REM Sleep


Rapid eye movement sleep.

A phase of sleep distinguishable by random/rapid movement of the eyes, accompanied with low muscle tone throughout the body, and the propensity of the sleeper to dream vividly, and often emotionally intense.

Also known as paradoxical sleep and sometimes desynchronized sleep because of physiological similarities to waking states, including rapid, low-voltage desynchronized brain waves.

Electrical and chemical activity regulating this phase of sleep originates in the brain stem.

The amygdala is implicated in the processing of emotional content and behaviors related and to anxiety and panic, in addition to responses to pleasant and rewarding stimuli.

The amygdala plays a roll in cataplexy, with episodes of muscle paralysis during wakefulness that can be triggered by strong, positive emotions in persons with narcolepsy.

Dopamine signaling in the amygdala regulates REM sleep and possibly cataplexy as well.

Dopamine released in the amygdala can accelerate transitions from non-REM to REM sleep.

The amygdala is important in emotional processing both in normal REM sleep and in disorders of REM sleep.

In healthy persons both negative and positive emotions (anxiety, fear, and joy) are common during dreams.

REM sleep is believed to play a crucial role in the processing of emotional memories, strengthening some, weakening others, and activation of the amygdala occurs during REM sleep.

REM sleep is characterized most notably by an abundance of the neurotransmitter acetylcholine, combined with a nearly complete absence of monoamine neurotransmitters histamine, serotonin, and norepinephrine.

Other phases of sleep are referred to as non-REM sleep.

REM and non-REM sleep alternate within one sleep cycle, which lasts about 90 minutes in adult humans.

When sleep cycles continue, they shift towards a higher proportion of REM sleep.

The transition to REM sleep bring electrical bursts called PGO waves originating in the brain stem.

REM sleep suspends central homeostasis, allowing large fluctuations in respiration, thermoregulation, and circulation which do not occur in any other modes of sleeping or waking.

With REM sleep the body loses muscle tone, a state known as REM atonia.

REM sleep has similarities to wakefulness, although the body is paralyzed.

In REM sleep the brain acts somewhat awake, with cerebral neurons firing with the same intensity as in wakefulness.

Electroencephalography during REM deep sleep reveal fast, low amplitude, desynchronized neural brainwaves that resemble the pattern seen during wakefulness which differ from the slow δ (delta) waves pattern of NREM deep sleep.

The θ (theta) rhythm in the hippocampus shows 40–60 Hz gamma waves, in the cortex, as it does in waking.

Cortical and thalamic neurons in the waking and REM sleeping brain fire more readily than in the NREM deep sleeping brain.

During REM sleep, electrical connectivity among different areas of the brain manifests differently than during wakefulness.

Brain energy use in REM sleep, as measured by oxygen and glucose metabolism, equals or exceeds energy use in waking.

The rate in non-REM sleep is 11–40% lower.

Neural activity during REM sleep originates in the brain stem, especially the pontine tegmentum and locus coeruleus.

REM sleep is immediately preceded by ponto-geniculo-occipital waves, which appear as bursts of electrical activity originating in the brain stem.

These ponto-geniculo-occipital waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep.

The highest amplitude in the visual cortex cause of the rapid eye movements in paradoxical sleep.

Positron emission tomography (PET) within the forebrain, the limbic and paralimbic systems show more activation than other areas.

REM sleep activated areas are inverse to those activated during non-REM sleep and display greater activity than in quiet waking.

The anterior paralimbic REM activation area includes areas linked with emotion, memory, fear, and sex, and may thus relate to the experience of dreaming during REMS.

The distribution of brain activity during REM sleep varies in with the type of activity seen in the prior period of wakefulness.

Mental activity areas in superior frontal gyrus, medial frontal areas, intraparietal sulcus, and superior parietal cortex show equal activity in REM sleep as in wakefulness.

Experimental suppression of the amygdala results in less REM sleep.

Waking and paradoxical sleep involve higher use of the neurotransmitter acetylcholine, which may cause the faster brainwaves, compared to slow-wave sleep.

Acetylcholinesterase inhibitors, increase available acetylcholine, and induces paradoxical sleep.

Carbachol, which mimics the effect of acetylcholine on neurons, also induces paradoxical sleep.

The neurotransmitters, orexin and gamma-Aminobutyric acid (GABA), promote wakefulness, diminish during deep sleep, and inhibit paradoxical sleep.

Orexins are peptides produced by neurons in the lateral hypothalamus and the innervate the cortex, the brainstem and other regions where it promotes wakefulness and regulates REM sleep.

Chemical changes in the brain show continuous periodic oscillation.

REM-on neurons are primarily cholinergic, involving acetylcholine.

REM-off neurons activate serotonin and noradrenaline, which among other functions suppress the REM-on neurons.

Acetylcholine manifests in the cortex equally during wakefulness and REM, it appears in higher concentrations in the brain stem during REM.

The withdrawal of orexin and GABA may cause the absence of the other excitatory neurotransmitters.

Most rapid eye movement sleep are in fact less rapid than those normally exhibited by waking humans, being shorter in duration and more likely to loop back to their starting point.

In slow-wave sleep the eyes can drift apart; however, the eyes of the paradoxical sleeper move in tandem.

These eye movements follow the ponto-geniculo-occipital waves originating in the brain stem.

Congenitally blind people, move their eyes in REM sleep.

During paradoxical sleep the body’s homeostasis is suspended: the heart rate, cardiac pressure, cardiac output, arterial pressure, and breathing rate quickly become irregular when the body moves into REM sleep.

During REM sleep respiratory reflexes such as response to hypoxia diminish, and the brain exerts less control over breathing.

The fluctuations of heart rate and arterial pressure tend to coincide with ponto-geniculo-occipital waves and rapid eye movements, twitches, or sudden changes in breathing.

Nocturnal penile tumescence normally accompanies REM sleep in humans.

If a male has erectile dysfunction (ED) while awake, but has nocturnal penile tumescence episodes during REM, it would suggest that the ED is from a psychological rather than a physiological cause.

In females, nocturnal clitoral tumescence causes enlargement, with accompanying vaginal blood flow and 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.

Body temperature is not well regulated during REM sleep, as neurons which typically activate in response to cold temperatures do not fire during REM sleep, as they do in NREM sleep and waking.

Hot or cold environmental temperatures can reduce the proportion of REM sleep, as well as amount of total sleep.

REM atonia, an almost complete paralysis of the body, is accomplished through the inhibition of motor neurons.

In REM sleep, motor neurons throughout the body undergo a process called hyperpolarization: their already-negative membrane potential decreases by another 2–10 millivolts, raising the threshold which a stimulus must overcome to excite them.

Muscle inhibition may result from unavailability of monoamine neurotransmitters, by restraining the abundance of acetylcholine in the brainstem.

Lack of REM atonia causes REM behavior disorder.

REM behavior disorder sufferers physically act out their dreams.

This is different from conventional sleepwalking, which takes place during slow-wave sleep, not REM.

Narcolepsy involves excessive and unwanted REM atonia—that is, cataplexy and excessive daytime sleepiness while awake, hypnagogic hallucinations before entering slow-wave sleep, or sleep paralysis while waking.

Patients with suspected sleep disorders are typically evaluated by polysomnogram.

Rapid eye movement sleep (REM) is associated with dreaming.

Waking up sleepers during a REM phase is a method for obtaining dream reports.

80% of people can give some kind of dream report under these circumstances.

Lucid dreams are reported far more often in REM sleep.

It is estimated, 80% of dreams occur during REM.

Some dreaming can take place during non-REM sleep. ..

Light sleepers can experience dreaming during stage 2 non-REM sleep.

Deep sleepers, upon awakening in the same stage, are more likely to report “thinking” but not “dreaming”.

After waking from REM sleep, the mind seems more receptive to semantic priming effects.

People awakened from REM perform better on tasks like anagrams and creative problem solving testing.

REM sleep aids the process of creativity.

Creativity has been attributed to changes during REM sleep in cholinergic and noradrenergic neuromodulation.

During a night of sleep, there are about four or five periods of REM sleep.

REM sleep periods are shorter, about 15 minutes, at the beginning of the night and longer, about 25 minutes toward the end.

Some individuals tend to wake, or experience a period of very light sleep, for a short time immediately after a bout of REM.

REM sleep times varies with age: A newborn baby spends more than 80% of total sleep time in REM.

About 20-25% of adult sleep is REM, approximating 90-120 minutes of a night’s sleep.

The first REM episode occurs about 70 minutes after falling asleep.

Cycles of about 90 minutes each follow, with each cycle including a larger proportion of REM sleep.

The increased REM sleep later in the night is connected with the circadian rhythm.

The increased REM sleep later in the night occurs even in people who didn’t sleep in the first part of the night.

In the weeks after a human baby is born, neural patterns in sleep begin to show a rhythm of REM and non-REM sleep.

Infants spend more time in REM sleep than adults.

The proportion of REM sleep then decreases significantly in childhood.

Older people tend to sleep less overall but sleep in REM for about the same absolute time, and therefore spend a greater proportion of sleep in REM.

Rapid eye movement sleep can be subclassified into tonic and phasic phases.

Tonic REM is characterized by theta rhythms in the brain.

Phasic REM is characterized by ponto-geniculo-occipital waves and actual rapid eye movements.

Processing of external stimuli is heavily inhibited during phasic REM..

Sleepers are more difficult to arouse from phasic REM than in slow-wave sleep.

Selective REMS deprivation causes a significant increase in the number of attempts to go into REM stage while asleep. On recovery nights, an individual will usually move to stage.

REM sleep is biologically necessary.

REM deprivation leads to psychological disturbances, such as anxiety, irritability, hallucinations, and difficulty concentrating and appetite may increase.

REM sleep deprivation can improve certain types of depression when depression appears to be related to an imbalance of certain neurotransmitters.

Although sleep deprivation has been shown to alleviate depression, albeit temporarily.

Combining sleep-schedule alterations with pharmacotherapy may prolong this effect.

Antidepressants and stimulants (such as amphetamine and cocaine) interfere with REM sleep by stimulating the monoamine neurotransmitters which must be suppressed for REM sleep to occur.

These drugs may stop REM sleep entirely for weeks or months.

Sleep deprivation stimulates hippocampal neurogenesis much as antidepressants do.

REM sleep may help preserve certain procedural memory, spatial memory, and emotional memory.

Prevails most after birth, and diminishes with age.

Postulated to aid the developing brain by providing the neural stimulation that newborns need to form mature neural connections.

Sleep 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.

Humans are more likely to wake from REM sleep than from NREM sleep.

Patients treated with percutaneous coronary intervention experience a high prevalence of obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep. 



Diabetes mellitus is an independent predictor of OSA during REM sleep



OSA during the REM sleep cycle is associated with intense hypoxemic insult and cardiovascular instability.


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