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sleep, resting state in which an individual becomes relatively quiescent and relatively unaware of the environment. During sleep, which is in part a period of rest and relaxation, most physiological functions such as body temperature, blood pressure, and rate of breathing and heartbeat decrease. However, sleep is also a time of repair and growth, and some tissues, e.g., epithelium, proliferate more rapidly during sleep. Sleep also aids in the strengthening of memories, and researchers have discovered that an increased circulation of fluids in the brain during sleep removes waste products from the brain.
In humans, sleep occurs in cyclical patterns; in each cycle of 11-2 to 2 hr, the sleeper moves through four stages of sleep, from Stage 1 to Stage 4, and back again to Stage 1. In the first stage, low-frequency, low-amplitude theta waves characterize brain activity. The stage usually lasts only several minutes, before the individual drifts into Stage 2 sleep, and the brain moves into low-frequency, high-amplitude waves. Stage 3 signals an increase of low-frequency, high-amplitude delta waves, and at Stage 4 sleep these delta waves account for more than half of all brain wave activity (see electroencephalography). Rapid-eye-movement (REM) sleep occurs during Stage 1 sleep at the end of each cycle, and people woken up at this time usually report that they have been dreaming. Dream deprivation or sleep deprivation results in detrimental changes in personality, perceptual processes, and intellectual functioning. There is some evidence that emotional and environmental deprivation disrupts the sleep patterns of young children, which in turn inhibits the secretion of growth hormone, normally secreted maximally during sleep.
The amount of sleep needed depends on both the individual and the environment: For instance, worrying, critical individuals tend to need both more sleep and more dream sleep than easygoing ones, and stress and worry during the day result in an increase in REM sleep. It has been hypothesized that while deeper stages of sleep are physically restorative, REM sleep is psychically restorative. REM sleep is also believed to integrate new information in the brain and to reactivate the sleeping brain without waking the sleeper. There is evidence that the hypothalamus and thalamus of the brain initiate sleep and that part of the midbrain acts as an arousal system. See also dream; insomnia; narcolepsy; sleep apnea.
in man and higher animals, a periodic physiological state of the brain and body outwardly manifested by inertia and reduced responsiveness to external stimuli. During sleep, conscious mental activity is subjectively inhibited, although it is restored from time to time during dreams, which are subsequently often forgotten. Periods of inactivity are characteristic of lower animals, but the extent to which they correspond functionally to the sleep exhibited by higher animals has not been determined.
Physiological manifestations. Research that has been conducted since the 1950’s on the internal organization and mechanisms of sleep has relied chiefly on electrophysiological methods to reveal that sleep is not a single homogeneous state but a series of at least two states (sleep phases). The states differ sharply in manifestations, brain mechanisms, and functions and are still not completely understood. Scientists who have done research in this area include the American scientists N. Kleitman, E. Aserinsky, and W. Dement and the French scientist M. Jouvet.
The first sleep phase—nonrapid-eye-movement sleep (NREM sleep)—is characterized by a shift in the electroencephalogram (EEG) in the form of a slowing of the rhythm of oscillations of the potential. In man, a regular succession of changes in physiological parameters permit four stages to be distinguished in NREM sleep. (In animals, the differentiation of stages is less pronounced.) The first stage—drowsiness—is manifested by the inhibition of the main rhythm of calm wakefulness (alpha rhythm at a frequency of 8-13 oscillations per sec) and the replacement of the main rhythm by a flattened EEG curve in the form of a slightly oscillating, almost straight line against a background of slow- and fast-frequency low-amplitude oscillations. The oscillations are sometimes in the form of distinct rhythms in frequency ranges of 5-6 and 18-35 oscillations per sec. The second stage—sleep spindling—is the onset of sleep proper. It is distinguished by the appearance in the EEG of a spindle-like short series of waves in the beta rhythm at a frequency of 13-16 oscillations per sec. The waves are sometimes combined with sharp waves (diphasic slow-frequency, high-amplitude waves, or the K-complex). The third stage is marked by regular slow waves (delta rhythm at a frequency of 1-4 oscillations per sec) with some spindling superimposed. In the fourth stage slow high-amplitude waves at a frequency of 0.5-2 oscillations per sec are dominant. The third and fourth stages are often referred to as slow-wave sleep (SWS) or deep sleep.
NREM sleep is characterized by a decrease in skeletal muscle tone (according to electromyographic data). Respiration and heart rates also slow down, although they accelerate somewhat in SWS sleep. The eyes are either motionless or make slow oscillating movements in the first and second stages. When a person is awakened from NREM sleep, he usually denies having experienced mental activity while asleep or (generally in the first and second stages) reports having been engaged in thoughtlike activity, such as pondering the past day’s events. Dreaming is rare. In SWS sleep such manifestations of unconscious mental activity as sleepwalking (somnambulism), sleeptalking, and nightmares in children may occur, of which nothing is recalled upon awakening. The effectiveness of arousal in the NREM phase diminishes from the first to fourth stages, resulting in a steady deepening of sleep in these stages.
The second phase of sleep is known as rapid-eye-movement sleep (REM sleep), fast sleep, active sleep, or paradoxical sleep. It is characterized by a unique combination of manifestations of deep sleep and superficial sleep. In this phase the EEG reflects the transition from a slow to a more rapid low-amplitude rhythm similar to the first stage of NREM sleep and even wakefulness. Under normal conditions, REM sleep occurs after the period of NREM sleep and is characterized by tonic (stable) and phasic (brief) manifestations. Tonic manifestations include the above-described change in the EEG, a sharp decrease in the tone of the neck muscles, the inhibition of cerebrospinal reflexes, and an increase in cerebral blood flow. Experiments on animals have also revealed that the brain temperature rises and a characteristic regular rhythm develops in the brain’s limbic system. Phasic manifestations include sawtooth discharges in the EEG, rapid eye movements (solitary or grouped together), twitching of the muscles of the face and extremities, irregular cardiac and respiratory rhythms, and increases in blood pressure.
Unusual manifestations of the activity of a cat’s brain have been revealed by attached electrodes. The manifestations are in the form of surges of potential, or pontogeniculo-occipital peaks, which arise in the pons reticular formation and spread to the subcortical and cortical parts of the visual system. Of those awakened from REM sleep, 80-90 percent describe dreams characterized by coherent, vivid and life-like visual images with elements of unreality and fantasy that are usually without any direct bearing on the events of the preceding day.
Temporal organization. NREM and REM sleep phases constitute a sleep cycle lasting 90-100 min that recurs three to five times a night during normal sleep. In the initial cycles, NREM sleep encompasses all its stages and REM sleep is brief. The first period of REM sleep usually occurs 60-90 min after falling asleep and lasts several min. SWS sleep decreases in duration in subsequent cycles until it does not occur at all in the morning sleep cycles, and REM sleep lengthens considerably.
The cycle of NREM and REM sleep is a manifestation of one of the basic biological rhythms of the body. The two sleep phases and the cyclicity of sleep are characteristic of all warm-blooded animals, including mammals and birds, with the exception of echidnas. Cycles of NREM and REM sleep are virtually identical from marsupials to man.
The sleep of newborns is characterized by multiple phases and consists primarily of REM sleep. NREM sleep develops toward the end of the second or the beginning of the third week of life. As children grow, their sleep gradually becomes monophasic and clearly confined to a particular period of the daily biorhythm. REM sleep becomes briefer, and by the age of 10–15 years it constitutes an average of 20 percent of the total sleep time, as it does in adults. The length of REM sleep remains unchanged until the age of 60-70 years, when it again decreases. NREM sleep, including SWS sleep, increases in duration during childhood simultaneously with the decrease in REM sleep. SWS sleep constitutes 25 percent of sleep time during this period. Between the ages of 20 and 30 SWS sleep steadily decreases in length until it completely disappears in old age.
SWS sleep and REM sleep are very important factors in the integral activity of the brain. The brain responds to the selective elimination of a phase by compensatory increases in the deprived phase, which is manifested by an increase in the duration of the phase in the initial recovery periods of sleep. Total sleep deprivation results in a decrease in work capacity and in mental disturbances, including hallucinations. In the recovery period, there is a compensatory increase in SWS sleep and then in REM sleep.
Mechanisms. Sleep arises from a ramified system of neuronal structures embracing virtually all parts of the brain, with different parts of the system performing different functions. The mechanisms directly responsible for inducing NREM sleep are associated with the medulla oblongata and thalamus; they are called synchronizing mechanisms. The mechanisms that directly induce REM sleep are associated with the pons reticular formation.
The onset of both NREM and REM sleep depends on the activity of neurons located in the brainstem. These neurons influence other neurons (specifically, those in the higher parts of the brain) through the chemical transmitter serotonin. Neuronal structures located at the base of the prosencephalon and diencephalon play a special role in the mechanisms governing the natural alternation of wakefulness and sleep phases. Signals from various parts of the brain as well as from the external and internal environments may affect sleep through the above-mentioned mechanisms. The activity of individual neurons in different parts of the cerebral cortex and subcortical structures during NREM sleep is almost the same as during calm wakefulness. The activity is more intense during REM sleep, that is, it is comparable to neuronal activity during active wakefulness. The fact that the brain is active during sleep is also evidenced by increases in cerebral blood flow and oxygen absorption during NREM sleep and especially during REM sleep.
Despite their qualitative differences, the mechanisms of sleep and wakefulness constitute a single self-regulating functional system that enables the body to adapt to the various conditions of existence.
Theories. The principal theories of sleep as an interruption in the activity of the nerve cells (neurons) of the brain are being substantially reappraised on the basis of recent findings on the processes and cerebral mechanisms of sleep. One of these theories is based on the toxic origin of sleep. The French scientists R. Legendre and H. Pieron theorized that wakefulness is accompanied by the body’s formation of special substances—hypnotoxins—that poison brain cells and thereby induce sleep. During sleep the body supposedly frees itself from these substances. In the 1970’s, the hypnotoxin theory was partially revived after substances of a polypeptide nature were isolated from the blood of a sleeping animal; injection of the substances into another animal caused it to fall asleep quickly.
According to I. P. Pavlov’s theory of diffuse cortical inhibition, sleep is caused by the inhibition of the neurons of the cerebral hemispheres and subcortical structures. The inhibition spreads from a specific part of the cortex, where internal inhibition develops as a result of conditioned-reflex activity. Although the direct investigation of neuronal activity in higher parts of the brain showed that the onset of sleep is associated with the reorganization of neuronal activity and not its inhibition, this theory was important in the analysis of the participation of external conditions in the onset of sleep and the identification of the role of the cerebral cortex.
In the 1920’s a theory was advanced that linked the alternation of sleep and wakefulness to the activity of a special sleep-inducing center in the diencephalic structures, including the hypothalamus and thalamus. This theory was proposed by the Austrian scientist C. von Economo, who conducted clinical and anatomical observations of individuals with lethargic encephalitis. The theory was also based on experiments conducted by the Swiss scientist W. Hess on the direct electrostimulation of animal diencephalic structures through attached electrodes. The role of the hypothalamicohypophyseal system in the origin of sleep was demonstrated by the Soviet scientist A. V. Tonkikh. The theory’s shortcomings were associated with its attempt to correlate a complex function with a specific brain center. Nevertheless, the theory of a sleep center was the starting point for modern sleep research. The theory emphasized the unequal participation of different parts of the brain in the onset of sleep and the relationship between sleep and the active state of some of these parts. Subsequent studies by F. Bremer of Belgium, H. Magoun of the USA, and G. Moruzzi of Italy helped elucidate the function of the reticular formation of the brainstem in maintaining wakefulness. These studies became the basis of a theory that linked the onset of sleep to the suppression of the ascending influences of the reticular formation that activate the higher parts of the brain. However, the onset of sleep depends not so much on the inhibition of the cerebral apparatus controlling wakefulness as it does on the activity of special hypnogenic mechanisms.
All the theories mentioned above regard sleep as a state of rest and an interlude in neuronal activity during which neurons are inhibited, producing a regeneration of the energy resources spent during the period of wakefulness. However, the results of the direct study of the activity of cerebral neurons and many energy parameters, including cerebral blood flow and O2 absorption, contradict this view. Since the 1960’s attention has been drawn to the idea of sleep as an integral brain activity uniquely organized and associated with the analysis of information obtained during the preceding period of wakefulness. It is believed that during sleep the brain assesses, screens, and transfers information to long-term memory, reorganizes and improves existing brain programs on the basis of this information, and develops psychological-defense mechanisms to cope with emotional stress. Although this theory has not been proven, it is supported by the results of research on the influence of different types of sleep on the learning process, memory, and emotional reactions.
Other theories have also been proposed on the nature of sleep. For example, theories exist that associate sleep with biosynthesis processes in the brain (chiefly of proteins and nucleic acids) and with the training of the oculomotor system.
REFERENCESAnokhin, P. K. Biologiia i neirofiziologüa uslovnogo refleksa. Moscow, 1968.
Latash, L. P. Gipotalamus, prisposobitel’naia aktivnost’ i elektroentsefalogramma. Moscow, 1968.
Vein, A. M. Bodrstvovanie i son. Moscow, 1970.
Shepoval’nikov, A. N. Aktivnost’ spiashchego mozga. Leningrad, 1971.
Sleeping Brain. Edited by M. H. Chase. Los Angeles, 1972.
Jouvet, M. “Neurophysiology of the States of Sleep.” Physiological Review, 1967, vol. 47, no. 2.
Jouvet, M. “Some Monoaminergic Mechanisms Controlling Sleep and Waking.” In Brain and Human Behavior. Heidelberg-New York, 1972. Pages 131-60.
Sleep, Physiology and Pathology. Philadelphia-Toronto, 1969.
Koella, W. P. Sleep. Springfield, 111., 1967.
Basic Sleep Mechanisms. Edited by O. Petre-Quadens and J. Schlag. New York-London, 1974.
Sleep disturbances are not independent diseases but the consequences of various factors, most often neuroses. They are associated with 80 percent of all cases of neuroses. Emotional instability, anxiety, depression, fear, and excessive fatigue contribute significantly to the development of sleep disturbances. Other causative factors may be schizophrenia, manic-depressive psychosis, and other mental diseases, many neurological diseases, diseases of the internal organs and endocrine system, metabolic disturbances accompanied by pain, the poisoning of the nervous system, and a decrease in the oxygen saturation of the brain. Apparently healthy individuals also suffer from sleep disturbances. The populations of economically developed countries are apt to suffer from different forms of insomnia as a result of the nervous tension brought on by modern life-styles.
Pathologically excessive sleep, or hypersomnia, is a characteristic manifestation of various diseases. Narcolepsy is a condition characterized by attacks of uncontrollable sleepiness, nightmares while falling asleep, and poor sleep at night. Pickwickian syndrome (cardiopulmonary insufficiency associated with obesity) is accompanied by constant drowsiness during the day and sleep disturbances at night. Lethargy is manifested either by daytime sleep from which arousal is impossible or by hypersomnia. In the latter case, a lethargic individual usually awakens to eat or perform physiological functions.
The treatment of sleep disturbances depends on the nature of the main disease. Emotional stability must be achieved through the proper organization of work and rest, the use of psychotropic drugs, and psychotherapy. Hypnotics are used only in conjunction with causal treatment and only when prescribed by a physician. It is best to start and continue as long as possible with small doses of the weakest hypnotics. Individual techniques for falling asleep should be devised. Narcolepsy is treated with preparations that stimulate brain activity, and the principal means of treating pickwickian syndrome is by losing weight. Periodic somnolence of a psychogenic nature is treated as a neurosis. In cases of lethargy resulting from an organic brain affection, the underlying disease is treated.
REFERENCEVein, A. M. Narusheniia sna i bodrstvovaniia. Moscow, 1974.
A. M. VEIN
sleep(operating system, multitasking)
The alternative is to poll or "busy wait" for the event but this uses processing power.
Also used in the phrase "sleep on" (or "block on") some external event, meaning to wait for it.
E.g. the Unix command of the same name which pauses the current process for a given number of seconds.
sleep(1) An inactive state. See sleep mode.
(2) A delay in processing. In a programming language, a sleep statement creates a delay for a specified period of time.
(3) An inactive state of a program. The program resumes processing after receiving a signal.