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Neurobehavioral Consequences of Sleep Dysfunction

Neurobehavioral Consequences of Sleep Dysfunction

As chief of the division of sleep and chronobiology in the department of psychiatry at the University of Pennsylvania School of Medicine, David F. Dinges, Ph.D., focuses on ways sleep and the endogenous circadian pacemaker interact to control wakefulness and waking neurobehavioral functions such as physiological alertness, attention, cognitive performance, fatigue, mood, neuroendocrine profiles, immune responses and health. In an interview with Psychiatric Times, Dinges discussed neurobehavioral consequences of sleep loss, factors that impair sleeping, the pervasiveness of sleepiness and new ways to manage sleepiness.

Psychiatric Times: What is the function of sleep?

Dinges: This fundamental question has two levels. An extensive description of the neurobiological mechanisms of sleep will likely reveal multiple functions at a basic, probably subcellular, level. To date, these remain occult. At a more molar level, sleep promotes subsequent wakefulness. The stability of the wake state, alertness, and how well the brain functions cognitively and emotionally all depend upon an adequate duration of quality sleep. If you don't sleep enough, waking is eroded, even though you may not be aware of it.

So if sleep is essential for waking, then how much sleep is needed and for how long? Although the duration of sleep needed for stable waking functions varies among individuals and across the life span, daily sleep in our species is an average duration of eight hours. Because time is viewed in the information age as a commodity that can be bought, sold, traded and generally controlled at will, large segments of modern society have chronically reduced sleep durations. The reasons include sleep loss from occupational demands such as shift work or jet lag, sleep loss associated with aging and other developmental issues and, most pervasively, sleep loss associated with lifestyles that put a premium on waking activities. Because so many of us routinely reduce our sleep, we have created a new societal standard for wakefulness that is suboptimal. Far too many people are sleep-deprived to the point of requiring caffeine, exogenous stimulation and compensatory effort to remain awake. It is not uncommon to hear people attribute their sleepiness and even uncontrolled sleep attacks to a boring or sedentary activity-not appreciating that their own inherent biological drive for sleep overwhelms wakefulness when stimulation or compensatory effort are no longer enough. In contrast, wakefulness following satiation of sleep drive is effortless and requires no stimulation. The neurobiology for wakefulness and the neurobiology for sleep can be thought of as being in opposition [Edgar et al., 1993]. There is evidence that the endogenous circadian pacemaker located in the suprachiasmatic nucleus is a wake-promoting system [Edgar et al., 1993].

Its primary neurobiological effect is to promote wakefulness at the right time of day. In diurnal animals like us, that's when the sun is out. The sleep drive or so-called "sleep homeostat" is in counterregulation to these waking mechanisms. The longer you're awake, or the less sleep you get night after night, the greater the drive to sleep. In reality, the circadian pacemaker and sleep homeostat interact dynamically, tipping the balance toward sleep at night and waking during the day. Even though your circadian system may be promoting wakefulness at the right time of day, if you have too great a sleep debt, your ability to function will be compromised. You will experience problem sleepiness, with its attendant risk for reductions in attention, recall and cognitive throughput, and increased errors and uncontrolled sleep attacks [National Heart, Lung, Blood Institute and National Center on Sleep Disorders Research Working Group, 1999]. My message to psychiatrists and other physicians is simple: Take sleepiness seriously in patients or yourself, as it may have a basis in sleep pathology. Problem sleepiness poses a risk to the patient's safety, (e.g., while driving) and quality of life (e.g., attending school or work).

PT: What do recent studies tell us about the functions of REM [rapid eye movement] and non-REM sleep?

Dinges: There is accumulating evidence from animal and human studies that long-term memory consolidation may be one of the primary activities during REM sleep. Without adequate REM sleep, it appears that some memories from the preceding day do not get consolidated.

In contrast, the functions of non-REM sleep remain unknown, although it has been suggested that non-REM has a priority role in recovery. But what's recovered? One theory posits that sleep restores glycogen depleted during waking [Benington and Heller, 1995]. The neurobiological functions of non-REM and REM sleep will likely be discovered in the next five years as the field of basic sleep science completes elucidation of the molecules and brain sites involved in the different sleep states.

There may be parallel functions for sleep in recovery or calibration in emotional processing. However, the relationship of sleep to affect is poorly understood. There is indirect evidence that emotional stability may be a function of obtaining adequate sleep. There is much comorbidity between insomnia and depression. Insomnia symptoms appear to be a risk factor for developing clinically significant depression [Ford and Kamerow, 1989]. Sleep deprivation can acutely relieve depression in some patients and trigger mania in many bipolar patients [Wu and Bunney, 1990]. We've not been able to explain these unexpected effects of sleep loss, but they suggest that the link between loss of sleep and emotional valence may be fundamental to the neurobiology of each. Now we can speculate that every night sleep rebuilds, metaphorically at least, cognitive and emotional capabilities.

Sleep may serve important functions for other physiological systems [Dinges and Chugh, 1997], including immune system integrity and responses. Some of the molecules that turn sleep on-cytokines such as interleukin-1-are active when we develop fever. They not only produce the febrile response, but they also make us sleepy and alter sleep responses [Krueger and Majde, 1994]. There is also evidence that sleep deprivation, especially chronic, may compromise host defense against infection from endogenous pathogens [Everson, 1993]. Therefore sleep may be protective immunologically, either directly or indirectly.

The lethal effects of chronic sleep deprivation have been well-documented in rodents using a yoked control paradigm [Rechtschaffen et al., 1983]. From this model there is evidence that sleep loss involves a progression of ever greater physical debilitation which apparently does not involve failure of a vital organ. Rather, it compromised physiological adaptation reflected in disturbances in thermoregulatory, metabolic and immune systems [Dinges and Chugh, 1997]. Neuroimaging studies of the brains of sleep-deprived rodents, experimentally sleep-deprived humans and patients with fatal familial insomnia [Medori et al., 1992] reveal marked hypometabolism in thalamic regions, among other areas, of the wake brain [Dinges and Chugh, 1997]. Since the thalamus is actively involved with the cortex and reticular formation in the initiation and maintenance of non-REM sleep, these imaging studies may suggest a sustained pressure for, if not outright co-occurrence of, aspects of sleep in the presence of waking.

Sleep may help maintain a range of functions involving health and adaptive behavior. Yet it remains for many people undervalued relative to its role in waking functions. We have had success in making people aware of sleep problems, like obstructive sleep apnea and the ability of medicine to treat these conditions. However, we still have a long way to go to get physicians and patients to understand that identification, prevention and treatment of sleepiness, regardless of its cause, is essential for full behavioral health. The widespread tolerance of sleepiness as an acceptable consequence of modern life, and the failure to appreciate its potentially devastating neurobehavioral effects on children, adolescents, adults and the elderly is an ongoing crisis. As the core specialty for behavioral health, psychiatry has a pivotal role to play in educating the public about sleep, sleep disorders and problem sleepiness. However, too few psychiatrists obtain training in sleep.

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