Rapid Eye Movement Sleep

REM sleep behavior disorder (RBD) is a parasomnia characterized by violent behaviors during REM sleep, usually corresponding to enacted nightmares and dreams, that may injure the patients and their bed-partners or disturb sleep [1].

From: Sleep Medicine Reviews, 2017

REM Sleep

Jerome M. Siegel, in Principles and Practice of Sleep Medicine (Fourth Edition), 2005

WHAT IS REM SLEEP?

REM sleep was discovered by Aserinsky and Kleitman in 1953.1 They found that it was characterized by the periodic recurrence of rapid eye movements, linked to a dramatic reduction in the amplitude of the electroencephalogram (EEG). They found that the EEG of REM sleep closely resembled the EEG of alert waking and reported that subjects awakened from REM sleep reported vivid dreams. Dement identified a similar state of low-voltage EEG with eye movements in cats.2 Jouvet then repeated this observation, finding in addition a loss of muscle tone (atonia) in REM sleep and using the name paradoxical sleep to refer to this state. The "paradox" was that the EEG resembled that of waking, whereas behaviorally the animal remained asleep and unresponsive.3 Subsequent authors have described this state as "activated" sleep, or "dream" sleep. Recent work in humans has shown that some mental activity can be present in non-REM sleep but has supported the original finding linking our most vivid dreams to the REM sleep state.1

Most early work was done in cats, and it is in the cat that most of the "classic" signs of REM sleep and their generating mechanisms were discovered. Figure 10-1, top, shows the principal electrical signs of REM sleep. These include the reduction in EEG amplitude, particularly in the amplitude of its lower-frequency components. REM sleep is also characterized by a suppression of muscle tone (atonia), visible in the electromyogram (EMG). Erections tend to occur in men and clitoral enlargement in women. Thermoregulation largely ceases, and animal body temperatures drift toward environmental temperatures, as in reptiles.4 Pupils constrict, reflecting a parasympathetic dominance in the control of the iris. These changes that are present throughout the REM sleep period have been termed its tonic features.

Also visible are large electrical potentials that can be most easily recorded in the lateral geniculate nucleus.5 These potentials originate in the pons, appear after a few milliseconds in the lateral geniculate nucleus, and can be observed with further delay in the occipital cortex, leading to the name ponto-geniculo-occipital (PGO) spikes. They occur as large-amplitude, isolated potentials appearing 30 or more seconds before the onset of REM sleep, as defined by EEG and EMG criteria. After REM sleep begins, they arrive in bursts of 3 to 10 waves usually correlated with rapid eye movements. PGO-linked potentials can also be recorded in the motor nuclei of the extraocular muscles, where they trigger the rapid eye movements of REM sleep. They are present, in addition, in thalamic nuclei other than the geniculate and in neocortical regions other than the occipital cortex. In humans, rapid eye movements are loosely correlated with contractions of the muscles of the middle ear of the sort that accompany speech generation and that are part of the protective response to loud noise.6 Other muscles also contract during periods of rapid eye movement, briefly breaking through the tonic muscle atonia of REM sleep. There are periods of marked irregularity in respiratory and heart rates during REM sleep, in contrast to non-REM sleep, during which respiration and heart rate are highly regular. There does not appear to be any single pacemaker for all of this irregular activity. Rather, the signals producing twitches of the peripheral or middle ear muscles may lead or follow PGO spikes and rapid eye movements. Bursts of brainstem neuronal activity may likewise lead or follow the activity of any particular recorded muscle.789 These changes that occur episodically in REM sleep have been called its phasic features.

As we will see later, certain manipulations of the brainstem can eliminate only the phasic events of REM sleep, whereas others can cause the phasic events to occur in waking; yet other manipulations can affect tonic components. These tonic and phasic features are also expressed to varying extents in different species, and not all of these features are present in all species that have been observed to have REM sleep.

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Volume 2

Jerome M. Siegel, in Encyclopedia of Sleep and Circadian Rhythms, 2023

Abstract

The key brain structure for generating REM sleep is the pons and adjacent portions of the midbrain. These areas and the hypothalamus contain cells that are maximally active in REM sleep, called REM-on cells, and cells that are minimally active in REM sleep, called REM-off cells. Subgroups of REM-on cells use the transmitter gamma-aminobutyric acid (GABA), acetylcholine, glutamate, or glycine. Subgroups of REM-off cells use the transmitter norepinephrine, epinephrine, serotonin, histamine and GABA. Destruction of large regions within the midbrain and pons can prevent the occurrence of REM sleep. Damage to portions of the brainstem can cause abnormalities in certain aspects of REM sleep. Hypocretin neurons have an important role in the regulation of REM sleep and other sleep–wake phenomena.

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Stress and Arousal/Sleep

C.A. Lowry, ... K.P. Wright, in Encyclopedia of Behavioral Neuroscience, 2010

REM sleep

REM sleep is defined by low-amplitude desynchronized theta EEG activity with the presence of saw-tooth waves at the cortex. REM sleep is also characterized by the presence of pontine–geniculate–occipital (PGO) waves as well as hippocampal theta EEG activity. Compared to NREM sleep, REM sleep is considered the sleep state with the highest physiological arousal. Respiration, heart rate, and brain glucose utilization are more variable and activity can be as high as that observed during wakefulness. However, skeletal muscle activity is actively inhibited during REM sleep. REMs and other phasic activity such as middle ear muscle activity may be present during REM sleep.

Cholinergic neurons in the reticular formation are active during REM sleep, primarily those located in the pontine tegmentum. However, there are special populations referred to as REM-ON neurons that fire only during REM sleep, REM-OFF neurons that fire during wakefulness and are off during REM sleep, and a population of cholinergic neurons that fire during both REM sleep and wakefulness. GABAergic REM-ON neurons are located in the sublaterodorsal nucleus/peri-LC and the periventricular gray matter, and GABAergic REM-OFF neurons are located in the ventrolateral part of the periaqueductal grey matter and the lateral pontine tegmentum. REM-ON neurons inhibit REM-OFF neurons and thus promote REM sleep. Reciprocal inhibitory interactions between the REM-ON and REM-OFF neurons are thought to be involved in REM-sleep regulation. In addition stimulation of serotonergic, noradrenergic, or histaminergic cells will inhibit REM sleep. Orexin/hypocretin neurons also regulate REM-sleep timing via activation of the LC. Disinhibition of GABAergic neurons in the pons may also be involved in REM-sleep generation.

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Handbook of Sleep Research

Pierre-Hervé Luppi, ... Patrice Fort, in Handbook of Behavioral Neuroscience, 2019

Abstract

Rapid eye movement sleep (REM or paradoxical sleep (PS)) is a state of sleep characterized by REMs, EEG activation, and muscle atony. In the present review, we present the most recent results on the neuronal network responsible for PS generation. We propose that muscle atony during PS is due to the activation of PS-on glutamatergic neurons localized in the caudal pontine sublaterodorsal tegmental nucleus (SLD) and the glycinergic/GABAergic premotoneurons localized in the medullary ventral reticular nuclei. The SLD neurons are inactivated during waking and slow-wave sleep by PS-off GABAergic neurons localized in the ventrolateral periaqueductal gray and the adjacent deep mesencephalic reticular nucleus. PS onset and maintenance is due to the inhibition of these PS-off neurons by PS-on GABAergic neurons localized in the posterior hypothalamus, the ventrolateral periaqueductal gray, and the lateral and dorsal paragigantocellular reticular nuclei.

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Schizophrenia and Its Associated Sleep Disorders

Kathleen L. Benson, in Therapy in Sleep Medicine, 2012

REM Sleep Onset Latency

Rapid eye movement (REM) sleep onset latency is defined as the elapsed time between sleep onset and the onset of the first REM sleep period, alternatively viewed as the length of the first NREM sleep period.

Significantly shortened REM latencies have been observed in approximately one half of studies comparing the sleep of unmedicated patients with schizophrenia to that of nonpsychiatric and psychiatric control subjects.22

Shortened REM latencies may be the result of an active advance of REM sleep mechanisms.22

Shortened REM latencies may also reflect the passive advance of the first REM sleep period due to SWS deficits in the first NREM period.27

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Neurological Aspects of Sleep

Bruce J. Fisch, in Neurology and General Medicine (Fourth Edition), 2008

REM Sleep

REM sleep is distinct from the other stages of sleep. Only three stages of sleep can be consistently distinguished in the neonatal period: active sleep, quiet sleep, and indeterminate or transitional sleep. Active sleep is the forerunner of REM sleep. As in adults, it is characterized by abrupt rapid eye movements, irregular respiration and heart rate, penile tumescence, muscular atonia (absent EMG activity), and a low-amplitude, irregular EEG pattern. Thermal regulation is markedly suppressed, so that neither shivering nor sweating is typically seen. In neonates, REM sleep onset is usually in active sleep, whereas in children or adults REM sleep rarely occurs during the first 60 minutes of sleep. Sleep onset with REM sleep beyond early childhood is therefore abnormal. Active sleep first appears at approximately 32 weeks of conceptional age. At term, REM (active) sleep occupies 50 percent of sleep time. After the first year of life, the majority of REM sleep occurs during the second half of the night, and REM sleep occupies 20 to 25 percent of total sleep time (Fig. 32-2). During REM sleep, brain metabolism increases dramatically to near-waking levels. The combination of atonia, active cerebral metabolism, and an EEG pattern that at times resembles alert wakefulness has led to the characterization of REM sleep as a metabolically awake brain in a paralyzed body.

REM sleep is enhanced by cholinergic agonists and suppressed by tricyclic antidepressant medications, adrenergic uptake blockers, clonidine, scopolamine, propranolol, lithium, and monoamine oxidase inhibitors. Alcohol ingestion immediately before sleep suppresses REM sleep during the first half of the night but then results in excessive REM activity later in the night. Prolonged REM suppression (produced by repeatedly awakening individuals from REM sleep or by pharmacological means) is followed by a period of excessive REM sleep, often referred to as REM rebound. These observations have important implications for sleep testing. For example, the sudden withdrawal of tricyclic antidepressant medication before testing may lead to the erroneous impression of narcolepsy because of early-onset and excessive REM sleep. Similarly, the duration of the history of sleep apnea correlates with the length of REM periods (REM rebound) that appear at the time of initial treatment using continuous positive airway pressure therapy.

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REM (Rapid Eye Movement) Sleep

P. Das, C.J. Bae, in Encyclopedia of the Neurological Sciences (Second Edition), 2014

Abstract

Rapid eye movement (REM) sleep is commonly associated with dreams, and is characterized by specific physiological features that distinguish it from other sleep stages. The electrophysiological features associated with REM sleep are rapid eye movements, low voltage-mixed frequency electroencephalogram (EEG), and muscle atonia. The key brain structures responsible for producing this sleep stage are located in the brainstem. The disruption of pathways involved with REM sleep can affect various electrophysiological components of REM sleep and can result in clinical conditions such as narcolepsy and REM sleep behavior disorder. The biological purpose of REM sleep is not clear, though it seems that it has a role in consolidating procedural memories.

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Rapid Eye Movement Sleep

Jerome M. Siegel, in Principles and Practice of Sleep Medicine (Sixth Edition), 2017

Summary

REM sleep was first identified by its most obvious behavior: rapid eye movements during sleep. In most adult mammals the EEG of the neocortex is low in voltage during REM sleep. The hippocampus has regular high-voltage theta waves throughout REM sleep. The tone of the postural muscles is greatly reduced or abolished during this state.

The key brain structure for generating REM sleep is the brainstem, particularly the pons and adjacent portions of the midbrain. Considerable progress has been made in identifying the neurons most closely linked to REM sleep within these regions and the transmitters that they employ. Massive damage to the REM-generating region can abolish REM sleep. Small lesions can cause REM sleep without atonia in animals or REM sleep behavior disorder in humans

Narcolepsy is characterized by abnormalities in the regulation of REM sleep. Most cases of human narcolepsy are caused by a loss of hypocretin (orexin) neurons, a cell group whose somas are localized to the hypothalamus. Hypocretin neurons have potent effects on alertness and motor control and normally are activated in relation to particular, generally positive emotions in humans as well as in animals. In the absence of this cell group, cataplexy, a REM sleep–like loss of muscle tone, occurs.

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Clinical Neurophysiology: Basis and Technical Aspects

Pierre-Hervé Luppi, Patrice Fort, in Handbook of Clinical Neurology, 2019

A network model for PS onset and maintenance

The onset of PS would be due to the activation by intrinsic and extrinsic factors of PS-on MCH/GABAergic neurons localized in the LH area. At PS onset, these neurons would inhibit the PS-off GABAergic neurons localized in the vlPAG and the dDpMe tonically inhibiting during W and SWS the glutamatergic PS-on neurons from the SLD. The disinhibited descending glutamatergic PS-on SLD neurons would induce muscle atonia via their excitatory projections to GABA/glycinergic premotoneurons localized in the raphe magnus, alpha, and ventral gigantocellular reticular nuclei. PS-on GABAergic neurons localized in the LH, DPGi, and vlPAG would also inactivate the PS-off orexin (hypocretin) and aminergic neurons during PS. The exit from PS would be due to the activation of waking/arousal systems, since PS episodes are almost always terminated by a transition to wakefulness state. The waking systems would reciprocally inhibit the GABAergic PS-on neurons localized in the LH, vlPAG, and DPGi. Since the duration of PS is negatively coupled with the metabolic rate, it can be proposed that the activity of the waking systems is triggered to end PS to restore crucial physiological parameters like thermoregulation.

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Nightmares and the Mood Regulatory Functions of Sleep

Patrick J. McNamara, ... Alina A. Gusev, in Sleep and Affect, 2015

The NREM-REM Cycle

REM sleep accounts for about 22% of total sleep time in humans. The other major form of human sleep is called non-REM and is composed of three key stages or phases of sleep, including N1, which is a transitional stage from wake into sleep; N2, which is a form of light sleep and which makes up the bulk of our sleep time; and N3 or slow-wave sleep (SWS), which appears to serve a variety of functions from physiologic repair to memory consolidation. Although the cortex is activated in REM, arousal thresholds in humans are variable in REM. A typical night of sleep will consist of NREM alternating with REM. As the night progresses, less time is devoted to SWS and more to REM. Thus, REM sleep tends to be more prominent toward the last part of the night (Carskadon & Rechtschaffen, 2000). REM sleep can be further divided into its tonic and phasic components.

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