The impact of REM sleep loss on human brain connectivity.

Brain function is vulnerable to the consequences of inadequate sleep, an adverse trend that is increasingly prevalent. The REM sleep phase has been implicated in coordinating various brain structures and is hypothesized to have potential links to brain variability. However, traditional imaging research have encountered challenges in attributing specific brain region activity to REM sleep, remained understudied at the whole-brain connectivity level. Through the spilt-night paradigm, distinct patterns of REM sleep phases were observed among the full-night sleep group (n = 36), the early-night deprivation group (n = 41), and the late-night deprivation group (n = 36). We employed connectome-based predictive modeling (CPM) to delineate the effects of REM sleep deprivation on the functional connectivity of the brain (REM connectome) during its resting state. The REM sleep-brain connectome was characterized by stronger connectivity within the default mode network (DMN) and between the DMN and visual networks, while fewer predictive edges were observed. Notably, connections such as those between the cingulo-opercular network (CON) and the auditory network, as well as between the subcortex and visual networks, also made significant contributions. These findings elucidate the neural signatures of REM sleep loss and reveal common connectivity patterns across individuals, validated at the group level.

Sleep architecture in idiopathic hypersomnia: the influence of age, sex, and body mass index.

This study aimed to progress the understanding of idiopathic hypersomnia (IH) by assessing the moderating influence of individual characteristics, such as age, sex, and body mass index (BMI) on sleep architecture. In this retrospective study, 76 IH participants (38.1 ± 11.3 years; 40 women) underwent a clinical interview, an in-laboratory polysomnography with a maximal 9-h time in bed and a multiple sleep latency test (MSLT). They were compared to 106 healthy controls (38.1 ± 14.1 years; 60 women). Multiple regressions were used to assess moderating influence of age, sex, and BMI on sleep variables. We used correlations to assess whether sleep variables were associated with Epworth Sleepiness Scale scores and mean sleep onset latency on the MSLT in IH participants. Compared to controls, IH participants had shorter sleep latency (p = 0.002), longer total sleep time (p < 0.001), more time spent in N2 sleep (p = 0.008), and showed trends for a higher sleep efficiency (p = 0.023) and more time spent in rapid eye movement (REM) sleep (p = 0.022). No significant moderating influence of age, sex, or BMI was found. More severe self-reported sleepiness in IH patients was correlated with shorter REM sleep latency and less N1 sleep in terms of proportion and duration (ps < 0.01). This study shows that, when compared to healthy controls, patients with IH had no anomalies in their sleep architecture that can explain their excessive daytime sleepiness. Moreover, there is no moderating influence of age, sex, and BMI, suggesting that the absence of major group differences is relatively robust.

[The relationship between rapid eye movement electromyogram activity and sleep stability in rapid eye movement sleep behavior disorder].

Objective: To investigate the relationship between the types of electromyogram (EMG) activity and sleep stability during rapid eye movement (REM) in patients with rapid eye movement sleep behavior disorder(RBD). Methods: One hundred and three patients with RBD who met the inclusion and exclusion criteria at the Second Affiliated Hospital of Air Force Military Medical University from January 2017 to December 2019 were retrospectively analyzed. The general situation, clinical symptoms, sleep and emotion questionnaires and nocturnal PSG data were collected. According to the different proportions of tonic and phasic EMG activity, the group with a higher proportion of tonic EMG than phasic EMG was defined as the tonic dominant group, and the group with a higher proportion of phasic EMG than tonic was defined as the phasic dominant group. The sleep instability index was calculated according to the ratio of the number of transitions from sleep to wakefulness to the total sleep time of each sleep stage. Multiple linear regression was used to explore the relationship between REM EMG activity and sleep instability index. Results: A total of 35 idiopathic RBD (iRBD) patients were included, aged(54.5±18.2)years, with 17 males and 18 females. There were 27 RBD with Parkinson's disease (PD), with an average age of (59.4±7.9)years, including 17 males and 10 females. Additionally, there were 41 RBD patients with narcolepsy, aged (21.2±13.2)years, consisting of 22 males and 19 females. Both iRBD and RBD patients with PD had lower objective total sleep time, sleep latency, sleep efficiency, wake time after sleep onset and the percentage of N3 sleep compared to RBD with episodic sleep disorder (all P<0.05). N1-W index[M(Q1, Q3),10.6 (6.5, 16.9)/h vs 7.3 (4.7, 10.5)/h], N2-W index [4.0 (2.2, 5.6)/h vs 2.3 (1.5, 3.9)/h], NREM-W index [ (5.8±2.9)/h vs (4.5±3.2)/h] and REM-W index[ 3.9 (1.9, 7.3)/h vs 2.7 (1.0, 4.0)/h] in the phasic dominant group were higher than those in the tonic dominant group. After adjusting for confounding factors, the effect of phasic EMG dominant group on REM-W was higher than that in the tonic dominant group (ß=2.05, 95%CI: 0.09-3.26, P=0.012). Conclusion: In RBD patients, the phasic EMG activity has a significant impact on sleep stability, especially on REM sleep stability.

[Effects of slow-wave sleep fragmentation and rapid eye movement sleep fragmentation on melatonin secretion]. / Vliyanie fragmentatsii 3-i stadii sna i paradoksal'noi fazy sna na sekretsiyu melatonina.

OBJECTIVE: To compare the effect of stage 3 fragmentation and the paradoxical phase of night sleep on melatonin (MT) secretion, and to evaluate the effects of changes in autonomic balance and activation reactions that occur in the orthodox and paradoxical phases of sleep. MATERIAL AND METHODS: Fifteen healthy men participated in three sessions: with stage 3 fragmentation, with fragmentation of paradoxical sleep, and in a control experiment in which sleep was not disturbed. In each experiment, 7 saliva samples were collected in the evening, at night and in the morning and the MT content was determined. Heart rate variability was analyzed using an electrocardiogram and autonomic balance was assessed. RESULTS: Sleep fragmentation was accompanied by activation reactions and reduced the duration of stage 3 and paradoxical phase sleep by 50% and 51% in the corresponding sessions. Fragmentation of paradoxical sleep also led to an increase in the duration of night wakefulness. Sleep disturbances caused an increase in MT secretion in the second half of the night and in the morning, especially pronounced in sessions with fragmentation of paradoxical sleep, in which upon awakening MT was 1.8 times higher than in the control. Stage 3 fragmentation was accompanied by increased sympathetic activation, while fragmentation of paradoxical sleep did not cause autonomic shifts. The subjects were divided into 2 clusters: with high and low MT in night and morning saliva samples. In all sessions, subjects with high MT had 1.7-2 times longer duration of night wakefulness; in sessions with fragmentation, they had significantly more activations in the paradoxical phase of sleep. CONCLUSION: Night sleep disturbances cause an increase in MT secretion, especially pronounced during the fragmentation of the paradoxical phase. An increase in MT levels does not depend on changes in autonomic balance and is apparently associated with activation of the serotonergic system, which accompanies disturbances in the depth and continuity of sleep.

Circadian rapid eye movement sleep expression is associated with brain microstructural integrity in older adults.

Rapid eye movement sleep (REMS) is increasingly suggested as a discriminant sleep state for subtle signs of age-related neurodegeneration. While REMS expression is under strong circadian control and circadian dysregulation increases with age, the association between brain aging and circadian REMS regulation has not yet been assessed. Here, we measure the circadian amplitude of REMS through a 40-h in-lab multiple nap protocol in controlled laboratory conditions, and brain microstructural integrity with quantitative multi-parameter mapping (MPM) imaging in 86 older individuals. We show that reduced circadian REMS amplitude is related to lower magnetization transfer saturation (MTsat), longitudinal relaxation rate (R1) and effective transverse relaxation rate (R2*) values in several white matter regions mostly located around the lateral ventricles, and with lower R1 values in grey matter clusters encompassing the hippocampus, parahippocampus, thalamus and hypothalamus. Our results further highlight the importance of considering circadian regulation for understanding the association between sleep and brain structure in older individuals.

Prefrontal coding of learned and inferred knowledge during REM and NREM sleep.

Idling brain activity has been proposed to facilitate inference, insight, and innovative problem-solving. However, it remains unclear how and when the idling brain can create novel ideas. Here, we show that cortical offline activity is both necessary and sufficient for building unlearned inferential knowledge from previously acquired information. In a transitive inference paradigm, male C57BL/6J mice gained the inference 1 day after, but not shortly after, complete training. Inhibiting the neuronal computations in the anterior cingulate cortex (ACC) during post-learning either non-rapid eye movement (NREM) or rapid eye movement (REM) sleep, but not wakefulness, disrupted the inference without affecting the learned knowledge. In vivo Ca2+ imaging suggests that NREM sleep organizes the scattered learned knowledge in a complete hierarchy, while REM sleep computes the inferential information from the organized hierarchy. Furthermore, after insufficient learning, artificial activation of medial entorhinal cortex-ACC dialog during only REM sleep created inferential knowledge. Collectively, our study provides a mechanistic insight on NREM and REM coordination in weaving inferential knowledge, thus highlighting the power of idling brain in cognitive flexibility.

Isoflurane anesthesia and sleep deprivation trigger delayed and selective sleep alterations.

Isoflurane anesthesia (IA) partially compensates NREM sleep (NREMS) and not REM sleep (REMS) requirement, eliciting post-anesthetic REMS rebound. Sleep deprivation triggers compensatory NREMS rebounds and REMS rebounds during recovery sleep as a result of the body's homeostatic mechanisms. A combination of sleep deprivation and isoflurane anesthesia is common in clinical settings, especially prior to surgeries. This study investigates the effects of pre-anesthetic sleep deprivation on post-anesthetic sleep-wake architecture. The effects of isoflurane exposure (90 min) alone were compared with the effects of isoflurane exposure preceded by experimental sleep deprivation (6 h, gentle handling) on recovery sleep in adult mice by studying the architecture of post-anesthetic sleep for 3 consecutive post-anesthetic days. Effects of isoflurane anesthesia on recovery sleep developed only during the first dark period after anesthesia, the active phase in mice. During this time, mice irrespective of preceding sleep pressure, showed NREMS and REMS rebound and decreased wakefulness during recovery sleep. Additionally, sleep deprivation prior to isoflurane treatment caused a persistent reduction of theta power during post-anesthetic REMS at least for 3 post-anesthetic days. We showed that isoflurane causes NREMS rebound during recovery sleep which suggests that isoflurane may not fully compensate for natural NREMS. The study also reveals that isoflurane exposure preceded by sleep deprivation caused a persistent disruption of REMS quality. We suggest that preoperative sleep deprivation may impair postoperative recovery through lasting disruption in sleep quality.

Homeostatic regulation of rapid eye movement sleep by the preoptic area of the hypothalamus.

Rapid eye movement sleep (REMs) is characterized by activated electroencephalogram (EEG) and muscle atonia, accompanied by vivid dreams. REMs is homeostatically regulated, ensuring that any loss of REMs is compensated by a subsequent increase in its amount. However, the neural mechanisms underlying the homeostatic control of REMs are largely unknown. Here, we show that GABAergic neurons in the preoptic area of the hypothalamus projecting to the tuberomammillary nucleus (POAGAD2→TMN neurons) are crucial for the homeostatic regulation of REMs in mice. POAGAD2→TMN neurons are most active during REMs, and inhibiting them specifically decreases REMs. REMs restriction leads to an increased number and amplitude of calcium transients in POAGAD2→TMN neurons, reflecting the accumulation of REMs pressure. Inhibiting POAGAD2→TMN neurons during REMs restriction blocked the subsequent rebound of REMs. Our findings reveal a hypothalamic circuit whose activity mirrors the buildup of homeostatic REMs pressure during restriction and that is required for the ensuing rebound in REMs.

Out-of-body experiences in relation to lucid dreaming and sleep paralysis: A theoretical review and conceptual model.

Out-of-body experiences (OBEs) are characterized by the subjective experience of being located outside the physical body. Little is known about the neurophysiology of spontaneous OBEs, which are often reported by healthy individuals as occurring during states of reduced vigilance, particularly in proximity to or during sleep (sleep-related OBEs). In this paper, we review the current state of research on sleep-related OBEs and hypothesize that maintaining consciousness during transitions from wakefulness to REM sleep (sleep-onset REM periods) may facilitate sleep-related OBEs. Based on this hypothesis, we propose a new conceptual model that potentially describes the relationship between OBEs and sleep states. The model sheds light on the phenomenological differences between sleep-related OBEs and similar states of consciousness, such as lucid dreaming (the realization of being in a dream state) and sleep paralysis (feeling paralyzed while falling asleep or waking up), and explores the potential polysomnographic features underlying sleep-related OBEs. Additionally, we apply the predictive coding framework and suggest a connecting link between sleep-related OBEs and OBEs reported during wakefulness.

Automatic Sleep Stage Classification Using Nasal Pressure Decoding Based on a Multi-Kernel Convolutional BiLSTM Network.

Sleep quality is an essential parameter of a healthy human life, while sleep disorders such as sleep apnea are abundant. In the investigation of sleep and its malfunction, the gold-standard is polysomnography, which utilizes an extensive range of variables for sleep stage classification. However, undergoing full polysomnography, which requires many sensors that are directly connected to the heaviness of the setup and the discomfort of sleep, brings a significant burden. In this study, sleep stage classification was performed using the single dimension of nasal pressure, dramatically decreasing the complexity of the process. In turn, such improvements could increase the much needed clinical applicability. Specifically, we propose a deep learning structure consisting of multi-kernel convolutional neural networks and bidirectional long short-term memory for sleep stage classification. Sleep stages of 25 healthy subjects were classified into 3-class (wake, rapid eye movement (REM), and non-REM) and 4-class (wake, REM, light, and deep sleep) based on nasal pressure. Following a leave-one-subject-out cross-validation, in the 3-class the accuracy was 0.704, the F1-score was 0.490, and the kappa value was 0.283 for the overall metrics. In the 4-class, the accuracy was 0.604, the F1-score was 0.349, and the kappa value was 0.217 for the overall metrics. This was higher than the four comparative models, including the class-wise F1-score. This result demonstrates the possibility of a sleep stage classification model only using easily applicable and highly practical nasal pressure recordings. This is also likely to be used with interventions that could help treat sleep-related diseases.

Rapid eye movement dependency is associated with increased inflammatory activity in obstructive sleep apnea syndrome.

OBJECTIVE: Rapid eye movement (REM)-dependent obstructive sleep apnea syndrome (OSAS) is a specific subtype of OSAS having some phenotypic characteristics like a preference for a younger age, female gender, and milder severity. Such favorable features could make it possible to consider an overall benign course for this phenotype. However, accumulating data introduced its association with several cardiometabolic and vascular disorders recently. The primary objective of this study was to address the disease from the inflammation perspective and evaluate the potential inflammatory status in this variant via two accessible blood parameters: platelet distribution width (PDW) and systemic immune-inflammation index (SII). The secondary aim was to investigate whether this status, together with other disease characteristics, demonstrates consistency under different definitions of REM-dependent OSAS published previously. PATIENTS AND METHODS: The medical records of 35 patients with mild-to-moderate REM-dependent OSAS, 35 age- and sex-matched patients with REM-independent OSAS, and 25 non-OSA controls were retrospectively analyzed. Baseline features, polysomnographic characteristics, PDW, and SII were compared between the groups. Secondly, the analyses were repeated using different definitions of REM-dependent OSAS. Bivariate analyses were performed, and a multiple stepwise regression model was applied to adjust for body mass index (BMI) and cardiovascular risk (CVR) factors.  RESULTS: Mean PDW and SII were increased in patients with REM-dependent OSAS as compared to non-OSA controls (p = .022 and .029). The significance remained stable after adjustment for BMI and CVRs and was consistent according to different definitions. The Comparison of patients with REM-independent OSAS and non-OSA controls, as well as the two different subtypes of OSAS, did not yield significance. CONCLUSION: Based on the current findings, patients with REM-dependent OSAS appear to be susceptible to inflammation and should be carefully monitored for the negative consequences of that issue. To our knowledge, this study is the first to evaluate SII and PDW in REM-dependent OSAS.

Thalamocortical Dynamics during Rapid Eye Movement Sleep in the Mouse Somatosensory Pathway.

Rapid eye movement (REM) sleep, also referred to as paradoxical sleep for the striking resemblance of its electroencephalogram (EEG) to the one observed in wakefulness, is characterized by the occurrence of transient events such as limb twitches or facial and rapid eye movements. Here, we investigated the local activity of the primary somatosensory or barrel cortex (S1) in naturally sleeping head-fixed male mice during REM. Through local field potential recordings, we uncovered local appearances of spindle waves in the barrel cortex during REM concomitant with strong delta power, challenging the view of a wakefulness-like activity in REM. We further performed extra- and intracellular recordings of thalamic cells in head-fixed mice. Our data show high-frequency thalamic bursts of spikes and subthreshold spindle oscillations in approximately half of the neurons of the ventral posterior medial nucleus which further confirmed the thalamic origin of local cortical spindles in S1 in REM. Cortical spindle oscillations were suppressed, while thalamus spike firing increased, associated with rapid mouse whisker movements and S1 cortical activity transitioned to an activated state. During REM, the sensory thalamus and barrel cortex therefore alternate between high (wake-like) and low (non-REM sleep-like) activation states, potentially providing a neuronal substrate for mnemonic processes occurring during this paradoxical sleep stage.

Spinal projecting neurons in rostral ventromedial medulla co-regulate motor and sympathetic tone.

Many behaviors require the coordinated actions of somatic and autonomic functions. However, the underlying mechanisms remain elusive. By opto-stimulating different populations of descending spinal projecting neurons (SPNs) in anesthetized mice, we show that stimulation of excitatory SPNs in the rostral ventromedial medulla (rVMM) resulted in a simultaneous increase in somatomotor and sympathetic activities. Conversely, opto-stimulation of rVMM inhibitory SPNs decreased both activities. Anatomically, these SPNs innervate both sympathetic preganglionic neurons and motor-related regions in the spinal cord. Fiber-photometry recording indicated that the activities of rVMM SPNs correlate with different levels of muscle and sympathetic tone during distinct arousal states. Inhibiting rVMM excitatory SPNs reduced basal muscle and sympathetic tone, impairing locomotion initiation and high-speed performance. In contrast, silencing the inhibitory population abolished muscle atonia and sympathetic hypoactivity during rapid eye movement (REM) sleep. Together, these results identify rVMM SPNs as descending spinal projecting pathways controlling the tone of both the somatomotor and sympathetic systems.

REM Sleep Preserves Affective Response to Social Stress-Experimental Study.

Sleep's contribution to affective regulation is insufficiently understood. Previous human research has focused on memorizing or rating affective pictures and less on physiological affective responsivity. This may result in overlapping definitions of affective and declarative memories and inconsistent deductions for how rapid eye movement sleep (REMS) and slow-wave sleep (SWS) are involved. Literature associates REMS theta (4-8 Hz) activity with emotional memory processing, but its contribution to social stress habituation is unknown. Applying selective sleep stage suppression and oscillatory analyses, we investigated how sleep modulated affective adaptation toward social stress and retention of neutral declarative memories. Native Finnish participants (N = 29; age, M = 25.8 years) were allocated to REMS or SWS suppression conditions. We measured physiological (skin conductance response, SCR) and subjective stress response and declarative memory retrieval thrice: before laboratory night, the next morning, and after 3 d. Linear mixed models were applied to test the effects of condition and sleep parameters on emotional responsivity and memory retrieval. Greater overnight increase in SCR toward the stressor emerged after suppressed SWS (intact REMS) relative to suppressed REMS (20.1% vs 6.1%; p = 0.016). The overnight SCR increase was positively associated with accumulated REMS theta energy irrespective of the condition (r = 0.601; p = 0.002). Subjectively rated affective response and declarative memory recall were comparable between the conditions. The contributions of REMS and SWS to habituation of social stress are distinct. REMS theta activity proposedly facilitates the consolidation of autonomic affective responses. Declarative memory consolidation may not have greater dependence on intact SWS relative to intact REMS.

The effect of REM-sleep disruption on affective processing: A systematic review of human and animal experimental studies.

Evidence on the importance of rapid-eye-movement sleep (REMS) in processing emotions is accumulating. The focus of this systematic review is the outcomes of experimental REMS deprivation (REMSD), which is the most common method in animal models and human studies on REMSD. This review revealed that variations in the applied REMSD methods were substantial. Animal models used longer deprivation protocols compared with studies in humans, which mostly reported acute deprivation effects after one night. Studies on animal models showed that REMSD causes aggressive behavior, increased pain sensitivity, reduced sexual behavior, and compromised consolidation of fear memories. Animal models also revealed that REMSD during critical developmental periods elicits lasting consequences on affective-related behavior. The few human studies revealed increases in pain sensitivity and suggest stronger consolidation of emotional memories after REMSD. As pharmacological interventions (such as selective serotonin reuptake inhibitors [SSRIs]) may suppress REMS for long periods, there is a clear gap in knowledge regarding the effects and mechanisms of chronic REMS suppression in humans.

Older adults at greater risk for Alzheimer's disease show stronger associations between sleep apnea severity in REM sleep and verbal memory.

BACKGROUND: Obstructive sleep apnea (OSA) increases risk for cognitive decline and Alzheimer's disease (AD). While the underlying mechanisms remain unclear, hypoxemia during OSA has been implicated in cognitive impairment. OSA during rapid eye movement (REM) sleep is usually more severe than in non-rapid eye movement (NREM) sleep, but the relative effect of oxyhemoglobin desaturation during REM versus NREM sleep on memory is not completely characterized. Here, we examined the impact of OSA, as well as the moderating effects of AD risk factors, on verbal memory in a sample of middle-aged and older adults with heightened AD risk. METHODS: Eighty-one adults (mean age:61.7 ± 6.0 years, 62% females, 32% apolipoprotein E ε4 allele (APOE4) carriers, and 70% with parental history of AD) underwent clinical polysomnography including assessment of OSA. OSA features were derived in total, NREM, and REM sleep. REM-NREM ratios of OSA features were also calculated. Verbal memory was assessed with the Rey Auditory Verbal Learning Test (RAVLT). Multiple regression models evaluated the relationships between OSA features and RAVLT scores while adjusting for sex, age, time between assessments, education years, body mass index (BMI), and APOE4 status or parental history of AD. The significant main effects of OSA features on RAVLT performance and the moderating effects of AD risk factors (i.e., sex, age, APOE4 status, and parental history of AD) were examined. RESULTS: Apnea-hypopnea index (AHI), respiratory disturbance index (RDI), and oxyhemoglobin desaturation index (ODI) during REM sleep were negatively associated with RAVLT total learning and long-delay recall. Further, greater REM-NREM ratios of AHI, RDI, and ODI (i.e., more events in REM than NREM) were related to worse total learning and recall. We found specifically that the negative association between REM ODI and total learning was driven by adults 60 + years old. In addition, the negative relationships between REM-NREM ODI ratio and total learning, and REM-NREM RDI ratio and long-delay recall were driven by APOE4 carriers. CONCLUSION: Greater OSA severity, particularly during REM sleep, negatively affects verbal memory, especially for people with greater AD risk. These findings underscore the potential importance of proactive screening and treatment of REM OSA even if overall AHI appears low.

Selective Enhancement of REM Sleep in Male Rats through Activation of Melatonin MT1 Receptors Located in the Locus Ceruleus Norepinephrine Neurons.

Sleep disorders affect millions of people around the world and have a high comorbidity with psychiatric disorders. While current hypnotics mostly increase non-rapid eye movement sleep (NREMS), drugs acting selectively on enhancing rapid eye movement sleep (REMS) are lacking. This polysomnographic study in male rats showed that the first-in-class selective melatonin MT1 receptor partial agonist UCM871 increases the duration of REMS without affecting that of NREMS. The REMS-promoting effects of UCM871 occurred by inhibiting, in a dose-response manner, the firing activity of the locus ceruleus (LC) norepinephrine (NE) neurons, which express MT1 receptors. The increase of REMS duration and the inhibition of LC-NE neuronal activity by UCM871 were abolished by MT1 pharmacological antagonism and by an adeno-associated viral (AAV) vector, which selectively knocked down MT1 receptors in the LC-NE neurons. In conclusion, MT1 receptor agonism inhibits LC-NE neurons and triggers REMS, thus representing a novel mechanism and target for REMS disorders and/or psychiatric disorders associated with REMS impairments.

Unraveling the complexity of rapid eye movement microstates: insights from nonlinear EEG analysis.

Although rapid eye movement (REM) sleep is conventionally treated as a unified state, it comprises two distinct microstates: phasic and tonic REM. Recent research emphasizes the importance of understanding the interplay between these microstates, hypothesizing their role in transient shifts between sensory detachment and external awareness. Previous studies primarily employed linear metrics to probe cognitive states, such as oscillatory power, while in this study, we adopt Lempel-Ziv Complexity (LZC), to examine the nonlinear features of electroencephalographic (EEG) data from the REM microstates and to gain complementary insights into neural dynamics during REM sleep. Our findings demonstrate a noteworthy reduction in LZC during phasic REM compared to tonic REM states, signifying diminished EEG complexity in the former. Additionally, we noted a negative correlation between decreased LZC and delta band power, along with a positive correlation with alpha band power. This study highlights the potential of nonlinear EEG metrics, particularly LZC, in elucidating the distinct features of REM microstates. Overall, this research contributes to advancing our understanding of the complex dynamics within REM sleep and opens new avenues for exploring its implications in both clinical and nonclinical contexts.