States of Brain Activity—Sleep, Brain Waves, Epilepsy, Psychoses, and Dementia

All of us are aware of the many different states of brain activity, including sleep, wakefulness, extreme excitement, and even different levels of mood such as exhilaration, depression, and fear. All these states result from different activating or inhibiting forces generated usually within the brain. In Chapter 59 , we began a partial discussion of this subject when we described different systems that are capable of activating large portions of the brain. In this chapter, we present brief surveys of specific states of brain activity, beginning with sleep.

Sleep

Sleep is defined as unconsciousness from which a person can be aroused by sensory or other stimuli. It is to be distinguished from coma, which is unconsciousness from which a 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 described in the following section.

Two Types of Sleep—Slow-Wave Sleep and Rapid Eye Movement Sleep

Each night, a person goes through stages of two major types of sleep that alternate with each other ( Figure 60-1 ). These types are called (1) rapid eye movement sleep (REM sleep), in which the eyes undergo rapid movements even though the person is still asleep, and (2) slow-wave sleep or non-REM (NREM) sleep , in which the brain waves are strong and of low frequency, as we discuss later.

Figure 60-1, Progressive change in the characteristics of the brain waves during alert wakefulness, rapid eye movement (REM) sleep, and stages one through four of sleep.

REM sleep occurs in episodes that occupy about 25% 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 often associated with vivid dreaming. Most sleep during each night is of the slow-wave (NREM) variety, which is the deep, restful sleep that the person experiences during the first hour of sleep after having been awake for many hours.

REM (Paradoxical, Desynchronized) Sleep

In a normal night of sleep, bouts of REM sleep lasting 5 to 30 minutes usually appear on average every 90 minutes in young adults. When a person is extremely sleepy, each bout of REM sleep is short and may even be absent. As the person becomes more rested through the night, the durations of the REM bouts increase.

REM sleep has several important characteristics:

1.
It is an active form of sleep usually associated with 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 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%. An 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 the presence of marked activity in the brain.

In summary, REM sleep is a type of sleep in which the brain is quite active. However, the person is not fully aware of the surroundings and therefore is truly asleep.

Slow-Wave Sleep

We can understand the characteristics of deep slow-wave sleep by remembering the last time we were kept awake for more than 24 hours and the deep sleep that occurred during the first hour after going to sleep. This sleep is exceedingly restful and is associated with decreases in peripheral vascular tone and many other vegetative functions of the body. For example, 10% to 30% decreases occur 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. Also, the dreams of slow-wave sleep are usually not remembered because consolidation of the dreams in memory does not occur.

Basic Theories of Sleep

Sleep Is 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 became fatigued during the waking day and became inactive as a result. An important experiment changed this thinking to the current view that sleep is caused by an active inhibitory process, because it was discovered that transecting the brain stem at the level of the midpons creates a brain cortex that never goes to sleep. In other words, a center located below the midpontile level of the brain stem appears to be required to cause sleep by inhibiting other parts of the brain.

Neuronal Centers, Neurohumoral Substances, and Mechanisms That Can Cause Sleep—Possible 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 raphe nuclei in the lower half of the pons and in the medulla is the most conspicuous stimulation area for causing almost natural sleep. These nuclei comprise 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, as discussed in Chapter 49 . 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 the production of sleep.
2.
Stimulation of some areas in the nucleus of the tractus solitarius can also cause sleep. This nucleus is the termination in the medulla and pons for visceral sensory signals entering by way of the vagus and glossopharyngeal nerves.
3.
Sleep can be promoted by stimulation of several regions in the diencephalon , 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 Wakefulness

Discrete lesions in the raphe nuclei lead to a high state of wakefulness. This phenomenon is also true of bilateral lesions in the medial rostral suprachiasmal area in the anterior hypothalamus. In both cases, the excitatory reticular nuclei of the mesencephalon and upper pons seem to become released from inhibition, thus causing intense wakefulness. Indeed, sometimes lesions of the anterior hypothalamus can cause such intense wakefulness that the animal actually dies of exhaustion.

Other Possible Transmitter Substances Related to Sleep

Experiments have shown that the cerebrospinal fluid and the blood or urine of animals that have been kept awake for several days contain 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 delta sleep–inducing peptide , a nonapeptide found in the cerebrospinal fluid after electrical stimulation of the thalamus to induce sleep. Several other potential sleep factors, mostly peptides, have been isolated from the cerebrospinal fluid or neuronal tissues of the brain stem of animals kept awake for days. It is possible that prolonged wakefulness causes progressive accumulation of a sleep factor or factors in the brain stem or cerebrospinal fluid that lead(s) to sleep.

Possible Cause of REM Sleep

It is not understood why slow-wave sleep is broken periodically by REM sleep. 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 formation might, through their extensive efferent fibers, activate many portions of the brain. This mechanism theoretically could cause the increased 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 definitive explanation. Therefore, we might suggest the following possible mechanism for causing the sleep-wakefulness cycle.

When the sleep centers are not activated, the mesencephalic and upper pontile reticular activating nuclei are released from inhibition, which allows the reticular activating nuclei to become spontaneously active. This spontaneous activity 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 in the activating system presumably become fatigued. Consequently, the positive feedback cycle between the mesencephalic 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 transitions from sleep to wakefulness and from wakefulness to sleep. It could also explain arousal—that is, the insomnia that occurs when a person’s mind becomes preoccupied with a thought—and the wakefulness that is produced by bodily physical activity.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here