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Physiological Basis of Insomnia 35 decreased HFP compared to the good sleepers. These physiological findings in “preinsomnia” patients suggest that their existing hyperreactivity to sleep-related stress and caffeine could be secondary to elevated sympathetic nervous system activity, and this could be a marker for the development of chronic insomnia at a later date. The finding of elevated physiological activity prior to mood change, personality change, or complaint of chronic insomnia provides another clue that underlying physiology could be the key to the later development of additional insomnia symptoms. DISCUSSION It is generally accepted that there are changes in several physiological systems in association with psychophysiological insomnia. The current experiments attempted to refine our understanding of the relationship among physiological arousal, poor EEG sleep, psychological status, and subjective report of insomnia. The finding that experimentally produced chronic physiological arousal in normal young adults produces the mood and personality changes seen in patients with insomnia provides a compelling description of how chronic insomnia could develop in physiologically susceptible individuals. The studies showing that, by itself the poor sleep of patients with insomnia does not produce the arousal, mood, and personality characteristics of patients and that the production of much worse EEG sleep in patients with insomnia does not magnify symptoms leads to the conclusions that the symptoms produced by chronic physiological arousal were not mediated by the poor sleep that was produced and the symptom complex that was associated with psychophysiological insomnia is not really a sleep disorder, but rather an arousal disorder. Finally, the importance of physiological arousal as the harbinger of insomnia was enhanced by the finding of elevated heart rate and abnormal cardiac spectral activity in normal subjects with no sleep complaint who were found to have EEG-defined SI. These several approaches identify tangible physiopathology that should be open to identification and amenable to treatment. We have recognized for many years that some patients have lifelong problems with excessive sleepiness secondary to disorders such as narcolepsy or idiopathic hypersomnolance. The extent to which these disorders demonstrate a failure of the sleep system vs a failure of the arousal system can be debated. Certainly, these disorders are commonly treated with medications that have direct impact by increasing central nervous system arousal. Recognition that another group of patients suffers from the opposite lifelong problem (hyposomnolence or hyperarousal) has been more difficult. At this point, much work has identified the physiological markers of chronic hyperarousal in patients. Behavioral relaxation techniques can provide effective help for patients with some situational hyperarousal, but as behavioral techniques such as sleep extension eventually fail in patients with idiopathic hypersomnolance, behavioral techniques may also fail in patients suffering from chronic hyperarousal. Identifying arousal disorders as a major component of both hypersomnolance and insomnia can help direct research toward more effective pharmacological control of the underlying physiologic arousal disorder.
36 Bonnet and Arand ACKNOWLEDGMENT This chapter was supported by the Dayton Department of Veterans Affairs Medical Center, Wright State University School of Medicine, and the Sleep–Wake Disorders Research Institute. REFERENCES 1. Kales, J. D., Kales, A., Bixler, E. O., et al. (1984) Biopsychobehavioral correlates of insomnia, V: Clinical characteristics and behavioral correlates. Am. J. Psychiatry 141, 1371–1376. 2. Tan, T. L., Kales, J. D., Kales, A., Soldatos, C. R., and Bixler, E. O. (1984) Biopsychobehavioral correlates of insomnia. IV: Diagnosis based on DSM-III. Am. J. Psychiatry 141, 357–362. 3. Kales, A., Caldwell, A. B., Soldatos, C. R, Bixler, E. O., and Kales, J. D. (1983) Biopsychobehavioral correlates of insomnia. II. Pattern specificity and consistency with the Minnesota Multiphasic Personality Inventory. Psychosom. Med. 45, 341–355. 4. Hauri, P. J. (1983) A cluster analysis of insomnia. Sleep 6, 326–338. 5. Healey, E. S., Kales, A., Monroe, L. J., Bixler, E. O., Chamberlin, K., and Soldatos, C. R. (1981) Onset of insomnia: Role of life-stress events. Psychosom. Med. 43, 439–451. 6. Monroe, L. J. (1967) Psychological and physiological differences between good and poor sleepers. J. Abnorm. Psychol. 72, 255–264. 7. Haynes, S. N., Follingstad, D. R., and McGowen, W. T. (1974) Insomnia: Sleep patterns and anxiety level. J. Psychosom. Res. 18, 69–74. 8. Freedman, R. R. and Sattler, H. L. (1982) Physiological and psychological factors in sleep-onset insomnia. J. Abnorm. Psychol. 91, 380–389. 9. Freedman, R. R. (1986) EEG power spectra in sleep-onset insomnia. Electroencephal. Clin. Neurophysiol. 63, 408–413. 10. Haynes, S. N., Adams, A., and Franzen, M. (1981) The effects of presleep stress on sleep-onset insomnia. J. Abnorm. Psychol. 90, 601–606. 11. Bonnet, M. H. and Arand, D. L. (1998) Heart rate variability in insomniacs and matched normal sleepers. Psychosom. Med. 60, 610–615. 12. Johns, M. W., Gay, T. J. A., Masterton, J. P., and Bruce, D. W. (1971) Relationship between sleep habits, adrenocortical activity and personality. Psychosom. Med. 33, 499–508. 13. Mendelson, W. B., Garnett, D., Gillin, C. G., and Weingartner H. (1984) The experience of insomnia and daytime and nighttime functioning. Psychiat. Res. 12, 235–250. 14. Adam, K., Tomeny, M., and Oswald, I. (1986) Physiological and psychological differences between good and poor sleepers. J. Psychiatr. Res. 20, 301–316. 15. Frankel, B., Buchbinder, R., Coursey, R., and Snyder, F. (1973) Sleep patterns and psychological test characteristics of chronic primary insomniacs. Sleep Res. 2, 149. 16. Borkovec, T. D. (1982) Insomnia. J. Cons. Clin. Psychol. 50, 880–895. 17. Mendelson, W. B., James, S. P., Garnett, D., Sack, D. A., and Rosenthal, N. E. (1986) A psychophysiological study of insomnia. Psychiatry Res. 19, 267–284. 18. Seidel, W. F., Ball, S., Cohen, S., Patterson, N., Yost, D., and Dement, W. C. (1984) Daytime alertness in relation to mood, performance, and nocturnal sleep in chronic insomniacs and noncomplaining sleepers. Sleep 7, 230–238. 19. Bonnet, M. H. (1986) Effect of 64 hours of sleep deprivation upon sleep in geriatric normals and insomniacs. Neurobiol. Aging 7, 89–96. 20. Stepanski, E., Zorick, F., Roehrs, T., Young, D., and Roth, T. (1988) Daytime alertness in patients with chronic insomnia compared with asymptomatic control subjects. Sleep 11, 54–60. 21. Haynes, S. N., Fitzgerald, S. G., Shute, G. E., and Hall, M. (1985) The utility and validity of daytime naps in the assessment of sleep-onset insomnia. J. Behav. Med. 8, 237–247.
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
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Page 21 and 22: 4 Attarian et al. until the 1970s t
Page 23 and 24: 6 Attarian et al. Table 2 Diagnosti
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Page 27 and 28: 10 Attarian et al. REFERENCES 1. Ma
Page 29 and 30: 12 Attarian Another study in Austri
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Page 33 and 34: 16 Attarian communities. A structur
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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
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Page 51: 34 Bonnet and Arand The Development
Page 55 and 56: 38 Bonnet and Arand 45. Bonnet, M.
Page 57 and 58: 40 Attarian Table 1 Types of Insomn
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Page 61 and 62: 44 Fig. 1. Example of a 1-week slee
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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
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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 79 and 80: 62 Garcia neurodevelopmental disabi
Page 81 and 82: 64 Garcia 35. Czeisler, C., kronaue
Page 83 and 84: 66 Garcia
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Page 89 and 90: 72 Attarian Affective disorder is s
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86 Attarian insomnia or for other s
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88 Attarian
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90 Duntley tion systems found that
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92 Duntley Case 1 A 36-year-old fem
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94 Fig. 2. The objective amount of
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96 Duntley PROGNOSIS AND COMPLICATI
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98 Duntley
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100 Attarian EPIDEMIOLOGY There are
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102 Attarian CLINICAL MANIFESTATION
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104 Attarian DIAGNOSTIC WORKUP The
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106 Attarian 13. Hauri, P. J. (1998
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108 Plotkin
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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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