Sleep is defined as unconsciousness from which the person can be aroused by sensory or other stimuli. It is to be distinguished from coma, which is uncon-sciousness from which the person cannot be aroused. There are multiple stages of sleep, from very light sleep to very deep sleep; sleep researchers also divide sleep into two entirely different types of sleep that have different qualities, as follows.
Two Types of Sleep. During each night, a person goes through stages of two typesof sleep that alternate with each other. They are called (1) slow-wave sleep, because in this type of sleep the brain waves are very strong and very low fre-quency, as we discuss later, and (2) rapid eye movement sleep(REM sleep), because in this type of sleep the eyes undergo rapid movements despite the fact that the person is still asleep.
Most sleep during each night is of the slow-wave variety; this is the deep, restful sleep that the person experiences during the first hour of sleep after having been awake for many hours. REM sleep, on the other hand, occurs in episodes that occupy about 25 per cent of the sleep time in young adults; each episode normally recurs about every 90 minutes. This type of sleep is not so restful, and it is usually associated with vivid dreaming.
Most of us can understand the characteristics of deep slow-wave sleep by remembering the last time we were kept awake for more than 24 hours and then the deep sleep that occurred during the first hour after going to sleep. This sleep is exceedingly restful and is associated with decrease in both peripheral vascular tone and many other vegetative functions of the body. For instance, there are 10 to 30 per cent decreases in blood pressure, respiratory rate, and basal metabolic rate.
Although slow-wave sleep is frequently called “dreamless sleep,” dreams and sometimes even nightmares do occur during slow-wave sleep. The difference between the dreams that occur in slow-wave sleep and those that occur in REM sleep is that those of REM sleep are associated with more bodily muscle activity, and the dreams of slow-wave sleep usually are not remembered. That is, during slow-wave sleep, consolidation of the dreams in memory does not occur.
In a normal night of sleep, bouts of REM sleep lasting 5 to 30 minutes usually appear on the average every 90 minutes. When the person is extremely sleepy, each bout of REM sleep is short, and it may even be absent. Conversely, as the person becomes more rested through the night, the durations of the REM bouts increase.
There are several important characteristics of REM sleep:
1.It is usually associated with active dreaming and active bodily muscle movements.
2.The person is even more difficult to arouse by sensory stimuli than during deep slow-wave sleep, and yet people usually awaken spontaneously in the morning during an episode of REM sleep.
3.Muscle tone throughout the body is exceedingly depressed, indicating strong inhibition of the spinal muscle control areas.
4.Heart rate and respiratory rate usually become irregular, which is characteristic of the dream state.
5.Despite the extreme inhibition of the peripheral muscles, irregular muscle movements do occur. These are in addition to the rapid movements of the eyes.
6.The brain is highly active in REM sleep, and overall brain metabolism may be increased as much as 20 per cent. The electroencephalogram (EEG) shows a pattern of brain waves similar to those that occur during wakefulness. This type of sleep is also called paradoxical sleep because it is a paradox that a person can still be asleep despite marked activity in the brain.
In summary, REM sleep is a type of sleep in which the brain is quite active. However, the brain activity is not channeled in the proper direction for the person to be fully aware of his or her surroundings, and there-fore the person is truly asleep.
Sleep Is Believed to Be Caused by an Active Inhibitory Process.
An earlier theory of sleep was that the excitatory areas of the upper brain stem, the reticular activating system, simply fatigued during the waking day and became inactive as a result. This was called the passive theoryof sleep. An important experiment changed this viewto the current belief that sleep is caused by an activeinhibitory process: it was discovered that transectingthe brain stem at the level of the midpons creates a brain whose cortex never goes to sleep. In other words, there seems to be some center located below the mid-pontile level of the brain stem that is required to cause sleep by inhibiting other parts of the brain.
Neuronal Centers, Neurohumoral Substances, and Mechanisms That Can Cause Sleep— A Possible Specific Role for Serotonin
Stimulation of several specific areas of the brain can produce sleep with characteristics near those of natural sleep. Some of these areas are the following:
1.The most conspicuous stimulation area for causing almost natural sleep is the raphe nuclei in thelower half of the pons and in the medulla.Thesenuclei are a thin sheet of special neurons located in the midline. Nerve fibers from these nuclei spread locally in the brain stem reticular formation and also upward into the thalamus, hypothalamus, most areas of the limbic system, and even the neocortex of the cerebrum. In addition, fibers extend downward into the spinal cord, terminating in the posterior horns where they can inhibit incoming sensory signals, including pain. It is also known that many nerve endings of fibers from these raphe neurons secrete serotonin. When a drug that blocks the formation of serotonin is administered to an animal, the animal often cannot sleep for the next several days. Therefore, it has been assumed that serotonin is a transmitter substance associated with production of sleep.
2.Stimulation of some areas in the nucleus of thetractus solitarius can also cause sleep. This nucleusis the termination in the medulla and pons for visceral sensory signals entering by way of the vagus and glossopharyngeal nerves.
3.Stimulation of several regions in the diencephalon can also promote sleep, including (1) the rostral part of the hypothalamus, mainly in the suprachiasmal area, and (2) an occasional area in the diffuse nuclei of the thalamus.
Lesions in Sleep-Promoting Centers Can Cause Intense Wake-fulness. Discrete lesions in theraphe nucleilead to ahigh state of wakefulness. This is also true of bilateral lesions in the medial rostral suprachiasmal area in theanterior hypothalamus. In both instances, the excita-tory reticular nuclei of the mesencephalon and upper pons seem to become released from inhibition, thus causing the intense wakefulness. Indeed, sometimes lesions of the anterior hypothalamus can cause such intense wakefulness that the animal actually dies of exhaustion.
Other Possible TransmitterSubstances Related to Sleep.
Experiments have shown that the cerebrospinal fluid as well as the blood or urine of animals that have been kept awake for several days contains a substance or substances that will cause sleep when injected into the brain ventricular system of another animal. One likely substance has been identified as muramyl peptide, a low-molecular-weight substance that accumulates in the cerebrospinal fluid and urine in animals kept awake for several days. When only micrograms of this sleep-producing substance are injected into the third ventricle, almost natural sleep occurs within a few minutes, and the animal may stay asleep for several hours. Another substance that has similar effects in causing sleep is a nonapeptide isolated from the blood of sleeping animals. And still a third sleep factor, not yet identified molecularly, has been isolated from the neuronal tissues of the brain stem of animals kept awake for days. It is possible that prolonged wakeful-ness causes progressive accumulation of a sleep factor or factors in the brain stem or in the cerebrospinal fluid that lead to sleep.
Possible Cause of REM Sleep. Why slow-wave sleep isbroken periodically by REM sleep is not understood. However, drugs that mimic the action of acetylcholine increase the occurrence of REM sleep. Therefore, it has been postulated that the large acetylcholine-secreting neurons in the upper brain stem reticular for-mation might, through their extensive efferent fibers, activate many portions of the brain. This theoretically could cause the excess activity that occurs in certain brain regions in REM sleep, even though the signals are not channeled appropriately in the brain to cause normal conscious awareness that is characteristic of wakefulness.
Cycle Between Sleep and Wakefulness
The preceding discussions have merely identified neuronal areas, transmitters, and mechanisms that are related to sleep. They have not explained the cyclical, reciprocal operation of the sleep-wakefulness cycle. There is as yet no explanation. Therefore, we can let our imaginations run wild and suggest the following possible mechanism for causing the sleep-wakefulness cycle.
When the sleep centers are not activated, the mes-encephalic and upper pontile reticular activating nuclei are released from inhibition, which allows the reticular activating nuclei to become spontaneously active. This in turn excites both the cerebral cortex and the peripheral nervous system, both of which send numerous positive feedback signals back to the same reticular activating nuclei to activate them still further. Therefore, once wakefulness begins, it has a natural tendency to sustain itself because of all this positive feedback activity.
Then, after the brain remains activated for many hours, even the neurons themselves in the activating system presumably become fatigued. Consequently, the positive feedback cycle between the mesen-cephalic reticular nuclei and the cerebral cortex fades, and the sleep-promoting effects of the sleep centers take over, leading to rapid transition from wakefulness back to sleep.
This overall theory could explain the rapid transi-tions from sleep to wakefulness and from wakefulness to sleep. It could also explain arousal, the insomnia that occurs when a person’s mind becomes preoccu-pied with a thought, and the wakefulness that is pro-duced by bodily physical activity.
Sleep causes two major types of physiologic effects: first, effects on the nervous system itself, and second, effects on other functional systems of the body. The nervous system effects seem to be by far the more important because any person who has a transected spinal cord in the neck (and therefore has no sleep-wakefulness cycle below the transection) shows no harmful effects in the body beneath the level of transection that can be attributed directly to a sleep-wakefulness cycle.
Lack of sleep certainly does, however, affect the functions of the central nervous system. Prolonged wakefulness is often associated with progressive mal-function of the thought processes and sometimes even causes abnormal behavioral activities.
We are all familiar with the increased sluggishness of thought that occurs toward the end of a prolonged wakeful period, but in addition, a person can become irritable or even psychotic after forced wakefulness. Therefore, we can assume that sleep in multiple ways restores both normal levels of brain activity and normal “balance” among the different functions of the central nervous system. This might be likened to the “rezeroing” of electronic analog computers after pro-longed use, because computers of this type gradually lose their “baseline” of operation; it is reasonable to assume that the same effect occurs in the central nervous system because overuse of some brain areas during wakefulness could easily throw these areas out of balance with the remainder of the nervous system.
We might postulate that the principal value of sleepis to restore natural balances among the neuronal centers. The specific physiologic functions of sleepremain a mystery, and they are the subject of much research.
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