol. 20, 427–434. 5. Richman, N. (1984) Sleep problems in young children. Arch. Dis. Child 56, 491. 6. Van Tassel, E. (1985) The relative influence of child and environmental characteristics on sleep disturbances in the first and second years of life. J. Dev. Behav. Pediatr. 6, 81. 7. Roberts, K. (1951) Eating, sleeping, and elimination practices of a group of two and one half year old children. Am. J. Dis. Child 82, 121.
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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
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
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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
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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
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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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