Rapid eye movement sleep

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Overview

Rapid eye movement (REM) sleep is the normal stage of sleep characterized by rapid movements of the eyes. REM sleep is classified into two categories: tonic and phasic.^[1] It was discovered by Nathaniel Kleitman and Eugene Aserinsky in the early 1950s. Their seminal article was published September 4, 1953.^[1] Criteria for REM sleep include not only rapid eye movements, but also low muscle tone and a rapid, low voltage EEG -- these features are easily discernible in a polysomnogram, the sleep study typically done for patients with suspected sleep disorders.

REM sleep in adult humans typically occupies 20-25% of total sleep, lasting about 90-120 minutes. During a normal night of sleep, humans usually experience about 4 or 5 periods of REM sleep; they are quite short at the beginning of the night and longer toward the end. It is common for one to wake for a short time at the end of an REM phase. The relative amount of REM sleep varies considerably with age. A newborn baby spends more than 80% of total sleep time in REM (see also Active Sleep). During REM, the summed activity of the brain's neurons is a quite similar to that during waking hours; for this reason, the phenomenon is often called paradoxical sleep. This means that there are no dominating brain waves during REM sleep.

REM sleep is physiologically different from the other phases of sleep, which are collectively referred to as non-REM sleep. Most of our vividly recalled dreams occur during REM sleep.

Physiology of REM sleep

Polysomnographic record of REM Sleep. EEG highlighted by red box. Eye movements highlighted by red line.

See also: Neurology of dreams

Physiologically, certain neurons in the brain stem, known as REM sleep-on cells, (located in the pontine tegmentum), are particularly active during REM sleep, and are probably responsible for its occurrence. The release of certain neurotransmitters, the monoamines (norepinephrine, serotonin and histamine), is completely shut down during REM. This causes REM atonia, a state in which the motor neurons are not stimulated and thus the body's muscles don't move. Lack of such REM atonia causes REM Behavior Disorder; sufferers act out the movements occurring in their dreams.

Heart rate and breathing rate are irregular during REM sleep, again similar to the waking hours. Body temperature is not well regulated during REM. Erections of the penis (Nocturnal Penile Tumescence or NPT) is an established accompaniment of REM sleep and is used diagnostically to determine if male erectile dysfunction is of organic or psychological origin. Clitoral enlargement, with accompanying vaginal blood flow and transudation (i.e. lubrication) is also present during REM.

The eye movements associated with REM are generated by the pontine nucleus with projections to the superior colliculus and are associated with PGO (pons, geniculate, occipital) waves.

REM sleep disorders

See also: Sleep disorder

REM sleep can occur within about 90 minutes, but in those with a sleep onset REM period, it may be as little as 15-25 minutes. This is considered a sign of narcolepsy.^[1]

Theories about the function(s) of REM sleep

The function of REM sleep is not well understood; several theories have been advanced.

According to one theory, certain memories are consolidated during REM sleep. Numerous studies have suggested that REM sleep is important for consolidation of procedural memory and spatial memory. (Slow-wave sleep, part of non-REM sleep, appears to be important for declarative memory.) A recent study^[1] shows that artificial enhancement of the REM sleep improves the next-day recall of memorized pairs of words. Tucker et al.^[1] demonstrated that a daytime nap containing solely non REM sleep enhances declarative memory but not procedural memory. However, in people who have no REM sleep (because of brain damage), memory functions are not measurably affected.^[1]

Another theory suggests that monoamine shutdown is required so that the monoamine receptors in the brain can recover to regain full sensitivity. Indeed, if REM sleep is repeatedly interrupted, the person will "make up" for it with longer REM sleep at the next opportunity. Acute REM sleep deprivation can improve certain types of depression, and depression appears to be related to an imbalance of certain neurotransmitters. Most antidepressants selectively inhibit REM sleep due to their effects on monoamines. However, this effect decreases after long-term use.

According to a third theory, known as the Ontogenetic Hypothesis of REM sleep, this sleep phase (also known as Active Sleep in neonates) is particularly important to the developing brain, possibly because it provides the neural stimulation that newborns need to form mature neural connections and for proper nervous system development.^[1] Studies investigating the effects of Active Sleep deprivation have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, decreased brain mass,^[1] and result in an abnormal amount of neuronal cell death.^[1] REM sleep is necessary for proper central nervous system development.^[1] Further supporting this theory is the fact that the amount of REM sleep decreases with age, as well as the data from other species (see below).

Some researchers argue that the perpetuation of a complex brain process such as REM sleep indicates that it serves an important function for the survival of mammalian species. It fulfills important physiological needs vital for survival to the extent that prolonged REM sleep deprivation leads to death in experimental animals. In both humans and experimental animals, REM sleep loss leads to several behavioral and physiological abnormalities. Loss of REM sleep has been noticed during various natural and experimental infections. Survivability of the experimental animals decreases when REM sleep is totally attenuated during infection. This leads to the possibility that the quality and quantity of REM sleep is generally essential for normal body physiology.

The Sentinel hypothesis of REM sleep was put forward by Frederic Snyder in 1966. It is based upon the observation that REM sleep in several mammals (the rat, the hedgehog, the rabbit, and the rhesus monkey) is followed by a brief awakening. (This does not occur for either cats or humans, although humans are more likely to wake from REM sleep than from non-REM sleep.) Snyder hypothesized that REM sleep activates an animal periodically, to scan the environment for possible predators. This hypothesis does not explain the muscle paralysis of REM sleep.^[1][1][1]

REM sleep in animals

REM sleep occurs in all mammals and birds. It appears that the amount of REM sleep per night in a species is closely correlated with the developmental stage of newborns. The platypus for example, whose newborns are completely helpless and undeveloped, has more than seven hours of REM sleep per night.^{[citation needed]}

History

The phenomenon of REM sleep and its association with dreaming was discovered by Eugene Aserinsky and Nathaniel Kleitman with assistance from William C. Dement, a medical student at the time, in 1952 during their tenures at the University of Chicago.

References

Further reading

• Frederic Snyder (1966). "Toward an Evolutionary Theory of Dreaming". American Journal of Psychiatry 123: 121–142.
• (2003) in Edward F. Pace-Schott: Sleep and Dreaming: Scientific Advances and Reconsiderations. Cambridge University Press. ISBN 0521008697. 

See also

• Eye Movement Desensitization and Reprocessing
• Nystagmus
• Polyphasic sleep
• Sleep and learning
• Dream
• NREM
• Lucid Dream

Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .