Circadian Disorders

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Disorders of the circadian timing system are more common than previously thought. Circadian dysfunction is thought to be a common contributing factor in both sleep-wake disorders and affective disorders. The etiological bases of most circadian disorders are not known. However, such problems are thought to result from either compromised pacemaker function or faulty signaling to effector systems, or from other factors. Circadian function disorders are often manifest in the elderly, the blind, and individuals with hypothalamic, pituitary, or optic tumors.

Individuals with circadian sleep disorders typically are only symptomatic when forced to conform to a societal schedule. The underlying circadian pacemaker is usually functional but either is unable to entrain or has a deficient capacity for phase delays-advances. The circadian sleep disorders include delayed and advanced sleep phase syndrome and non-24-hr sleep-wake syndrome. Certain forms of sleep-wake disorders such as irregular sleep-wake syndrome are linked to defective pacemaker function.

Shift-work sleep disorder constitutes a significant epidemiological problem. Some 8 million workers in the United States currently work a schedule that requires night, swing or rotating shifts. The night shift sleep-wake schedule is in direct opposition to the

Figure 8 Thermoregulation is impaired in an environment with temporal cues. Effects of 6-hr exposures to cold (20oC ambient temperature) on body temperature in monkeys normally maintained at 280C when (A) entrained to an LD 12:12 cycle and (B) free-running in constant light (lighting regimen indicated at the base of each graph). The shaded areas show the body temperature rhythm (x + SD) for the three previous control days, and the solid line is the body temperature on the day of the cold pulse. The cold pulse had virtually no physiological effect in LD but produced a significant fall in core body temperature when the animals were isolated from environmental time cues. [Reproduced by permission from Fuller, C. A., Sulzman, F. M., and Moore-Ede, M. C. (1978). Thermoregulation is impaired in an environment without circadian time cues. Science 199, 794-796.]

Figure 8 Thermoregulation is impaired in an environment with temporal cues. Effects of 6-hr exposures to cold (20oC ambient temperature) on body temperature in monkeys normally maintained at 280C when (A) entrained to an LD 12:12 cycle and (B) free-running in constant light (lighting regimen indicated at the base of each graph). The shaded areas show the body temperature rhythm (x + SD) for the three previous control days, and the solid line is the body temperature on the day of the cold pulse. The cold pulse had virtually no physiological effect in LD but produced a significant fall in core body temperature when the animals were isolated from environmental time cues. [Reproduced by permission from Fuller, C. A., Sulzman, F. M., and Moore-Ede, M. C. (1978). Thermoregulation is impaired in an environment without circadian time cues. Science 199, 794-796.]

Figure 9 Sleep times as self-reported (striped horizontal bars) and via polygraphic recordings (dark horizontal bars) in an individual with delayed sleep phase insomnia. When attending school 5 days week, days 1-18, she lay awake in bed for several hours (open horizontal bars) before falling asleep but could sleep at a delayed phase with no difficulty on weekends (days 1,7, 8,14, and 15) and on vacation (days 19-45). On days 46-59, she was evaluated in the laboratory and on days 51 and 52 was subjected to an acute phase advance, which confirmed her inability to sleep at the desired time (2200-0600 hr). She was treated by chronotherapy on days 58-65 by phase-delaying her bedtime 3 hr each day until the desired phase relationship with the 24-hr clock was obtained. [Reproduced by permission from Moore-Ede, M. C., Sulzman, F. M., and Fuller, C. A. (1982). The Clocks That Time Us: Physiology of the Circadian Timing System. Harvard University Press, Cambridge, MA].

Figure 9 Sleep times as self-reported (striped horizontal bars) and via polygraphic recordings (dark horizontal bars) in an individual with delayed sleep phase insomnia. When attending school 5 days week, days 1-18, she lay awake in bed for several hours (open horizontal bars) before falling asleep but could sleep at a delayed phase with no difficulty on weekends (days 1,7, 8,14, and 15) and on vacation (days 19-45). On days 46-59, she was evaluated in the laboratory and on days 51 and 52 was subjected to an acute phase advance, which confirmed her inability to sleep at the desired time (2200-0600 hr). She was treated by chronotherapy on days 58-65 by phase-delaying her bedtime 3 hr each day until the desired phase relationship with the 24-hr clock was obtained. [Reproduced by permission from Moore-Ede, M. C., Sulzman, F. M., and Fuller, C. A. (1982). The Clocks That Time Us: Physiology of the Circadian Timing System. Harvard University Press, Cambridge, MA].

sleep-wake schedule dictated by the circadian clock. Similar to jet lag, many workers report insomnia during their off hours and hypersomnolence during their work hours. Consequently, alterness and performance suffer on the job and place the worker at greater risk for sleepiness-related accidents. Most workers also complain of additional symptoms including gastrointestinal discomfort and malaise. It is thought that the extreme work shift schedules of workers are largely responsible for two infamous disasters, the grounding of the oil tanker Exxon Valdez in 1989 and the Chernobyl nuclear plant explosion in 1986. In a similar vein, a 1992 study demonstrated that nurses on shiftwork schedules were up to 3 times more likely to misdiagnose and provide improper treatment than their daytime counterparts. Furthermore, a well-documented link exists between shift-work and both gastrointestinal and cardiovascular diseases. Often confounding the treatment of shift-work disorders is the fact that shift-workers tend to implement counter-measures in the form of caffeine, nicotine, alcohol, and sedatives.

Circadian dysfunction is also implicated in a number of affective disorders. One particularly notable example is winter depression or seasonal affective disorder (SAD). SAD is characterized by depression, lethargy, loss of libido, hypersomnia, weight gain, carbohydrate cravings, anxiety, and an inability to concentrate and focus. Onset of SAD occurs during the late autumn or winter and occurs 6 months out of phase in the northern and southern hemispheres. SAD patients experience a spontaneous remission in late spring or early summer. SAD is set apart from nonseasonal depression by three atypical symptoms: hyperphagia, carbohydrate craving, and hypersomnia. Bright light therapy has proven extremely effective in ameliorating its symptoms. Administration of a few hours of early morning or evening bright light (>2500 lx) can frequently help to resynchronize biological rhythms. This may be primarily due to the ability of light to entrain the daily melatonin rhythm or to suppress inappropriate daytime melatonin secretion.

Figure 9 demonstrates the efficacy of chronother-apy in an individual suffering from delayed sleep phase insomnia, a common sleep disorder.

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