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Sleep Disorders and Sleep Deprivation: An Unmet Public

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<strong>Sleep</strong> <strong>Disorders</strong> <strong>and</strong> <strong>Sleep</strong> <strong>Deprivation</strong>: <strong>An</strong> <strong>Unmet</strong> <strong>Public</strong> Health Problem<br />

http://www.nap.edu/catalog/11617.html<br />

76 SLEEP DISORDERS AND SLEEP DEPRIVATION<br />

• Causing clinically significant distress or impairment in social, occupational,<br />

or other important areas of functioning.<br />

• Not occurring exclusively during the course of another sleep disorder.<br />

• Not due to the direct physiological effects of a substance or a medical<br />

condition (APA, 1994).<br />

Insomnia symptoms are remarkably common, affecting at least 10 percent<br />

of adults in the United States (Ford <strong>and</strong> Kamerow, 1989; Ohayon et<br />

al., 1997; Simon <strong>and</strong> VonKorff, 1997; Roth <strong>and</strong> <strong>An</strong>coli-Israel, 1999). Prevalence<br />

is higher among women <strong>and</strong> older individuals (Mellinger et al., 1985;<br />

Ford <strong>and</strong> Kamerow, 1989; Foley et al., 1995). Severe insomnia tends to be<br />

chronic, with about 85 percent of patients continuing to report the same<br />

symptoms <strong>and</strong> impairment months or years after diagnosis (Hohagen et al.,<br />

1993; Katz <strong>and</strong> McHorney, 1998). The comorbidity of sleep disorders with<br />

psychiatric disorders is covered later in this chapter.<br />

Etiology <strong>and</strong> Risk Factors<br />

The precise causes of insomnia are poorly understood but, in general<br />

terms, involve a combination of biological, psychological, <strong>and</strong> social factors.<br />

Insomnia is conceptualized as a state of hyperarousal (Perlis et al., 2005).<br />

Stress is thought to play a leading role in activating the hypothalamicpituitary<br />

axis <strong>and</strong> setting the stage for chronic insomnia. A key study showed<br />

that adults with insomnia, compared with normal sleepers, have higher levels,<br />

over a 24-hr period, of cortisol <strong>and</strong> adrenocorticotropic hormone (ACTH),<br />

which are hormones released by the hypothalamic-pituitary-adrenal axis after<br />

stress exposure (Vgontzas et al., 2001). The 24-hour pattern of cortisol<br />

<strong>and</strong> ACTH secretion is different, however, from that in individuals who are<br />

chronically stressed. Cognitive factors, such as worry, rumination, <strong>and</strong> fear<br />

of sleeplessness, perpetuate the problem through behavioral conditioning.<br />

Other perpetuating factors include light exposure <strong>and</strong> unstable sleep schedules<br />

(Partinen <strong>and</strong> Hublin, 2005).<br />

Insomnia patients often attribute their difficulty sleeping to an overactive<br />

brain. Several lines of evidence, from preclinical to sleep neuroimaging<br />

studies in insomnia patients, suggest that there are multiple neural systems<br />

arranged hierarchically in the central nervous system that contribute to<br />

arousal as well as insomnia complaints. Disturbances in these systems may<br />

differ according to the nature of insomnia. Structures that regulate sleep<br />

<strong>and</strong> wakefulness, for example the brainstem, hypothalamus <strong>and</strong> basal forebrain,<br />

are abnormally overactive during sleep in primary insomnia patients<br />

(Nofzinger et al., 2004b). In addition, limbic <strong>and</strong> paralimbic structures that<br />

regulate basic emotions <strong>and</strong> instinctual behaviors such as the amygdala,<br />

hippocampus, ventromedial prefrontal cortex <strong>and</strong> anterior cingulate cortex<br />

Copyright © National Academy of Sciences. All rights reserved.

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