Rapid Eye Movement (REM) sleep is a normal stage of sleep characterized by the rapid movement of the eyes. REM sleep is classified into two categories: tonic and phasic. It was identified and defined by Kleitman and Aserinsky in the early 1950s.
Criteria for REM sleep includes not only rapid eye movement, 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, about 90–120 minutes of a night's sleep. During a normal night of sleep, humans usually experience about four or five periods of REM sleep; they are quite short at the beginning of the night and longer toward the end. Many animals and some people tend to wake, or experience a period of very light sleep, for a short time immediately after a bout of REM. The relative amount of REM sleep varies considerably with age. A newborn baby spends more than 80% of total sleep time in REM. During REM, the activity of the brain's neurons is quite similar to that during waking hours, but the body is paralyzed due to atonia; for this reason, the REM-sleep stage may be called paradoxical sleep. This means there are no dominating brain waves during REM sleep.
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 do not 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) normally accompany REM sleep. If a male has erectile dysfunction (ED) while awake, but has NPT episodes during REM, it would suggest that the ED is from a psychological rather than a physiological cause. In females, erection of the clitoris (nocturnal clitoral tumescence or NCT) causes enlargement, with accompanying vaginal blood flow and transudation (i.e. lubrication). During a normal night of sleep the penis and clitoris may be erect for a total time of from one hour to as long as three and a half hours during REM. Research urologists have found that the increased blood flow during NPT and NCT episodes may prevent excessive collagen from forming in the erectile tissues (sinusoids) of the clitoris and penis. They are aware that the increased fiber formation in the erectile tissues could lead to tissue-cell death and eventual loss of erectile function.
In a study published in the journal Human Brain Mapping, participants who were in REM "dream" sleep were also monitored by special MRI imaging designed to visualise brain activity. The researchers found activity in areas of the brain that control sight, hearing, smell, touch, balance and body movement.
During dreaming, the primary visual cortex is inactive, while secondary areas are active. This is similar to when subjects are asked to imagine or recall a visual scene, and different from what happens when they are actually seeing the scene.
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 shows that artificial enhancement of the non-REM sleep improves the next-day recall of memorised pairs of words. Tucker et al. demonstrated that a daytime nap containing solely non-REM sleep enhances declarative memory but not procedural memory. The role of REM sleep in memory, however, is not without its doubts. Monoamine oxidase (MAO) inhibitors and tricyclic antidepressants can suppress REM sleep, yet these drugs show no evidence of impairing memory. On the contrary, some studies show MAO inhibitors improve memory. Moreover, one case study of an individual who had little or no REM sleep due to a shrapnel injury to the brainstem did not find the individual's memory to be impaired. (For a more detailed critique on the link between sleep and memory, see Ref.)
Intimately related to views on REM function in memory consolidation, Mitchison and Crick have proposed that by virtue of its inherent spontaneous activity, the function of REM sleep "is to remove certain undesirable modes of interaction in networks of cells in the cerebral cortex", which process they characterise as "unlearning". As a result, those memories which are relevant (whose underlying neuronal substrate is strong enough to withstand such spontaneous, chaotic activation), are further strengthened, whilst weaker, transient, "noise" memory traces disintegrate.
According to another theory, known as the Ontogenetic Hypothesis of REM sleep, this sleep stage (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. 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, and result in an abnormal amount of neuronal cell death. Further supporting this theory is the fact that the amount of REM sleep in humans decreases with age, as well as data from other species (see below).
One important theoretical consequence of the Onthogenetic Hypothesis is that REM sleep may have no essentially vital function in the mature brain, i.e., once the development of CNS has completed. However, because processes of neuronal plasticity do not cease altogether in the brain, REM sleep may continue to be implicated in neurogenesis in adults as a source of sustained spontaneous stimulation.
Yet 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 compensate for it with longer REM sleep, "rebound sleep", at the next opportunity. The only way to cure it is to sleep early. It has been suggested that Acute REM sleep deprivation can improve certain types of depression when depression appears to be related to an imbalance of certain neurotransmitters. This however is not proven. As of yet, there is no known test that will prove the theory of chemical imbalance. Most antidepressants selectively inhibit REM sleep due to their effects on monoamines. However, this effect decreases after long-term use.
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 and avian 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 hypothesised 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.
Studies have shown that people sleep more efficiently when they are sleep-deprived and that they enter REM sleep faster when this is the case. Sleep studies also show that patients who sleep less move to stage 3, stage 4 and REM sleep faster than patients who are not sleep deprived 
Sleep aids the process by which creativity forms associative elements into new combinations that are useful or meet some requirement. This occurs in REM sleep rather than in NREM sleep. Rather than being due to memory processes, this has been attributed to changes during REM sleep in cholinergic and noradrenergic neuromodulation. During REM sleep high levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the neocortex, and lower levels of acetylcholine and norepinephrine in the neocortex encourage the spread of associational activity within neocortical areas without control from the hippocampus. This is in contrast to waking consciousness, where higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing "neocortical structures to reorganise associative hierarchies, in which information from the hippocampus would be reinterpreted in relation to previous semantic representations or nodes."
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. Kleitmann and Aserinsky's seminal article was published September 10, 1953.
[Add reference: Carson III, Culley C., Kirby, Roger S., Goldstein, Irwin, editors, "Textbook of Erectile Dysfunction" Oxford, U.K.; Isis Medical Media, Ltd., 1999; Moreland, R.B. & Nehra, A.; Pathosphysiology of erectile dysfunction; a molecular basis, role of NPT in maintaining potency: pp. 105–15.]