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Non-rapid eye movement sleep
Non-rapid eye movement sleep
Non-rapid eye movement sleep
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Simplified hypnogram with NREM stages.

Non-rapid eye movement sleep (NREM), also known as quiescent sleep,[1] is, collectively, sleep stages 1–3, previously known as stages 1–4. Rapid eye movement sleep (REM) is not included. There are distinct electroencephalographic and other characteristics seen in each stage. Unlike REM sleep, there is usually little or no eye movement during these stages. Dreaming occurs during both sleep states, and muscles are not paralyzed as in REM sleep. People who do not go through the sleeping stages properly get stuck in NREM sleep, and because muscles are not paralyzed a person may be able to sleepwalk. According to studies, the mental activity that takes place during NREM sleep is believed to be thought-like, whereas REM sleep includes hallucinatory and bizarre content.[2] NREM sleep is characteristic of dreamer-initiated friendliness, compared to REM sleep where it is more aggressive, implying that NREM is in charge of simulating friendly interactions.[3] The mental activity that occurs in NREM and REM sleep is a result of two different mind generators, which also explains the difference in mental activity. In addition, there is a parasympathetic dominance during NREM. The reported differences between the REM and NREM activity are believed to arise from differences in the memory stages that occur during the two types of sleep.

Stages

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NREM sleep was divided into four stages in the Rechtschaffen and Kales (R&K) standardization of 1968. That has been reduced to three in the 2007 update by The American Academy of Sleep Medicine (AASM).[4]

  • Stage 1 – occurs mostly in the beginning of sleep, with slow eye movement. This state is sometimes referred to as relaxed wakefulness.[5] Alpha waves disappear and the theta wave appears. People aroused from this stage often believe that they have been fully awake. During the transition into stage-1 sleep, it is common to experience hypnic jerks.[6]
  • Stage 2 – no eye movement occurs, and dreaming is very rare. The sleeper is quite easily awakened. EEG recordings tend to show characteristic "sleep spindles", which are short bursts of high frequency brain activity,[7] and "K-complexes" during this stage.
  • Stage 3 – previously divided into stages 3 and 4, is deep sleep, slow-wave sleep (SWS). Stage 3 was formerly the transition between stage 2 and stage 4 where delta waves, associated with "deep" sleep, began to occur, while delta waves dominated in stage 4. In 2007, these were combined into just stage 3 for all of deep sleep.[8] Dreaming is more common in this stage than in other stages of NREM sleep though not as common as in REM sleep. The content of SWS dreams tends to be disconnected, less vivid, and less memorable than those that occur during REM sleep.[9] This is also the stage during which parasomnias most commonly occur.

Sleep spindles and K-complexes

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Sleep spindles are unique to NREM sleep. The most spindle activity occurs at the beginning and the end of NREM. Sleep spindles involve activation in the brain in the areas of the thalamus, anterior cingulate and insular cortices, and the superior temporal gyri. They have different lengths. There are slow spindles in the range of 11 – 13 Hz that are associated with increased activity in the superior frontal gyrus, and fast spindles in the range of 13 – 15 Hz that are associated with recruitment of sensorimotor processing cortical regions, as well as recruitment of the mesial frontal cortex and hippocampus. There is no clear answer as to what these sleep spindles mean, but ongoing research hopes to illuminate their function.[10]

K-complexes are single long delta waves that last for only a second.[11] They are also unique to NREM sleep. They appear spontaneously across the early stages, usually in the second stage, much like the sleep spindles. However, unlike sleep spindles, they can be voluntarily induced by transient noises such as a knock at the door. The function of these K-complexes is unknown and further research needs to be conducted.[12]

Dreaming

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Although study participants' reports of intense dream vividness during REM sleep and increased recollection of dreams occurring during that phase suggest that dreaming most commonly occurs during that stage,[13] dreaming can also occur during NREM sleep,[13] in which dreams tend to be more mundane in comparison.[14] It was initially thought that NREM sleep is the absence of dreaming, or dreams occur more rarely compared to REM sleep because 90–95% of those who wake up in the middle of REM sleep will report that they have had a dream, but only 5–10% of those waking up in the middle of non-REM sleep will report they've had a dream.[15] However, when asked for more general thought processes or feelings, 70% of people who awaken from NREM sleep reports of having dream-like feelings, which is characteristic of NREM dreams, potentially disproving that theory.[16][17]

Research has also shown that dreams during the NREM stage most commonly occur during the morning hours which is also the time period with the highest occurrence of REM sleep. This was found through a study involving subjects taking naps over specific intervals of time and being forcefully awakened, their sleep was separated into naps including only REM sleep and only NREM sleep using polysomnography. This implies that the polysomnographic occurrence of REM sleep is not required for dreaming. Rather, the actual mechanisms that create REM sleep cause changes to one's sleep experience. Through these changes, by morning, a sub-cortical activation may occur during NREM that is comparable to the type that occurs during REM. Such a sub-cortical activation may result in dreaming during the NREM stage during the morning hours.[18]

Self in dreaming

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It is suggested that dreaming involves two selfs: aggressive self (REM) and friendly self (NREM). It seems that in NREM dreams, the self is put in different situations, largely negative, but is found to respond in a way that befriends or embraces the unfamiliar.[3] It is sometimes thought that in NREM sleep, the dreamers are "aware of being aware", also known as "secondary awareness",[19] which allows them to make better decisions and potentially reflect on them.[16]

Muscle movements

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During non-REM sleep, the tonic drive to most respiratory muscles of the upper airway is inhibited. This has two consequences:

  1. The upper airway becomes more floppy.
  2. The rhythmic innervation results in weaker muscle contractions because the intracellular calcium levels are lowered, as the removal of tonic innervation hyperpolarizes motoneurons, and consequently, muscle cells.

However, because the diaphragm is largely driven by the autonomous system, it is relatively spared of non-REM inhibition. As such, the suction pressures it generates stay the same. This narrows the upper airway during sleep, increasing resistance and making airflow through the upper airway turbulent and noisy. For example, one way to determine whether a person is sleeping is to listen to their breathing - once the person falls asleep, their breathing becomes noticeably louder. Not surprisingly, the increased tendency of the upper airway to collapse during breathing in sleep can lead to snoring, a vibration of the tissues in the upper airway. This problem is exacerbated in overweight people when sleeping on the back, as extra fat tissue may weigh down on the airway, closing it. This can lead to sleep apnea.[citation needed]

Parasomnias

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Main article: Parasomnia

The occurrence of parasomnias is very common in the last stage of NREM sleep. Parasomnias are sleep behaviors that affect the function, quality, or timing of sleep, caused by a physiological activation in which the brain is caught between the stages of falling asleep and waking. The autonomous nervous system, cognitive process, and motor system are activated during sleep or while the person wakes up from sleep.

Some examples of parasomnias are somnambulism (sleep walking), somniloquy (sleep talking), sleep eating, nightmares or night terrors, sleep paralysis, and sexsomnia (or "sleep sex"). Many of these have a genetic component, and can be quite damaging to the person with the behavior or their bed partner. Parasomnias are most common in children, but most children have been found to outgrow them with age. However, if not outgrown, they can cause other serious problems with everyday life.[20]

Polysomnography

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Polysomnography (PSG) is a test used in the study of sleep; the test result is called a polysomnogram. Below are images of the NREM stages 1, 2 and 3.

The figures represent 30-second epochs (30 seconds of data). They represent data from both eyes, EEG, chin, microphone, EKG, legs, nasal/oral air flow, thermistor, thoracic effort, abdominal effort, oximetry, and body position, in that order. EEG is highlighted by the red box. Sleep spindles in the stage 2 figure are underlined in red.

Stage N1: Stage N1 Sleep. EEG highlighted by red box.

Stage N2: Stage N2 Sleep. EEG highlighted by red box. Sleep spindles highlighted by red line.

Stage N3: Stage 3 Sleep. EEG highlighted by red box.

Slow-wave sleep

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Main article: Slow-wave sleep

Slow-wave sleep (SWS) is made up of the deepest stage of NREM, and is often referred to as deep sleep.

The highest arousal thresholds (e.g. difficulty of awakening, such as by a sound of a particular volume) are observed in stage 3. A person will typically feel groggy when awakened from this stage, and indeed, cognitive tests administered after awakening from stage 3 indicate that mental performance is somewhat impaired for periods up to 30 minutes or so, relative to awakenings from other stages. This phenomenon has been called "sleep inertia."

After sleep deprivation there is usually a sharp rebound of SWS, suggesting there is a "need" for this stage.[21]

Slow Wave Sleep (SWS) is a highly active state unlike a state of brain quiescence as previously thought. Brain imaging data has shown that during NREM sleep the regional brain activity is influenced by the waking experience just passed.

A study was done involving an experimental and a control group to have them learn to navigate a 3D maze. The blood flow in the parahippocampal gyrus increased in conjunction with the individual's performance through the 3D maze. Participants were then trained in the maze for 4 hours and later, during the various sleep cycles of NREM sleep, REM sleep and wakefulness, they were scanned twelve times using a PET scan during the night. The PET scan demonstrated a higher blood flow in the hippocampus during SWS/NREM sleep due to the training from the previous day while the control group exhibited no increased blood flow and they had not received the training the prior day. The brain activity during sleep, according to this study, would show the events of the previous day do make a difference. One theory suggests a model of hippocampal-neocortical dialogue. "Two stages of hippocampal activity have been proposed, the first being the recording of the memory during waking and the second involving the playback of the memory during NREM sleep. This process of reactivation of memory firing sequences is believed to gradually reinforce initially weak connections between neocortical sites allowing the original information to be activated in the cortex independently of the hippocampus, and thus ensuring refreshed encoding capacity of the hippocampus." Maquet concluded that the areas of the brain involved with information processing and memory have increased brain activity during the slow wave sleep period. Events experienced in the previous day have more efficient and clearer memory recall the next day thus indicating that the memory regions of the brain are activated during SWS/NREM sleep instead of being dormant as previously thought.[22]

NREM SWS, also known as slow wave activity (SWA), is regarded as highly important in brain development due not only to its homeostatic behavior but also because of its distinct correlation with age.[23] Children sleep longer and deeper than adults. The difference in depth of sleep has been quantified by EEG recordings of SWA.[24] An increase in SWA peaks just before puberty and exponentially decreases from adolescence to adulthood in both longitudinal and cross-sectional studies of typically developing participants.[25][23][24][26] This phenomenon is understood as memories and learned skills being metabolized during NREM sleep;[23] the decrease in SWA is considered a reflection of synaptic rewiring and, therefore, an effect of behavioral maturation concluding.[25] The critical period from childhood to emerging adulthood is also considered a sensitive period for mental disorders to manifest. For example, children with attention deficit hyperactivity disorder (ADHD), a brain disorder that affects cognitive and motor control, have shown considerably different cortical thickening trajectories in contrast with typically developing children per MRI data. Cortical thickness is a common measure of brain maturation; the main difference in children with ADHD shows a delay in cortical thickness, specifically in the frontal lobe.[26] Significant correlations in the trajectory of gray matter thickness and SWA suggest that SWA may be able to indicate levels of cortical maturation on an individual level.[25] However, there has yet to be a study in which the diagnosis of ADHD can be given directly from SWA readings.

Memory

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Main article: Sleep and memory

Non-rapid eye movement sleep is known for its beneficial effect on memory consolidation, especially for declarative memory (while procedural memory improvement is more associated with REM-sleep),[27] even if establishing a clear-cut distinction between stages' influence on type of learning may not be possible.[28]

Generally, both REM and NREM are associated with an increased memory performance, because newly encoded memories are reactivated and consolidated during sleep.[29]

NREM sleep has been demonstrated to be intimately correlated with declarative memory consolidation in various studies, where subject slept after a declarative memory-task; these who had a sleep imbued of NREM stages, had a better performance after the nap or the night, compared to subjects who have been awake or had more REM-sleep.[30][31][32]

The importance of NREM sleep in memory consolidation has also been demonstrated using cueing; in this paradigm, while participants are sleeping and are in NREM sleep stages, cues are proposed (which can be, for example, aurally-presented sounds or words, odors, and so on).[33][34][35] The fact that this procedure was effective on the improvement of the later memory performance, indicates that during these stages, there is a reactivation of the memory traces and a subsequent consolidation, which are facilitated by the cues; importantly, this does not work if the cueing is presented when subjects are awake or in REM stages.[33][34]

Furthermore, the specific and crucial role of SWS (Slow-Wave Sleep, a stage of NREM sleep) in memory consolidation has been demonstrated in a study[36] where, through electrical stimulations, slow oscillations were induced and boosted; because of this SWA increase, participants had a better performance in declarative memory tasks. Not only SWA helps learning, but it is also crucial, because its suppression has been demonstrated to impair declarative memory consolidation.[37]

On the other hand, sleep spindles (especially associated with N2 NREM sleep stage, but can also occur during N3 NREM sleep stage) are also crucial for declarative consolidation; indeed they are enhanced (increasing in density) after declarative learning,[38] their increase is associated with a better memory performance (which has been proved using pharmacological manipulation of spindles' density, and measuring outcomes on learning tasks).[39]

A working model of sleep and memory stabilization

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Schreiner and Rasch (2017)[35] proposed a model illustrating how the cueing beneficial effect on memory during sleep could function, which includes theta and gamma waves and sleep spindles.

Increased theta activity represents the successful reestablishment of the memory after the cueing: if such an increase is observed, it means that the association between the cue and the memory trace is strong enough, and that the cue is presented in an effective way and time. Theta waves interacts with gamma activity, and - during NREM - this oscillatory theta-gamma produces the relocation of the memory representation, from the hippocampus to the cortex. On the other hand, sleep spindles increase occurs right after or in parallel to the theta augmentation, and is a necessary mechanism for the stabilization, the reinforcement and also the integration of the newly encoded memory trace.[35]

Importantly, in this working model, slow oscillations have the role of a 'time-giving pace maker',[35] and seem to be a prerequisite for the success of cueing.

According to this model, enhancing only slow waves or only spindles, is not sufficient to improve memory function of sleep: both need to be increased to obtain an influence and this latter.[35]

NREM in other animals

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Not much is known about NREM, so scientists have conducted studies in other animals to potentially understand more, in particular why the brain has evolved to have two distinct states.[40] In their studies, it was found that between birds and certain mammals like dolphins, their brains exhibit similar behavior. It was found that certain species of birds have half their brain's hemisphere release brain waves similar to a human's during NREM sleep, and the other half of it fully conscious, allowing them to fly while sleeping.[41] Certain species of dolphins also exhibit similar behavior as birds in order to be able to swim while sleeping.[42]

In rats, after a 24-hour sleep deprivation, it was found that there was an increase of slow-wave activity in NREM sleep,[43] which corresponds directly with the human brain which when sleep deprived, prioritizes NREM sleep over REM sleep, implying that the NREM sleep is responsible for regulating and compensating for missed sleep.[44]

References

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Further reading

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Non-rapid eye movement sleep

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Non-rapid eye movement (NREM) sleep is one of the two primary phases of human sleep, alongside rapid eye movement (REM) sleep, and constitutes approximately 75-80% of total sleep duration in adults. It is characterized by the absence of rapid eye movements, reduced muscle activity, and progressive deepening of sleep through three distinct stages (N1, N2, and N3), during which brain wave patterns shift from lighter theta waves to deeper delta waves, facilitating physiological restoration and cognitive processing. Unlike REM sleep, which features vivid dreaming and brain activity resembling wakefulness, NREM sleep emphasizes bodily repair and memory consolidation without significant eye movements or muscle atonia. NREM sleep progresses through its stages in cycles lasting about 90-120 minutes, repeating 4-6 times per night, with deeper stages more prevalent in the first half of the sleep period. Stage N1 represents the transition from to , lasting 1-5 minutes and involving light sleep with brain waves (4-7 Hz), slowed breathing, and relaxed muscles, comprising roughly 5% of total . Stage N2, the longest phase at about 45-50% of sleep time, features sleep spindles (bursts of 11-16 Hz activity) and K-complexes on (EEG), which help maintain and contribute to encoding, with further reductions in and body temperature. Stage N3, or deep , involves high-amplitude delta waves (0.5-4 Hz) and is the most restorative, making difficult and accounting for 20-25% of , particularly in younger individuals where it peaks during childhood before declining with age. The physiological functions of NREM sleep are essential for overall health, primarily supporting restorative processes such as tissue repair, muscle growth, and protein synthesis through the release of , especially during stage N3. It bolsters immune function by enhancing production and other immune responses, reducing inflammation and aiding recovery from illness or stress. Cognitively, NREM sleep facilitates —declarative memories in stage N3 via slow waves and procedural memories in stage N2 through spindles—while promoting synaptic by downscaling neural connections to prevent overload from daytime learning. Disruptions in NREM sleep are linked to impaired physical recovery, weakened immunity, and cognitive deficits, underscoring its role in maintaining metabolic balance, including glucose regulation and control.

Definition and Overview

Definition

Non-rapid eye movement (NREM) sleep is one of the two primary phases of , distinguished by the lack of rapid eye movements and comprising approximately 75-80% of total time in healthy adults. This phase is subdivided into three stages—N1, N2, and N3—based on the (AASM) scoring criteria, first established in its 2007 manual for the scoring of and associated events and retained in subsequent versions (e.g., Version 3, 2023). These stages reflect a progression from light to deep , characterized by distinct electroencephalographic patterns, though without the rapid eye movements or muscle atonia seen in the other phase. The classification of NREM sleep evolved from earlier systems; the seminal 1968 manual by Rechtschaffen and Kales defined four NREM stages (1–4), with stages 3 and 4 representing based on amplitude. In 2007, the AASM task force revised this framework, merging stages 3 and 4 into a single N3 stage due to insufficient evidence supporting their separation, thereby simplifying scoring while maintaining focus on slow-wave activity for identification. Physiologically, NREM sleep is marked by a progressively decreasing threshold from , requiring stronger stimuli to awaken an individual, particularly in deeper stages where thresholds can exceed 100 decibels of noise. It features dominance, which lowers , , and metabolic rate while promoting restorative processes. Sensory responsiveness is also reduced, as the inhibits the relay of external stimuli to the , facilitating disconnection from the environment. Throughout a typical night's sleep, NREM phases alternate with in ultradian cycles lasting 90 to 120 minutes, with earlier cycles shorter (70–100 minutes) and later ones longer, occurring 4 to 6 times in an 8-hour period.

Comparison to REM Sleep

Non-rapid eye movement (NREM) sleep is distinguished from primarily by its patterns and muscle activity. During NREM sleep, EEG recordings show high-amplitude, low-frequency slow waves, particularly in deeper stages, reflecting synchronized neural activity across brain regions. In contrast, REM sleep features low-voltage, mixed-frequency EEG waves resembling those of , indicative of desynchronized, activated brain states. Additionally, NREM sleep maintains skeletal muscle tone, allowing for potential movement, whereas REM sleep is characterized by muscle atonia, a temporary that prevents acting out dreams, mediated by brainstem mechanisms. Sleep architecture further highlights these differences through cycle progression and age-related changes. A typical night's sleep consists of 4–6 cycles, each lasting about 90 minutes, beginning with NREM sleep that dominates the early cycles and accounts for roughly 75–80% of total time in adults. REM periods are shorter initially but lengthen toward morning, comprising 20–25% of . With advancing age, the proportion and duration of NREM sleep decline significantly, while REM sleep remains relatively stable, contributing to fragmented sleep in older adults. Arousal thresholds and functional roles also differ markedly. Light stages of NREM sleep have the lowest arousal thresholds, making awakening relatively easy compared to REM sleep, though deep NREM (stage N3) exhibits thresholds as high as or higher than REM due to profound neural inhibition. NREM sleep is closely linked to restorative processes, including tissue repair, immune function, and growth hormone release, emphasizing its role in physical recovery. In comparison, REM sleep supports cognitive and emotional processing but is associated with higher vulnerability to certain arousals, such as those triggered by intense stimuli. Recent multimodal neuroimaging studies from the 2020s have elucidated these contrasts at the neural level. (fMRI) combined with EEG reveals that NREM sleep promotes global brain synchronization, with widespread low-frequency oscillations facilitating metabolic clearance and network . Conversely, REM sleep shows localized, phasic activations in areas like the and , akin to dreaming-related processing, without the broad coherence seen in NREM. These findings underscore NREM's unique contribution to whole-brain maintenance versus REM's targeted reactivation.

Stages of NREM Sleep

N1 Stage

The N1 stage, the lightest phase of non-rapid eye movement (NREM) sleep, typically accounts for about 5% of total time in healthy adults. This transitional period usually lasts 1 to 7 minutes at the onset of or during brief arousals later in the night. Characterized by a shift from the relaxed wakefulness of (8-13 Hz) to low-amplitude mixed-frequency electroencephalographic (EEG) activity dominated by theta waves (4-7 Hz), N1 marks the initial descent into . Slow, rolling eye movements are detectable via (EOG), and vertex sharp waves—brief, high-amplitude potentials over the central —may emerge on EEG, reflecting early neural adjustments. Physiologically, N1 involves subtle but noticeable changes that ease the body toward rest. Heart rate and breathing slow gradually from waking levels, while skeletal muscle tone relaxes slightly, though not as profoundly as in deeper stages. Hypnic jerks, involuntary muscle twitches often perceived as a falling sensation, frequently occur during this stage, potentially triggered by the brain's lingering wakeful signals. These events are benign and common, affecting up to 70% of individuals at sleep onset. As a critical bridge from , facilitates the progression to deeper NREM stages if undisturbed, but remains highly responsive. Individuals awakened from often experience brief disorientation, frequently denying they were due to the stage's shallow nature. Recent research (2022-2025) indicates that rhythms during promote neural synchronization, contributing to initial that dampens extraneous inputs and supports the transition to consolidated .

N2 Stage

The N2 stage, also known as stage 2 of non-rapid eye movement (NREM) sleep, represents an intermediate level of sleep that follows the lighter stage and constitutes approximately 45-55% of total sleep time in healthy adults. This stage typically lasts 10-25 minutes per , with durations lengthening in subsequent cycles throughout the night. As sleep progresses from N1, the exhibits distinct (EEG) patterns that help maintain sleep continuity, including sleep spindles and K-complexes. Sleep spindles are brief bursts of oscillatory activity in the 11-16 Hz frequency range, lasting 0.5-2 seconds, which appear prominently in the central and frontal EEG leads during N2. These transient events are generated by interactions between thalamic reticular neurons and thalamocortical circuits, contributing to sleep protection and cognitive processing. K-complexes, another hallmark of N2, consist of high-amplitude, biphasic waves—a sharp negative deflection followed by a positive component—lasting about 1 second and often preceding or following spindles. These EEG features distinguish N2 from lighter sleep and signal the brain's adaptation to deeper rest, though delta waves become more prominent in the subsequent N3 stage. Physiologically, N2 involves further reductions in heart rate variability and core body temperature compared to N1, promoting metabolic conservation and relaxation of skeletal muscles. The arousal threshold during N2 is higher than in N1, making brief awakenings less likely, yet lower than in N3, allowing for occasional micro-arousals in response to stimuli. Recent research highlights the protective role of sleep spindles in N2, demonstrating that higher spindle density elevates the arousal threshold against environmental noise, thereby stabilizing sleep architecture.

N3 Stage

The N3 stage, also known as , represents the deepest phase of non-rapid eye movement (NREM) sleep and typically constitutes 15-25% of total sleep time in healthy adults, though this proportion decreases with aging due to reduced slow-wave activity. It is characterized by (EEG) patterns dominated by delta waves in the 0.5-4 Hz frequency range, with slow waves comprising more than 20% of any 30-second epoch, high-voltage deflections exceeding 75 μV, and a markedly elevated arousal threshold that makes spontaneous awakenings rare. This stage predominantly occurs during the first half of the night, with longer episodes early in the that progressively shorten as the night advances. Physiologically, N3 sleep features the lowest , , and of the night, reflecting profound parasympathetic dominance and bodily restoration, with often dropping by 10-20%. release reaches its peak during this stage, supporting tissue repair, metabolic regulation, and overall recovery. Awakening from N3 sleep often induces , a state of transient grogginess, impaired , and reduced alertness that typically lasts 15-60 minutes, more pronounced than from lighter stages due to the depth of neural synchronization. Recent studies from 2024 have provided evidence of widespread cortical during delta bursts in N3 sleep, where synaptic strength reductions correlate with decreased slow-wave slopes, facilitating neural reset and desynchronization of cortical circuits for improved post-sleep performance. These processes briefly couple with sleep spindles to support , though detailed mechanisms are addressed elsewhere.

Neural and Physiological Characteristics

Electroencephalography Patterns

(EEG) is a primary method for characterizing non-rapid eye movement (NREM) sleep through the analysis of wave patterns recorded from the . During , the EEG typically exhibits alpha rhythms at 8-13 Hz, reflecting relaxed alertness. As sleep onset occurs, there is a progressive shift in dominant frequencies across NREM stages: in the initial N1 stage, alpha activity diminishes, giving way to waves (4-8 Hz) with low-voltage, mixed-frequency patterns; this evolves into more varied frequencies in N2; and culminates in dominance (0.5-4 Hz) in the deep N3 stage, where high-amplitude, slow oscillations predominate. A hallmark of NREM sleep EEG morphology is the presence of high-voltage, synchronized waves, particularly the slow delta oscillations in N3, which arise from coordinated neuronal firing across cortical networks. This contrasts sharply with the desynchronized, low-voltage, fast-activity patterns observed in rapid eye movement () sleep, which resemble wakeful states. These morphological differences underscore the distinct neural states between NREM and REM, with NREM promoting global brain essential for restorative processes. EEG measurements in sleep research involve placing electrodes on the according to the international 10-20 system to capture voltage fluctuations from underlying activity. Power spectral analysis is then applied to decompose these signals into bands (e.g., delta, , alpha), quantifying the relative power in each to identify sleep stages and track transitions. This approach allows for precise delineation of the shifts that define NREM progression. Recent advances in high-density EEG, utilizing arrays of 128 or more channels, have revealed regional variations in slow-wave propagation during NREM sleep. Studies such as those from 2011 and 2022 demonstrate that slow waves do not occur uniformly but travel across the cortex in directed paths, originating in prefrontal areas and propagating posteriorly, with variations influenced by local neural properties. These findings highlight the spatially heterogeneous nature of NREM brain activity, providing deeper insights into its regulatory mechanisms.

Sleep Spindles and K-Complexes

Sleep spindles are transient bursts of oscillatory activity characterized by waxing-and-waning electroencephalographic (EEG) waves in the 11–16 Hz range, typically lasting 0.5–2 seconds. These events are generated through interactions in thalamo-cortical circuits, where neurons initiate rhythmic bursts that propagate to cortical layers via thalamocortical relay cells. Sleep spindles predominantly occur during stage N2 of non-rapid (NREM) sleep. Two main types of sleep spindles have been identified based on their frequency and topographic distribution: slow spindles, oscillating at 9–12 Hz and localized primarily to frontal regions, and fast spindles, oscillating at 13–15 Hz and centered over centro-parietal areas. Slow spindles are more prominent during deeper NREM stages, while fast spindles predominate in lighter NREM sleep. K-complexes represent the largest transient EEG waveform in human sleep, consisting of a distinct biphasic morphology with a sharp negative deflection followed by a slower positive wave, lasting approximately 1 second (ranging from 0.5 to 1.5 seconds). They often occur in isolation or followed by a and can be elicited as a response to external auditory or somatosensory stimuli, serving as an threshold marker without fully awakening the sleeper. Like spindles, K-complexes are hallmark features of N2 sleep. Both s and K-complexes contribute to by modulating thalamic relay of external inputs to the cortex, thereby promoting sleep maintenance and continuity. They also play roles in stabilizing synaptic traces and facilitating , which supports processes like . Recent studies, including those from 2022, have linked higher density to enhanced cognitive performance and greater resilience against psychiatric vulnerabilities such as , with some evidence of correlations with intelligence. In deeper NREM stages like N3, spindles can couple with slow oscillations to coordinate cortical activity. Quantification of these events typically involves measuring spindle density as the number of spindles per minute of NREM , with normal ranges varying by age and region but often averaging 2–6 per minute in adults. For K-complexes, detection criteria include a peak-to-peak exceeding 75 μV, ensuring distinction from smaller delta waves.

Cognitive Aspects

Dreaming

Dreams during non-rapid eye movement (NREM) sleep are reported less frequently than those in rapid eye movement (REM) sleep, with early studies reporting recall rates upon awakening of about 7% for NREM compared to 81% for REM, though more recent estimates indicate NREM rates around 40-50%. Dream recall rates vary by NREM stage, being higher in N1 and N2 than in deep N3 slow-wave sleep. These dreams tend to occur more often in later sleep cycles, particularly in the early morning hours when NREM periods follow extended REM episodes, increasing the likelihood of recall. In terms of duration, NREM dreams are generally shorter, lasting from seconds to a few minutes, in contrast to the more prolonged and immersive experiences during REM. The content of NREM dreams is often described as mundane, thought-like, and realistic, featuring static scenes or reflective problem-solving rather than the dynamic, bizarre narratives common in dreams. They exhibit less emotional intensity, with reduced vividness in sensory elements such as visual , and a greater focus on everyday concerns or logical processing. Unlike the hallucinatory and story-like quality of REM dreams, NREM mentation more closely resembles waking thoughts or brief fragments of episodic memory. Neurologically, NREM dreaming involves greater activation in frontal brain regions compared to REM sleep, supporting higher and reflective elements in the dream content. This frontal involvement contributes to the more coherent, less visually dominant experiences, as posterior cortical areas show reduced low-frequency activity associated with dream recall. Recent studies from 2023 to 2025 using awakenings from N2 stage NREM sleep have reported fragmented, narrative-like dream elements, with recall linked to increased density preceding awakenings. These findings suggest that spindles in N2 may facilitate the integration of brief, thought-oriented mentation into accessible memories upon arousal.

Memory Consolidation

Non-rapid eye movement (NREM) sleep plays a critical role in the , transforming fragile, newly encoded traces into stable, long-lasting representations through active neural processes. During NREM sleep, particularly in stages N2 and N3, the brain engages in the reactivation and reorganization of engrams, facilitating the transfer of from short-term storage in the hippocampus to long-term storage in the . This process is essential for both declarative memories, such as facts and events, and procedural memories, like skills and habits. A key mechanism underlying this consolidation is the replay of hippocampal activity during (SWS), which corresponds to N3 stage, where sharp-wave ripples in the hippocampus synchronize with cortical slow oscillations, promoting the replay of waking experiences. This replay strengthens synaptic connections associated with recent learning. Complementing this, sleep spindles—brief bursts of activity in the 11-16 Hz range predominant in N2 stage—mediate the transfer of this reactivated information from the hippocampus to distributed neocortical networks, enabling systems-level consolidation. These processes form a two-stage model of : initial encoding and synaptic strengthening occur during , followed by stabilization and integration during NREM sleep, which protects memories from interference and enhances retrieval. Evidence for these mechanisms comes from targeted memory reactivation (TMR) studies, where sensory cues (e.g., sounds or odors) associated with learning are presented during to trigger specific replay. A 2020 meta-analysis of 91 experiments involving over 2,000 participants found that TMR during NREM sleep significantly enhances performance, with a moderate (Hedges' g = 0.28 overall, and up to 0.40 for tasks), indicating reliable improvements in recall and retention. More recent studies from the 2010s to 2020s, including those using odors during SWS, have shown TMR boosts declarative recall by 15-25% compared to control conditions without cues. These effects are stage-specific: N2 sleep spindles particularly support consolidation, as evidenced by enhanced motor skill performance following spindle-linked cues, while N3 slow waves are more critical for declarative memories, with a 2024 confirming stronger associations between slow oscillation-spindle coupling and declarative .

Functions and Mechanisms

Synaptic Homeostasis

The synaptic homeostasis hypothesis posits that wakefulness leads to a net increase in synaptic strength across cortical circuits due to experience-dependent potentiation, and non-rapid eye movement (NREM) sleep serves to downscale these strengthened synapses to prevent neural overload, restore efficiency, and maintain overall brain homeostasis. Proposed by Tononi and Cirelli in 2003, this framework emphasizes that the intensity of slow-wave activity (SWA) during NREM sleep, particularly in the delta frequency range (0.5–4 Hz), reflects the degree of synaptic potentiation accumulated during prior wakefulness and progressively declines as downscaling occurs. Refinements to the hypothesis have incorporated evidence that downscaling not only renormalizes synaptic weights but also supports selective synaptic stabilization, with NREM sleep acting as a period of global synaptic renormalization rather than uniform weakening. Supporting evidence includes measurements showing reduced cortical excitability following NREM sleep, as assessed by combined with (TMS-EEG), where TMS-evoked potentials and motor-evoked potentials are smaller and delayed during NREM compared to , indicating decreased synaptic responsiveness. Additionally, the magnitude of delta power during NREM sleep correlates with the history of learning and synaptic potentiation during , with local increases in SWA observed in regions engaged by specific tasks, such as , supporting the that sleep intensity tracks prior synaptic changes. In terms of NREM stages, slow waves predominant in stage N3 () are thought to drive synaptic depotentiation by coordinating widespread hyperpolarization and reduced firing during down-states, facilitating the uniform downscaling of potentiated synapses across networks. spindles, oscillatory bursts primarily in stage N2, play a complementary role in coordinating , potentially by modulating calcium influx and protecting or selectively reinforcing recently potentiated synapses during downscaling. Recent studies, such as a 2024 study in animal models including larval , demonstrate that NREM-equivalent sleep actively reduces number in visual regions following sleep deprivation-induced increases, providing direct causal evidence for as part of and highlighting its evolutionary conservation across vertebrates. This process contributes to outcomes like enhanced by freeing neural resources for new learning.

Recovery and Health Roles

Non-rapid eye movement (NREM) sleep plays a crucial role in physical restoration, particularly through the secretion of growth hormone during stage N3, also known as slow-wave sleep. This hormone, essential for tissue repair, muscle growth, and metabolic regulation, exhibits a strong sleep-dependent rhythm, with peak release occurring specifically in association with N3 sleep. Studies in children and adults confirm that the pulsatile secretion of growth hormone aligns closely with the onset and depth of slow-wave activity in NREM, underscoring its restorative function. Additionally, NREM sleep enhances immune function by regulating cytokine production, promoting anti-inflammatory responses that support overall immune homeostasis. Cytokines such as interleukin-1 and tumor necrosis factor-alpha, which are elevated during NREM, facilitate immune cell activity while modulating sleep architecture to aid recovery from infections. Recent research further links NREM duration to reduced . A 2024 study demonstrated an inverse association between intensity—a key marker of NREM—and low-grade inflammatory processes, suggesting that longer NREM periods help mitigate chronic inflammation through enhanced balance. In the context of stress resilience, post-stress NREM sleep is vital for emotional regulation and normalization. According to a 2025 review in , NREM following acute stress promotes neural and physiological recovery, dampening hypothalamic-pituitary-adrenal axis hyperactivity and restoring emotional balance via consolidated slow-wave activity. Insufficient NREM sleep is associated with adverse health outcomes, including metabolic disorders and increased cardiovascular risk. Shortened NREM duration disrupts glucose and insulin sensitivity, elevating the likelihood of and , as evidenced by epidemiological data linking NREM deprivation to cardiometabolic imbalances. Similarly, age-related declines in NREM sleep accelerate the loss of , exacerbating vulnerability to neurodegenerative changes by reducing protective mechanisms against brain aging. Emerging 2024 findings highlight NREM's involvement in glymphatic clearance, the brain's waste removal system, where slow-wave oscillations drive flow to eliminate metabolic byproducts like amyloid-beta, potentially preventing accumulation linked to neurological disorders.

Parasomnias and Disorders

Common Parasomnias

Non-rapid eye movement (NREM) sleep parasomnias, also known as disorders of arousal, encompass a spectrum of abnormal behaviors that emerge from incomplete transitions between and , primarily during N1, N2, or N3 stages. The most prevalent types include confusional arousals, which typically arise from N1 or N2 and involve brief episodes of confusion or disorientation upon partial awakening; (somnambulism), occurring predominantly in N3 and characterized by complex motor activities such as walking while asleep; and night terrors (sleep terrors), also linked to N3 and featuring intense fear, screaming, and autonomic activation without full recall. These parasomnias affect 1-17% of children, with higher rates in preschool-aged individuals, and prevalence generally decreases with age, often resolving by in most cases. Manifestations commonly involve partial arousals accompanied by amnesia for the event, limited responsiveness to external stimuli, and behaviors that range from simple agitation in confusional arousals to ambulatory actions in or panicked reactions in night terrors, all without achieving full . Genetic factors play a significant role, with associations to (HLA) alleles such as DQB1*05:01, which is more frequent in affected individuals and familial cases, suggesting a hereditary predisposition. Triggers for these episodes include , which increases pressure and promotes ; fever, which disrupts sleep architecture; and certain medications, such as sedatives or antidepressants, that alter arousal thresholds. Recent research highlights the variable night-to-night expression of these parasomnias, where episodes may fluctuate in frequency and intensity due to interplay of predisposing and precipitating factors, complicating consistent clinical observation. Differentiation from other sleep disorders relies on video-polysomnography (vPSG), which confirms the NREM origin by capturing behaviors synchronized with EEG patterns of incomplete arousals, distinguishing them from events involving full or REM sleep associations. This measurement technique, often involving overnight monitoring, reveals the absence of oriented responsiveness, reinforcing the diagnosis of these dissociated states.

Clinical Implications

Disruptions in non-rapid eye movement (NREM) sleep are implicated in several disorders, including NREM-dominant , where patients exhibit increased high-frequency electroencephalographic (EEG) activity during NREM stages compared to controls, contributing to fragmented sleep and daytime impairment. (OSA) significantly reduces N3 sleep duration, with patients showing lower amounts of (SWS) and increased lighter sleep stages relative to healthy individuals. Recent studies from 2023 to 2025 have established links between NREM sleep disturbances and psychiatric and neurodegenerative conditions; for instance, chronic with NREM instability predicts the onset of depressive disorders. Similarly, reduced NREM sleep, particularly SWS, accelerates progression by impairing amyloid clearance and exacerbating cognitive symptoms. The clinical implications of shortened NREM sleep duration extend to broader health risks, including cognitive decline, where briefer NREM/REM cycles over time correlate with the development of or four years later. Insufficient NREM sleep also promotes immune dysfunction through chronic and altered innate/adaptive immune responses, heightening vulnerability to infections and autoimmune conditions. Age-related loss of SWS, which declines progressively from early adulthood, is associated with heightened risk, as greater reductions in SWS percentage predict incident independently of genetic factors. Treatments for NREM-related disorders emphasize behavioral and pharmacological interventions tailored to underlying mechanisms. For parasomnias arising during NREM sleep, scheduled awakenings—where caregivers gently rouse the individual 15-30 minutes before typical episode onset—have demonstrated efficacy in reducing frequency and severity across multiple case series. Pharmacotherapy, such as low-dose clonazepam (0.5-2 mg at bedtime), effectively suppresses disorders of arousal like night terrors, with response rates around 75% in retrospective analyses of affected adults. Advances in 2025 include exploratory use of gamma-hydroxybutyrate to enhance SWS in conditions like major depression, potentially restoring NREM architecture and mitigating associated cognitive deficits. Efforts to target sleep spindles, key NREM features, via pharmacological enhancement are emerging, though clinical trials remain ongoing. Public health guidelines underscore the importance of sufficient sleep to preserve NREM integrity, with the recommending 7-9 hours per night for adults to minimize risks of cognitive and immune impairments from NREM deficits. Adhering to this duration supports optimal SWS accumulation, equivalent to 40-110 minutes nightly in healthy adults, thereby promoting long-term brain health and recovery processes.

Measurement Techniques

Polysomnography

(PSG), also known as a , serves as the gold standard for objectively measuring non-rapid (NREM) sleep in both clinical and contexts by recording multiple physiological signals overnight. The procedure involves attaching electrodes to the scalp, face, and body to monitor brain activity via (EEG), eye movements through (EOG), muscle tone with (EMG), and heart rhythm using (ECG), typically conducted in a from evening until morning. According to the (AASM) guidelines, data are scored in 30-second epochs, where each segment is classified based on predominant physiological features to delineate stages, including NREM phases. Identification of NREM sleep during PSG relies primarily on visual scoring of EEG waveforms by trained technicians, who look for characteristic patterns such as theta waves in stage , sleep spindles and K-complexes in stage N2, and high-amplitude delta waves in stages N3. Automated algorithms complement this by quantifying specific NREM markers, such as detecting sleep spindles (11-16 Hz oscillations) with accuracies approaching human experts and computing delta power (0.5-4 Hz) to assess depth. In applications, PSG is essential for diagnosing NREM-related parasomnias like or confusional arousals by capturing abnormal behaviors alongside physiological data, and it provides detailed assessments of sleep architecture, revealing disruptions in NREM continuity or duration. However, limitations include high costs—often exceeding $1,000 per study due to equipment and staffing—and the requirement for lab confinement, which can alter natural sleep patterns through unfamiliar environments. Updates in the 2020s have integrated video recording with PSG (video-PSG) to simultaneously capture behavioral manifestations during NREM sleep, enhancing of parasomnias by correlating movements with electrophysiological signals. Modern automated scoring systems for stage classification now achieve accuracies up to 90%, matching or surpassing among human scorers, particularly for NREM stages.

Advanced Methods

Wearable electroencephalography (EEG) devices represent a significant advancement in non-invasive NREM sleep monitoring, enabling home-based assessments that extend beyond laboratory constraints. Devices such as the Waveband (formerly known as Dreem) headband utilize dry electrodes to record EEG signals, facilitating the detection of NREM stages, including slow-wave sleep, with performance comparable to polysomnography (PSG) in controlled validations. These headbands allow for longitudinal home monitoring, capturing NREM architecture over extended periods without requiring clinical supervision, as demonstrated in studies involving older adults where they accurately identified sleep efficiency and stage distributions. Hybrid functional (fMRI) and EEG techniques provide deeper insights into the neural correlates of NREM sleep by combining high-spatial-resolution hemodynamic mapping with temporal EEG precision. Simultaneous EEG-fMRI acquisitions have revealed spatially structured patterns of brain activation during NREM transitions, such as decreased thalamic and cortical connectivity in . These methods are particularly valuable for studying NREM-specific phenomena like sleep spindles, where fMRI highlights subcortical involvement that standalone EEG cannot resolve. Recent advancements incorporate algorithms to enhance real-time detection of NREM features, such as sleep spindles, achieving high F1 scores up to around 80% in 2024 models trained on multichannel EEG data. frameworks like convolutional neural networks outperform traditional thresholding methods by identifying spindle oscillations (12-16 Hz) with reduced false positives, enabling on-device processing in wearables. Complementing this, —using wrist-worn accelerometers—has been refined with AI to estimate NREM-REM cycles through movement and patterns, offering a low-burden alternative for cycle duration assessment in settings. In research applications, these advanced methods support longitudinal investigations into age-related NREM decline, where wearable EEG tracks reductions in slow-wave activity over years, correlating with cognitive changes in cohorts followed from midlife. By 2025, multimodal approaches integrating (PET) with EEG have emerged to probe NREM metabolic dynamics, revealing coupled decreases in and during deep sleep stages, as confirmed in peer-reviewed studies published in October 2025. Such integrations facilitate the study of NREM's restorative roles, linking metabolic shifts to synaptic in aging populations. Despite these benefits, advanced methods exhibit limitations, including reduced precision in stage classification compared to PSG—particularly for light NREM (N1)—due to fewer electrodes and susceptibility to motion artifacts. Ongoing validation against gold-standard PSG remains essential to ensure reliability across diverse populations, as wearable accuracies can vary by 10-20% in real-world conditions.

Comparative and Evolutionary Aspects

NREM in Animals

Non-rapid eye movement (NREM) sleep exhibits notable physiological similarities across mammalian , characterized by distinct electroencephalographic (EEG) features such as slow-wave activity and sleep spindles, though variations exist in structure and distribution. In rats, NREM sleep is marked by prominent delta power (0.5–4 Hz) in the EEG, which reflects homeostatic sleep pressure and increases following deprivation, serving as a key marker of sleep depth and recovery. Similarly, in cats, NREM sleep includes stages with sleep spindles—transient bursts of 11–16 Hz activity—particularly in lighter stages, facilitating the progression through sleep cycles that alternate with rapid eye movement () sleep. Certain aquatic mammals, such as dolphins, display unihemispheric NREM sleep, where slow-wave activity occurs independently in each hemisphere, allowing one side to remain vigilant for and predator avoidance while the other rests. In birds, NREM sleep features high-amplitude slow waves analogous to those in mammals, often occurring unihemispherically to support functions like flight control and during migration or rest. Unlike mammals, birds lack a clear REM equivalent, with their sleep consisting primarily of NREM-like states interspersed with brief, REM-resembling episodes of low-voltage EEG. Studies from 2022 highlight how avian NREM, particularly , optimizes energy expenditure in ecologically demanding contexts, such as in seabirds or migratory species where total is minimized. Invertebrates exhibit basic rest states that parallel NREM sleep in vertebrates, characterized by quiescence, elevated arousal thresholds, and homeostatic regulation where rest duration increases proportionally with prior wakefulness. For instance, in fruit flies and nematodes, these states involve conserved molecular pathways for sleep homeostasis, though without the complex EEG signatures of higher animals. Research on NREM sleep in animals often employs chronic electrode implants in to analyze sleep cycles, enabling long-term recording of EEG patterns, delta power dynamics, and transitions between NREM and stages with high temporal resolution. Across most mammalian and avian , NREM sleep comprises 70–90% of total time, underscoring its dominant role in restoration and . These animal models share core NREM features with humans, such as slow-wave dominance, but adapted to species-specific ecological needs.

Evolutionary Perspectives

Non-rapid eye movement (NREM) sleep exhibits remarkable conservation across vertebrate species, indicating its evolutionary origins trace back more than 500 million years to the emergence of early vertebrates. This deep phylogenetic persistence suggests NREM sleep predates the divergence of major vertebrate lineages, with analogous states observed in , reptiles, birds, and mammals through behavioral quiescence, elevated thresholds, and EEG patterns resembling slow-wave activity. The posits that NREM sleep serves as an ancient drive for synaptic strength accumulated during , a process rooted in fundamental neural plasticity mechanisms that likely evolved with the advent of complex nervous systems in early animals. Adaptive functions of NREM sleep include substantial energy conservation, with whole-body metabolic rates typically decreasing by 10-15% compared to wakefulness, and cerebral glucose metabolism dropping by up to 40% during deep NREM stages. This metabolic reduction facilitates resource allocation for restorative processes while minimizing exposure risks, as the profound immobility and sensory disconnection of NREM promote predator avoidance by enabling concealed, deep rest in safe microhabitats. Phylogenetically, NREM-like states precede REM sleep, appearing as the basal sleep form in non-mammalian vertebrates, whereas REM emerges later in amniotes, underscoring NREM's foundational role in sleep architecture. Evolutionary hypotheses emphasize NREM's role in neural maintenance, particularly for downregulating synaptic overload in increasingly complex brains, thereby preventing cognitive overload and supporting learning efficiency. Recent genomic analyses reveal that core sleep-regulatory genes, such as those involved in circadian rhythms and neural excitability, share homology with mechanisms in early eukaryotes, suggesting sleep-like restorative processes originated over a billion years ago through endosymbiotic integrations like mitochondria. A 2025 study further supports this by identifying mitochondrial electron leakage in sleep-regulating neurons as a key driver of sleep pressure, linking cellular energy processes to the need for restorative across . In , increased encephalization has been associated with shorter overall duration, including NREM, suggesting enhanced neural efficiency and more effective synaptic during reduced sleep time.

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