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Scientific Dream Interpretation and Analysis |
SP r = √SSxSSy |
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Scientific Dream Interpretation and Analysis |
SP r = √SSxSSy |
We spend about one third of our lives sleeping. And when we are not sleeping, many of us want to be! We organize our time, our work, our relationships to meet the demands of sleep. Research and personal experience strongly suggest that sleep, or the lack thereof, has an significant impact on general health. According to surveys conducted by the National Sleep Foundation, more than 40 percent of adults experience daytime sleepiness severe enough to interfere with their daily activities at least a few days each month, while 20 percent report problem sleepiness a few days a week or more. Most of us are familiar with the powerful need for sleep. But does the body need sleep, in the way that it needs food and water? If so, why? Major questions about the nature of sleep, including what happens during sleep and what are the mechanisms of sleep, remain largely unanswered. But some progress has been made.
Until the 1950s, sleep was considered a state of inactivity. The brain was thought to be "turned off", and the body rested. We now know that the sleeping brain is equally and sometimes more active than the waking brain. Sleep, as well as wakefulness, is generated by the discharge of specific neurons in certain parts of the brain. Neurotransmitters produced in the brainstem, such as serotonin and norepinephrine, appear to play a role in keeping parts of the brain active while we are awake. As we fall asleep, neurons at the base of the brain begin firing and appear to "switch off" the signals that keep us awake. Research also suggests that adenosine builds up in our blood while we are awake and causes drowsiness, then gradually breaks down while we sleep.
Wall
In 1952 Eugene Aserinsky was a graduate student in the laboratory of Nathaniel Kleitman at the University of Chicago, where EEG recordings were being made from adults as they fell asleep. These revealed that after falling asleep, the EEG gradually changed from a desynchronized , low-voltage trace to a high-voltage trace with slow synchronized oscillations. At this point, it was assumed that deep sleep had been achieved and this status would be maintained until waking. The standard operating procedure was to record for 30 - 45 minutes to capture this transition and then turn the EEG recorder off to save chart paper. One night Aserinsky brought his son Armond, 8 years old, into the lab to be the subject. About 45 minutes after Armond had fallen asleep, his father was watching the pens on the EEG chart recorder register the slow oscilltations of deep sleep. Then, amazingly, the EEG shifted to another rhythm that looked more like waking even though Armond was still clearly sleeping and was totally immobile. We now know this stage of sleep is associated with rapid eye movements (REMs) and that while it usually does not occur in adults until about 90 minutes after falling asleep, in children, like Armond, it occurs sooner.
Linden
At least two distinct phases of sleep have been identified. During rapid eye movement (REM) sleep, synchronous rapid eye movements are seen, muscle atonia occurs, and the activity of the autonomic nervous system is irregular and accelerated. Non-REM (NREM) sleep displays lower, but not nonexistent, central nervous system activity, as seen in a slower and more regular EEG pattern. Clearly, sleep is an active and dynamic state.
Animal studies show that sleep is necessary for survival. For example, while rats normally live for two to three years, those deprived of REM sleep survive only about five weeks on average. Rats deprived of all sleep stages live only about three weeks. Sleep-deprived rats also develop low body temperatures and sores on their tails and paws. The sores may develop because the rats' immune systems become impaired. So the evidence suggests that there is a function of sleep other than to prevent sleepiness, just as there is a function of eating other than to prevent hunger.
Wall
Wake-Sleep Transition: As we lie down and close our eyes, (if we are tired) we begin to de-activate and move into low voltage, mixed-frequency EEG brain activity. People awakened from this sleep stage often report just barely being asleep, or just about to fall asleep.
Not too hard to wake people here, but they usually report being really asleep. Lasts 10-20 minutes
More slow-wave activity in the EEG readings and overall neuronal activity at it lowest. Brain temperatures lowest and sympathetic outflow, heart rate and blood pressure down. Stages 3 and 4 in humans are sometimes called slow-wave sleep.
Just exactly what starts REM sleep is complex and partially still being investigated. A system of neurons generating the EEG, eye movement, twitches and underlying muscle atonia of REM sleep have been identified in the brainstem . This system utilizes adrenergic (noradrenergic and serotonergic) REM sleep-off neurons, GABAergic, cholinergic, glycinergic and glutamatergic REM sleep-on cells as well as other neurons.
In REM or Rapid Eye Movement sleep, the EEG looks similar to stage 1 NREM and waking. Because it resembles waking, REM is often called "paradoxical" sleep. In REM there are bursts of neural activity, expecially in the Pons. These bursts generate high-voltage spike potentials, the ponto-geniculo-occipital or PGO spikes. The PGO spikes are named after structures in which these spikes are most detected (the pons, lateral geniculate nucleus, and occipital cortex). PGO spikes are one of the phasic or short-lasting events of REM sleep, including eye movements and cardio-respiratory irregularity.
The overall activity of the brain increases, and so the brain temperature and metabolic rate are high, equal to or greater than during the waking state. Atonia occurs (loss of muscle tone or outgoing motor commands to muscles) though small, phasic twitches occur and the skeletal muscles controlling the movements of the eyes, middle ear ossicles, and diaphragm are not atonic. The pupils are constricted (miosis), reflecting the high ratio of parasympathetic to sympathetic output to the pupil. Genital arousal regularly occur during REM sleep. There is a reduction in homeostatic mechanisms. Respiration is relatively unresponsive to changes in blood CO2, and response to heat and cold are absent or greatly reduced. Thus the body temperature drifts toward room temperature as with reptiles.
"EEG dysychronization results from a net tonic increase in reticular, thalamocortical, and cortical neuronal firing rates. PGO waves are the result of tonic disinhibition and phasic excitation of burst cells in the lateral pontomesencephalic tementum. Rapid eye movements are the consequence of phasic firing by reticular and vestivular cells; the latter directly excite oculomotor neurons. Muscular atonia is the consequence of tonic postsynaptic inhibition of spinal anterior horn cells by the pontomedullary reticular formation. " From Hobson et al., 2000 Behavioral and Brain Sciences 23
PGO waves:
In cat studies, oncoming REM seems to come from the lateral geniculate bodies of the thalamus, corresponding to the depolarization of the geniculate neurons by excitatory impulses arising in the pontine brain stem, and depolarization of neurons of the reticular formation and the PPT pedunculopontine region. The PPT, a cholinergically modulated area, is thought to be the origin of the process that initiates REM in the brain stem. signals originate in the pons (P) and radiate to the geniculate bodies (G) and the occipital cortex (O).
REM begins when PGO waves become cholenergically hyperexcitable, a condition that is regulated by the inner circadian clock in the thalamus.
More specifically, the " of serotonergic inhibition and neuromodulation that results from the "Don't Act Now" signals sent down into the pons from the hypothalamic circadian clock. "
This mode of active signals without input/output gating means we have a lot of "fictive movement" or movement hat is centrally commanded but peripherally inhibited.
Wilkerson
A classic view of sleep function is that sleep allows the central nervous system to repair and/or restore itself. According to this theory, sleep allows neurons that are used in wakefulness to shut down and repair themselves. Without sleep, neurons may become depleted in energy or "polluted" with the byproducts of normal cellular activity, and malfunctioning may result. Given the detrimental physical, mental and behavioral effects of lack of sleep, this hypothesis seems intuitively reasonable.
Data to support this hypothesis is scant, but not non-existent. During deep sleep, the secretion of growth hormone occurs in children and young adults. Some cells in the body have shown increased production and reduced breakdown of proteins during deep sleep. Since proteins are needed for cell growth and repair, this may indicate that deep sleep has restorative power. Also, activity in parts of the brain that are known to control emotions, decision-making processes, and social interations is greatly reduced during deep sleep. Thus deep sleep may help maintain optimal emotional and social functioning during wakefulness. A study in rats also showed that certain nerve signaling pathways generated by the rats while awake were repeated during deep sleep. Scientists have theorized that this repitition may play a role in memory and learning.
Research has shown an increased amount of sleep in humans and other mammals after 24 hours of sleep deprivation. However, studies on humans sleeping in constant environments without external time cues show that sleep episodes tend to be shorter following long periods of wakefulness. Studies on the effects of exercise on subsequent sleep also do not appear to support the body restoration hypothesis. According to this theory, one would predict increased sleep following elevated catabolism produced by physical exertion, but studies show no effect on post-exercise sleep. Finally, I wonder, why would the brain get "tired" and need to restore itself any more than, say, the liver?
Energy Conservation HypothesisA second theory is that sleep serves an energy conservation function. According to this hypothesis, the body needs sleep in order to offset the high energy costs of endothermy. Sleep reduces the metabolic rate and body temperature in endothermic animals. When animals fall asleep their metabolic rates decrease by approximately ten percent. Heat is dissipated from the body through peripheral vasodilation, leading to a one to two degree reduction in body temperature. Data in favor of this hypothesis rest on the similarities between hibernation and sleep. Because hibernation has been shown to have an energy conservation function and because hibernation is an extension of some physiological processes of sleep, then it is argued that sleep has an energy conservation function. Furthermore, at lower ambient temperatures, energy savings can be much greater; heat loss from the body increases as the difference in temperature between the body and the environment increases. By sleeping, an animal can keep this temperature difference smaller by lowering the body's metabolic rate (and temperature), which could give an animal an advantage in environments with low ambient temperatures or scarce food sources.
Immune System/Sleep Relationship Hypothesis
A related theory to those above is that sleep may help the body conserve energy and other resources needed by the immune system to attack pathogens. Infections and the ensuing fever often induce sleep because cytokines, chemicals produced by the immune system to fight infection, have sleep-inducing properties. Furthermore, the current view of cytokines is that they are predominantly inflammatory mediators. There is increasing evidence that cytokines are expressed and perform functions in the normal brain. Specifically, blocking interleukin (IL)-1 and tumor necrosis factor (TNF-alpha) in the normal brain alters the regulation of sleep. Researchers are just beginning to unravel the complex interrelationship between the immune system and the sleep function, but the possibilities are intriguing.
Wall
When animals are sleep deprived, a protein known as di-muramyl peptide accumulates in their spinal fluid. The peptides do not originate in the brain. Instead, they come from bacteria in the body, suggesting that sleep deprivation may enable bacterial growth and that sufficient sleep impedes bacterial growth.
What's even more interesting is that these di-muramyl peptides enhance non-REM sleep (but not REM sleep). [REM=rapid eye movements] The peptides also cause fever. The two effects are dissociable, however; the sleep effect is independent of the fever. More interesting still is the fact that the peptides stimulate cells in the brain and the body to produce interleukin-1, a powerful immune-system molecule that promotes the destruction of both bacteria and tumor cells. Highly significant and desirable health effects are mediated by interleukin's ability to encourage the B lymphocytes to produce antibodies, which kill viruses, and to trigger the proliferation of T lymphocytes, which attack microbial invaders. The net effect is to mobilize the body's defensive forces.
It looks as if sleep research has inadvertently stumbled on something of capital importance. By depriving his animals of sleep, Krueger made them more vulnerable to infection, which stimulated their immune system, which made them more sleepy. Having noticed this, it was then possible to show that many immune proteins do, in fact, promote sleep. Taking a shot of sleep for your flu is sounding better and better, isn't it? No needles. No pills. Sleep alone is enough to change the state of the immune system.
Now we return to our first question. Why do we feel sleepy when we have an infection? Perhaps because interleukin-1, a protein that is part of the normal bodily response to infection, is also an effective sedative. Like the peptides, interleukin-1 enhances non-REM sleep. It also increases the size of the EEG waves associated with non-REM sleep. Thus both the length and depth of sleep are increased as an integral part of the body's attempt to repulse microbial invaders. The upshot is that there is a positive, circular interaction between the immune response and sleep. Sleep enhances the immune system, and the immune system enhances sleep.
Invaders are assaulting our body's portals at all times, not just during winter, when we tend to get sick more, and not just during local outbreaks of viruses. This means that the margin of safety of our health - the degree to which we are resistant to infection, and perhaps even cancer - may be determined by how well our sleep state enhances our immune system. The daily sequencing of normal brain-mind states, therefore, mediates our health.
It is non-REM sleep that is enhanced by the chemicals our bodies produce to fight infection. Why is REM sleep absent from the immune response picture? We're not sure, but it seems likely it is because REM sleep involves a loss of temperature control. When we are sick, our body temperature soars and drops, and we cannot risk entering REM sleep and abandoning temperature control.
REM as SupersleepWe have seen how non-REM sleep helps us battle infection. Once we are healthy, however, it seems that REM sleep is the key to staying on top of our game. We have noted thus far that REM sleep serves to restore our energy system. During REM sleep our memory is consolidated and made permanent. During this unique brain-mind state of REM sleep, then, our circuits are being cleared and our battery is being recharged. We wake up with the insight and energy needed to tackle problems that seemed insoluble the night before.
As the conservator of the aminergic system, REM sleep is more than twice as effective as non-REM sleep. The firing rates of neurons containing norepinephrine and serotonin drop to half their waking levels in non-REM sleep, but the output drops by far more than half again in REM sleep. Thus REM sleep is at least five times more conservative of the amines than non-REM sleep and ten times more conservative than waking.
These calculations are based on the assumptions that the release of the chemical modulators is directly proportional to the firing rate of the neurons and that there is no release when the cells don't fire at all. Both assumptions have not been proven directly, but the general conclusion that far fewer amines are released in REM sleep than in either non-REM sleep or waking has been proven by experiments that measure their concentration in the brain. The same methods have also shown reciprocal increases in acetylcholine.
REM, it seems, is some sort of supersleep. The first reason for according it this status is that, although it normally occupies only about 20 percent of the total time we sleep each night, it takes only six weeks of deprivation of REM sleep alone to kill rats compared with four weeks for complete sleep deprivation. Based on its relative duration of only 20 percent of sleep time, we would predict that five times as long a deprivation period would be required if both states were equally life-enhancing. On these terms, one minute of REM sleep is worth five minutes of non-REM sleep.
The second reason supporting the idea of REM as supersleep is one that is attractive for the nappers of the world: there is a surprisingly beneficial nature of short naps if they occur at times in the day when REM sleep probability is high. Daytime naps are different from night sleep in that we may fall directly into a REM period and stay there for the duration of the nap. Since the time of peak REM probability is greatest in the late morning, the tendency of naps to be composed of REM sleep is highest then and falls thereafter till the onset of night sleep (about twelve hours later). The implication is that a little bit of sleep, at the right time of day, may be more useful than the same amount later on.
The third reason is that, following the deprivation of even small amounts of REM sleep, there is a prompt and complete repayment. The subject who has been denied REM sleep launches into extended REM periods as soon as he is allowed to sleep normally. In recent drug studies, when REM sleep was prevented the payback seemed to be made with interest. More REM sleep was paid back than was lost.
Of course, all these considerations have ignored the prospect that we might derive benefits from the rise of acetylcholine during REM sleep too. Unfortunately, how acetylcholine might confer its positive trophotropic benefits is as yet obscure. One possibility is that exposure to high levels of acetylcholine might affect cell metabolism. If so, this would indicate a link between brain-mind states and genetics, an exciting scientific prospect.
The field of brain-mind research is on the threshold of an inevitable union with molecular biology. Since both REM sleep and DNA were discovered in 1953, this is a rather late marriage. The neuromodulator molecules - norepinephrine, serotonin, and acetylcholine - operate on the membrane surface of cells. Genes are large molecules that lie deep in the nucleus of the cell. Genes communicate via messenger molecules that ferry information from cell membranes to the nucleus. There is evidence that the neuromodulators may affect this communication. If this is the case, then norepinephrine, serotonin, and acetylcholine may affect the communication between genes. And since they affect the brain-mind states, they would provide a link between our genes and our states.
Thus we can contemplate a very intimate conjunction in biology: the coupling of sleep to our genes. From such a union the fathers of DNA and REM sleep, Francis Crick, James Watson, Eugene Aserinsky, and Nathaniel Kleitman, could expect a bevy of beautiful scientific grandchildren.
Many sleep scientists hypothesize that each of the three major brain-mind states - waking, sleeping, and dreaming - will prove to be quite different states at a very deep level, that of gene expression. Genes operate by making enzymes, and enzymes are essential to synthesizing norepinephrine, serotonin, and acetylcholine. We might expect, then, that in REM sleep the genetic manufacture of enzymes that synthesize the norepinephrine molecule would be turned on when acetylcholine interacts with the messenger cells communicating with the genes. A related concept would be that the disappearance of norepinephrine during REM sleep might signal genes to crank out more of the enzymes that make it. Either way, by the time we wake up enough norepinephrine will have been manufactured so that the aminergic system is ready to go. What scientists need, now, are ways to study the genetic biology of sleep. As genetics and brain-mind theory come together, we will find better explanations of how states affect energy, mood, and health.
Hobson
J. Allan Hobson, M.D., is professor of psychiatry at Harvard Medical School, director of the Laboratory of Neurophysiology at the Massachusetts Mental Health Center, and a member of the MacArthur Foundation Mind-Body Network who lectures regularly around the world. The author of The Dreaming Brain and Sleep, he lives in Brookline, Massachusetts.
"To Sleep, Perchance to Know Why," Stephanie Wall, World Wide Web.
The Accidental Mind, David J. Linden. The Belknap Press of Harvard University Press, 2007.
"New Trends in Dream Brain Research," Richard Catlett Wilkerson, World Wide Web.
"Sleep and the Immune System is Good Health Mediated by Brain-Mind States?," J. Allan Hobson, World Wide Web.