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Home » Geriatric Psychiatry

Psychiatric Times. Vol. 16 No. 10
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Neurobehavioral Consequences of Sleep Dysfunction

Geriatric Times Staff
By Leslie Knowlton | October 1, 1999

PT: What sleep disorders are not related to lifestyle? What do physicians need to know?

Dinges: Every physician should be aware of primary sleep disorders. These include obstructive sleep apnea, insomnias, narcolepsy and periodic leg movements. An excellent source for information is the standard textbook in the field [Kryger et al., 1994]. Sleep apnea involves collapse of the upper airway during sleep and chronic fragmentation of sleep, of which the sleeper is unaware. One of the most prevalent sleep disorders, one study identified apnea in 3% to 5% of the middle-aged adult working population [Young et al., 1993]. A clinical polysomnogram is needed to confirm it but, once diagnosed, apnea is treatable, generally with mechanical airway splints (e.g., CPAP [continuous positive airway pressure]) and increasingly for some patients with dental devices and surgical procedures. Not all treatments are equally effective in all patients, which is why patients need to be evaluated at a sleep disorders center. Apnea has a high correlation with obesity, and studies now also suggest that sleep apnea may contribute to myocardial ischemia and infarct in patients with coronary artery disease. The most common risk from apnea is sleepiness that can result in errors, accidents, motor vehicle crashes and a reduced quality of life [Weaver et al., 1997]. Signs of sleep apnea-which can include obesity, complaints of fatigue or evidence that the patient falls asleep at inappropriate times-need to be taken seriously.

Hypnotics and sedatives are not indicated until sleep apnea has been ruled out. Insomnia, which refers to a complaint that sleep is difficult to initiate or maintain, or that it is neither refreshing nor restorative, is the most common sleep complaint-approximately 10% of adults report chronic insomnia.

Insomnia can present with a variety of daytime sequelae and can result from a range of conditions and disorders (behavioral, psychological, medical, circadian and so forth). Approximately half of all the patients who complain of insomnia chronically have a psychiatric disorder, usually an affective disorder [Buysse et al., 1994]. Most patients with insomnia are not seen in sleep disorders centers, but either seek no treatment or are treated by primary care physicians or psychiatrists. To evaluate and treat insomnia safely and effectively, the psychiatrist must understand how other sleep disorders present (for differential diagnosis), have acumen in the nature of the insomnia being experienced, and understand when treatment should focus on behavioral interventions and/or hypnotic medications. It is also important to appreciate that insomnia complaints in the elderly are less likely to involve psychopathology and more likely to be associated with age-related changes in sleep and physical problems (e.g., pain, nocturia) or behaviors that disrupt sleep, such as too much caffeine(Drug information on caffeine) intake. Insomnia patients tend to self-medicate-alcohol and "natural" substances such as melatonin(Drug information on melatonin) are widely used. Several behavioral and pharmacological treatments have been shown to be effective and safe for insomnia. Over-the-counter melatonin is not recommended for insomnia by many sleep experts because too few randomized controlled clinical trials have been completed.

Narcolepsy is a sleep disorder that is serious but much rarer than either sleep apnea or insomnia. A genetically transmitted disorder, narcolepsy involves sleep disruption, waking cataplexy and severe daytime sleepiness with uncontrolled attacks of REM sleep during wakefulness, often triggered by intense affect. Narcolepsy is frequently misdiagnosed, to the detriment of the patient. For example, a psychiatrist misdiagnosed a young adult patient with narcolepsy as having multiple personality disorder-the issue came to a head when the patient kept collapsing into REM sleep during emotionally charged therapy sessions. Subsequent polysomnography confirmed full-blown narcolepsy.

Narcolepsy often begins in adolescent and young adult years like some other severe neurobehavioral disorders. If you have a patient who is excessively sleepy, reports that they get weak in the knees when they experience emotions of any kind and that they have fallen down or had uncontrolled sleep attacks, etc., you need to get them into a sleep disorders center. The clinical markers of narcolepsy include REM sleep during daytime naps. The excessive day-time sleepiness of narcolepsy is now being treated with Provigil (modafinil), a new wake-promoting compound that lacks many of the adverse effects of traditional dopaminergic drugs. There is both hope and concern about the off-label use of Provigil.

Periodic limb movements involve episodes of repetitive limb movements during sleep (usually the legs), which can cause frequent arousals or partially awaken the sleeper or bed partner. Usually patients are unaware of the movements. Like sleep apnea and insomnia, the prevalence of periodic limb movements increases in geriatric populations. It has been reported that as many as one in three persons over the age of 60 may experience this condition [Ancoli-Israel et al., 1991]. Periodic limb movements can be associated with problem sleepiness during the daytime or complaints of nonrefreshing sleep. Like sleep apnea and narcolepsy, polysomnography can be used to objectively confirm the presence of the disorder. Benzodiazepines are often used to treat periodic limb movements.

Other sleep disorders that I have not discussed include parasomnias such as night terrors, nightmares, sleep walking, enuresis and REM behavior disorder. The latter was discovered only a few years ago. Found primarily in elderly men, REM behavior disorder involves the loss of the normal skeletal muscle paralysis of REM sleep. The sleeper suddenly starts pounding and thrashing the bed partner. Psychiatrists should be familiar with the techniques and tests needed to identify and treat all of these sleep disorders.

PT: What can be done to evaluate and manage problem sleepiness?

Dinges: Sleepiness has to be recognized. Problem sleepiness can be easily missed. An article has recently appeared in the American Family Physician-a leading journal for primary care physicians-based on the report of a NIH [National Institutes of Health] National Center for Sleep Disorders Research Working Group on problem sleepiness [National Heart, Lung, Blood Institute and National Center on Sleep Disorders Research Working Group, 1999]. In it, we encourage physicians to ask patients about behavioral signs of excessive sleepiness, sleep disorders, and the quantity and quality of sleep. For example: Does the patient report dozing off or having difficulty staying awake during routine tasks, especially while driving?

Having identified excessive sleepiness in a patient, you should then attempt to determine why the patient is sleepy, in order to ensure effective treatment of the underlying cause (e.g., sleep apnea, narcolepsy, insomnia). Diagnosis and treatment may ultimately require evaluation in a sleep disorders center. Prescription of sedating or stimulant compounds should not be done until the cause of and treatment for excessive sleepiness are determined. All patients should be advised that pre-existing sleepiness heightens the sedative effects of alcohol(Drug information on alcohol). Stimulants do not play a major role in the treatment of problem sleepiness except for patients with narcolepsy.

PT: What are you working on now?

Dinges: While much is known about acute total sleep loss, little is known about chronic partial sleep deprivation, which afflicts millions of people as a result of medical and psychiatric conditions, and lifestyle. We are currently investigating the effects of chronic sleep restriction on neurobehavioral functions and emotional, physical and psychological responses. This NIH-supported project involves having people live in the laboratory for 20 days, with random assignment to a limited amount of sleep (four, six or eight hours per day). Our initial experiments have demonstrated that [restricting] sleep...even to six hours per day, results in accumulating cognitive deficits that reach severe levels of impairment within one week, without subjects being aware of their levels of problem sleepiness. We are also continuing our experiments on the use of brief daytime (prophylactic) naps to enhance both neurobehavioral functioning and growth hormone secretion when nocturnal sleep is restricted, which occurs during space flight. This work is being done for NASA [National Aeronautics and Space Administraion] through support from the National Space Biomedical Research Institute.

As part of our studies for the U.S. Air Force Office of Scientific Research, we are investigating the effects of sustained low-dose caffeine and naps during severe total and partial sleep loss. This research is focused on novel ways to safely promote wakefulness through pharmacological countermeasures, other than amphetamines, in emergency personnel who must undergo prolonged waking demands (e.g., military operations). It is in collaboration with projects of Charles Czeisler, M.D., at Harvard Medical School and Dale Edgar, M.D., at Stanford Medical School.

We are also studying human-centered technologies that purport to detect a person's alertness or drowsiness level. These experiments, which are being done for the U.S. Department of Transportation and NASA Ames Research Center, are intended to identify ways to reliably track a person's sleepiness level while driving, flying or during other activities. We've tested in a double-blind, controlled trial a number of biobehavioral technologies that claim to be able to detect drowsiness while driving. These devices detect changes in head movements, various measures of brain wave activity, eye blink rate, slow eyelid closures, eye movements, pupil responses, heart rate changes and so forth.

Many of these technologies continue to be marketed, but few have been validated. Thus far, we have only found one technique that reliably detected drowsiness-induced vigilance failures with a high level of accuracy. This approach involves monitoring the cumulative duration of slow eyelid closures [PERCLOS]. An unobtrusive automated PERCLOS system is currently being developed by Richard Grace, Ph.D., at Carnegie Mellon University. Our goal is to ensure that technologies that end up in the workplace, automobile or clinic meet scientific criteria for validity and reliability, practical criteria for implementation and proper use, and legal policy criteria for protecting individual rights. I am certain that unobtrusive, online monitoring of human alertness and performance in the workplace and most transportation modes will grow and become normative early in the next century, as other technologies permit flexibility in time utilization beyond a fixed biologically driven period for sleep. I am equally certain that problems with sleep and sleepiness will accompany these developments and remain important behavioral health issues.

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References
1.Ancoli-Israel S, Kripke DF, Klauber MR et al. (1991), Periodic limb movements in sleep in community-dwelling elderly. Sleep 14(6):496-500.
2.Benington JH, Heller HC (1995), Restoration of brain energy metabolism as the function of sleep. Prog Neurobiol 45(4):347-360.
3.Buysse DJ, Reynolds CF, Hauri PJ et al. (1994), Diagnostic concordance for DSM-IV sleep disorders: a report from the APA/NIMH DSM-IV field trial. Am J Psychiatry 151(9):1351-1360.
4.Dinges DF, Chugh DK (1997), Physiological correlates of sleep deprivation. In: Physiology, Stress and Malnutrition, Functional Correlates, Nutritional Intervention, Kinney JM, Tucker HN, eds. Philadelphia: Lippincott-Raven, pp 1-27.
5.Edgar DM, Dement WC, Fuller CA (1993), Effects of SCN lesions on sleep in squirrel monkeys: evidence for opponent processes in sleep-wake regulation. J Neurosci 13(3):1065-1079.
6.Everson CA (1993), Sustained sleep deprivation impairs host defense. Am J Physiol 265(5 PT 2):R1148-R1154.
7.Ford DE, Kamerow DD (1989), Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? JAMA 262(10):1479-1484 [see comments].
8.Krueger JM, Majde JA (1994), Microbial products and cytokines in sleep and fever regulation. Crit Rev Immunol 14(3-4):355-379.
9.Kryger M, Roth T, Dement W eds. (1994), Principles and Practice of Sleep Medicine. 2nd ed. Philadelphia: Saunders.
10.Medori R, Tritschler HJ, LeBlanc A et al. (1992), Fatal familial insomnia, a prion disease with a mutation at codon 178 of the prion protein gene. N Engl J Med 326(7):444-449 [see comments].
11.National Heart, Lung, Blood Institute and National Center on Sleep Disorders Research Working Group (1999), Recognizing problem sleepiness in your patients. Am Fam Physician 59(4):937-944.
12.Rechtschaffen A, Gilliland MA, Bergmann BM, Winter JB (1983), Physiological correlates of prolonged sleep deprivation in rats. Science 221(4606):182-184.
13.Young T, Palta M, Dempsey J et al. (1993), The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 328(17):1230-1235.
14.Weaver TE, Laizner A, Evans LK et al. (1997), An instrument to measure functional status outcomes for disorders of excessive sleepiness. Sleep 20(10):835-843.
15.Wu JC, Bunney WR (1990), The biological basis of an antidepressant response to sleep deprivation and relapse: review and hypothesis. Am J Psychiatry 147(1):14-21.


 
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