Rapid eye movement

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For other uses of the acronym REM, see: REM (disambiguation).

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 (Aserinsky E, Kleitman N. Regularly Occurring Periods of Eye Motility, and Concomitant Phenomena, during Sleep. Science 1953:118;273-274). 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.

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

REM sleep in adults typically occupies 20-25% of total sleep, lasting about 90-120 minutes. During a normal night of sleep, we usually experience about 4 or 5 periods of REM sleep; they are quite short at the beginning of the night and longer at the end. It is common to wake for a short time at the end of a 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 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 so physiologically different[citation needed] from the other phases of sleep that the others are collectively referred to as non-REM sleep. Most of our vividly recalled dreams occur during REM sleep.

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Physiology of 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 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

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.[2]

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 and spatial memories. (Slow-wave sleep, part of non-REM sleep, appears to be important for declarative memories.) A recent study (Marshall, Helgadóttir, Mölle & Born, 2006) shows that artificial enhancement of the REM sleep improves the next-day recall of memorized pairs of words. However, in people who have no REM sleep (because of brain damage), memory functions are not measurably affected.[3]

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 (Marks et al. 1995). 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 (Mirmiran et al. 1983), and result in an abnormal amount of neuronal cell death (Morrissey, Duntley & Anch, 2004). REM sleep is necessary for proper central nervous system development (Marks et al. 1995). 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).

REM sleep in other 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 8 hours of REM sleep per night.

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.

REM sleep suppression

Various drugs, including alcohol, benzodiazepines, and antidepressants are known to suppress REM sleep.

Initial studies associated lack of REM sleep with adverse consequences, backed up by animal studies which including the finding that REM deprivation is ultimately fatal to rats. However a number of studies on humans subsequently failed to confirm the findings, and the majority opinion is that REM deprivation has no ill effects. What is agreed is that suppressing REM sleep greatly increases the number of attempts the subject will make to enter REM sleep. Also once the suppression is stopped, the proportion of time spent in REM sleep will increase significantly, which is known as REM rebound[4].

References

  1. KrygerM, RothT, Dement W. 'Principles & Pracitces of Sleep Medicine' WB Saunders Company. 2000: PG. 15, 724.
  2. Sasaki Y (2000). "Sleep onset REM period appearance rate is affected by REM propensity in circadian rhythm in normal nocturnal sleep". Clin Neurophysiol. 111 (3): 428–33. PMID 10699402. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help); |access-date= requires |url= (help)
  3. Siegel, Jerome M. "The REM Sleep-Memory Consolidation Hypothesis".
  4. REM deprivation at Macalester College, Sleep deprivation.
  • Morrissey MJ, Duntley SP, Anch AM, Nonneman R. Active sleep and its role in the prevention of apoptosis in the developing brain. Med Hypotheses. 2004;62(6):876-9. PMID 15142640
  • Marks GA et al. A functional role for REM sleep in brain maturation. Behav Brain Res. 1995 Jul-Aug;69(1-2):1-11. PMID 7546299

See also

da:Rapid Eye Movement de:REM-Schlaf it:Rapid eye movement nl:REMslaap no:REM-søvn fi:REM (uni) sv:REM-sömn


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