Showing papers on "Rapid eye movement sleep published in 2022"

A cognitive process occurring during sleep is revealed by rapid eye movements

Abstract: Since the discovery of rapid eye movement (REM) sleep, the nature of the eye movements that characterize this sleep phase has remained elusive. Do they reveal gaze shifts in the virtual environment of dreams or simply reflect random brainstem activity? We harnessed the head direction (HD) system of the mouse thalamus, a neuronal population whose activity reports, in awake mice, their actual HD as they explore their environment and, in sleeping mice, their virtual HD. We discovered that the direction and amplitude of rapid eye movements during REM sleep reveal the direction and amplitude of the ongoing changes in virtual HD. Thus, rapid eye movements disclose gaze shifts in the virtual world of REM sleep, thereby providing a window into the cognitive processes of the sleeping brain. Description The meaning of rapid eye movement Sleep includes phases characterized by rapid eye movement (REM) that were known to be associated with dreaming. But are these eye movements related to the contents of consciousness in that sleep state? Senzai and Scanziani recorded head direction cells in the anterior dorsal nucleus of the thalamus in mice during wake and sleep (see the Perspective by De Zeeuw and Canto). The direction and amplitude of rapid eye movements encoded the direction and amplitude of the heading of mice in their virtual environment during REM sleep. It was possible to predict the actual heading in the real and virtual world of the mice during wake and REM sleep, respectively, using saccadic eye movements. —PRS Rapid eye movements during REM sleep represent gaze shifts in the virtual world of the sleeping brain.

Lucid Dreaming Occurs in Activated REM Sleep, Not a Mixture of Sleep and Wakefulness.

Abstract: STUDY OBJECTIVES 1) To replicate the finding that lucid dreams are associated with physiological activation, including heightened REM density, during REM sleep. 2) To critically test whether a previously reported increase in frontolateral 40 Hz power in lucid REM sleep, used to justify the claim that lucid dreaming is a "hybrid state" mixing sleep and wakefulness, is attributable to the saccadic spike potential (SP) artifact as a corollary of heightened REM density. 3) To conduct an exploratory analysis of changes in EEG features during lucid REM sleep. METHODS We analyzed 14 signal-verified lucid dreams (SVLDs) and baseline REM sleep segments from the same REM periods from six participants derived from the Stanford SVLD database. Participants marked lucidity onset with standard left-right-left-right-center (LR2c) eye-movement signals in polysomnography recordings. RESULTS Compared to baseline REM sleep, lucid REM sleep had higher REM density (p=0.002). Bayesian analysis supported the null hypothesis of no differences in frontolateral 40 Hz power after removal of the SP artifact (BH=0.18) and ICA correction (BH=0.01). Compared to the entire REM sleep period, lucid REM sleep showed small reductions in low-frequency and beta band spectral power as well as increased signal complexity (all p<0.05), which were within the normal variance of baseline REM sleep. CONCLUSIONS Lucid dreams are associated with higher-than-average levels of physiological activation during REM sleep, including measures of both subcortical and cortical activation. Increases in 40 Hz power in periorbital channels reflect saccadic and microsaccadic SPs as a result of higher REM density accompanying heightened activation.

Lucid dreaming occurs in activated rapid eye movement sleep, not a mixture of sleep and wakefulness.

Abstract: STUDY OBJECTIVES (1) To critically test whether a previously reported increase in frontolateral 40 Hz power in lucid REM sleep, used to justify the claim that lucid dreaming is a "hybrid state" mixing sleep and wakefulness, is attributable to the saccadic spike potential (SP) artifact as a corollary of heightened REM density. (2) To replicate the finding that lucid dreams are associated with physiological activation, including heightened eye movement density, during REM sleep. (3) To conduct an exploratory analysis of changes in EEG features during lucid REM sleep. METHODS We analyzed 14 signal-verified lucid dreams (SVLDs) and baseline REM sleep segments from the same REM periods from six participants derived from the Stanford SVLD database. Participants marked lucidity onset with standard left-right-left-right-center (LR2c) eye-movement signals in polysomnography recordings. RESULTS Compared to baseline REM sleep, lucid REM sleep had higher REM density (β = 0.85, p = 0.002). Bayesian analysis supported the null hypothesis of no differences in frontolateral 40 Hz power after removal of the SP artifact (BH = 0.18) and ICA correction (BH = 0.01). Compared to the entire REM sleep period, lucid REM sleep showed small reductions in low-frequency and beta band spectral power as well as increased signal complexity (all p < 0.05), which were within the normal variance of baseline REM sleep. CONCLUSIONS Lucid dreams are associated with higher-than-average levels of physiological activation during REM sleep, including measures of both subcortical and cortical activation. Increases in 40 Hz power in periorbital channels reflect saccadic and microsaccadic SPs as a result of higher REM density accompanying heightened activation.

Order matters: sleep spindles contribute to memory consolidation only when followed by rapid-eye-movement sleep.

Abstract: Sleep is known to benefit memory consolidation, but little is known about the contribution of sleep stages within the sleep cycle. The sequential hypothesis proposes that memories are first replayed during non-rapid-eye-movement (NREM or N) sleep and then integrated into existing networks during rapid-eye-movement (REM or R) sleep, two successive critical steps for memory consolidation. However, it lacks experimental evidence as N always precedes R sleep in physiological conditions. We tested this sequential hypothesis in patients with central hypersomnolence disorder, including patients with narcolepsy who present the unique, anti-physiological peculiarity of frequently falling asleep in R sleep before entering N sleep. Patients performed a visual perceptual learning task before and after daytime naps stopped after one sleep cycle, starting in N or R sleep and followed by the other stage (i.e. N-R vs. R-N sleep sequence). We compared over-nap changes in performance, reflecting memory consolidation, depending on the sleep sequence during the nap. Thirty-six patients who slept for a total of 67 naps were included in the analysis. Results show that sleep spindles are associated with memory consolidation only when N is followed by R sleep, that is in physiologically ordered N-R naps, thus providing support to the sequential hypothesis in humans. In addition, we found a negative effect of rapid-eye-movements in R sleep on perceptual consolidation, highlighting the complex role of sleep stages in the balance to remember and to forget.

Rapid eye movement sleep reduction in patients with epilepsy: A systematic review and meta-analysis

Abstract: Compared to healthy controls, adults with epilepsy have a disrupted sleep architecture. Changes in sleep macrostructure may be associated with the refractoriness of epilepsy. However, there is no consensus regarding the changes in sleep architecture in patients with epilepsy. This meta-analysis aimed to elucidate the differences in sleep architecture between patients with epilepsy and healthy controls.This study followed the Preferred Reporting Items for Systematic Reviews and Meta-analysis guidelines. The PubMed, Embase, and Cochrane Central databases were searched (until May 2021) for studies comparing polysomnographic sleep macrostructures between patients with epilepsy and healthy controls. A meta-analysis was performed using a random-effects model. The percentage of rapid eye movement (REM) sleep, slow-wave sleep (SWS), and sleep efficiency (SE) were compared between patients with epilepsy and healthy controls.Overall, 24 studies involving 789 patients with epilepsy and 599 healthy controls fulfilled the eligibility criteria. Compared to healthy controls, patients with focal epilepsy had decreased REM sleep and SE. Patients with generalised epilepsy had increased SWS and decreased SE. Subgroup analyses focussed on the potential effect of seizure control on sleep architecture. The results revealed that both antiseizure medication (ASM)-untreated and treated patients had decreased SE. ASM treatment may restore REM sleep in patients with generalised epilepsy but not in patients with focal epilepsy.This meta-analysis revealed statistically significant differences in the sleep macrostructure between patients with epilepsy and healthy controls. There were significant differences in the sleep macrostructure between ASM-untreated patients and healthy controls, which may be an intrinsic change attributable to epilepsy.

Rapid eye movement sleep behaviour disorder: Past, present, and future

Abstract: This manuscript presents an overview of REM sleep behaviour disorder (RBD) with a special focus on European contributions. After an introduction examining the history of the disorder, we address the pathophysiological and clinical aspects, as well as the diagnostic issues. Further, implications of RBD diagnosis and biomarkers are discussed. Contributions of European researchers to this field are highlighted.

Chaperone Hsp70 (HSPA1) Is Involved in the Molecular Mechanisms of Sleep Cycle Integration

Abstract: The molecular mechanisms of sleep cycle integration at the beginning and the end of the inactive period are not clear. Sleep cycles with a predominance of deep slow-wave sleep (SWS) seem to be associated with accelerated protein synthesis in the brain. The inducible Hsp70 chaperone corrects protein conformational changes and has protective properties. This research explores (1) whether the Hspa1 gene encoding Hsp70 protein activates during the daily rapid-eye-movement sleep (REMS) maximum, and (2) whether a lower daily deep SWS maximum affects the Hspa1 expression level during the subsequent REMS. Combining polysomnography in male Wistar rats, RT-qPCR, and Western blotting, we reveal a three-fold Hspa1 upregulation in the nucleus reticularis pontis oralis, which regulates REMS. Hspa1 expression increases during the daily REMS maximum, 5–7 h after the natural peak of deep SWS. Using short-term selective REMS deprivation, we demonstrate that REMS rebound after deprivation exceeds the natural daily maximum, but it is not accompanied by Hspa1 upregulation. The results suggest that a high proportion of deep SWS, usually observed after sleep onset, is a necessary condition for Hspa1 upregulation during subsequent REMS. The data obtained can inform the understanding of the molecular mechanisms integrating SWS and REMS and key biological function(s) of sleep.

Classifying Idiopathic Rapid Eye Movement Sleep Behavior Disorder, Controls, and Mild Parkinson's Disease Using Gait Parameters

Abstract: Subtle gait changes associated with idiopathic rapid eye movement sleep behavior disorder (iRBD) could allow early detection of subjects with future synucleinopathies.

Serum MicroRNAs Predict Isolated Rapid Eye Movement Sleep Behavior Disorder and Lewy Body Diseases

Abstract: Isolated rapid eye movement sleep behavior disorder (IRBD) is a well‐established clinical risk factor for Lewy body diseases (LBDs), such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB).

Generalized EEG Slowing Across Phasic REM Sleep, Not Subjective RBD Severity, Predicts Neurodegeneration in Idiopathic RBD

Abstract: Idiopathic rapid eye movement sleep behavior disorder (iRBD) is the prodromal marker of α-synuclein degeneration with markedly high predictive value. We aim to evaluate the value of electroencephalography (EEG) data during rapid eye movement (REM) sleep and subjective RBD severity in predicting the conversion to neurodegenerative diseases in iRBD patients.At the baseline, iRBD patients underwent clinical assessment and video-polysomnography (PSG). Relative spectral power for nine frequency bands during phasic and tonic REM sleep in three regions of interest, slow-to-fast ratios, clinical and PSG variables were estimated and compared between iRBD patients who converted to neurodegenerative diseases (iRBD-C) and iRBD patients who remained disease-free (iRBD-NC). Receiver operating characteristic (ROC) curves evaluated the predictive performance of slow-to-fast ratios, and subjective RBD severity as assessed with RBD Questionnaire-Hong Kong.Twenty-two (33.8%) patients eventually developed neurodegenerative diseases. The iRBD-C group showed shorter total sleep time (p < 0.001), lower stage 2 sleep percentage (p = 0.044), more periodic leg-movement-related arousal index (p = 0.004), increased tonic chin electromyelographic activity (p = 0.040) and higher REM density in the third REM episode (p = 0.034) than the iRBD-NC group. EEG spectral power analyses revealed that iRBD phenoconverters showed significantly higher delta and lower alpha power, especially in central and occipital regions during the phasic REM state compared to the iRBD-NC group. Significantly higher slow-to-fast ratios were observed in a more generalized way during the phasic state in the iRBD-C group compared to the iRBD-NC group. ROC analyses of the slowing ratio in occipital areas during phasic REM sleep yielded an area under the curve of 0.749 (p = 0.001), while no significant predictive value of subjective RBD severity was observed.Our study shows that EEG slowing, especially in a more generalized manner during the phasic period, may be a promising marker in predicting phenoconversion in iRBD, rather than subjective RBD severity.

Relevance of sleep and associated structural changes in GBA1 mouse to human rapid eye movement behavior disorder

Abstract: Abstract Rapid eye movement (REM) sleep behaviour disorder (RBD) is a REM parasomnia that often predicts the later occurrence of alpha-synucleinopathies. Variants in the gene encoding for the lysosomal enzyme glucocerebrosidase, GBA, strongly increase the risk of RBD. In a GBA1-mouse model recently shown to mimic prodromal stages of α-synucleinopathy, we now demonstrate striking REM and NREM electroencephalographic sleep abnormalities accompanied by distinct structural changes in the more widespread sleep neurocircuitry.

White matter microstructure in Parkinson’s disease with and without elevated rapid eye movement sleep muscle tone

Abstract: Abstract People with Parkinson’s disease who have elevated muscle activity during rapid eye movement sleep (REM sleep without atonia) typically have a worse motor and cognitive impairment compared with those with normal muscle atonia during rapid eye movement sleep. This study used tract-based spatial statistics to compare diffusion MRI measures of fractional anisotropy, radial, mean and axial diffusivity (measures of axonal microstructure based on the directionality of water diffusion) in white matter tracts between people with Parkinson’s disease with and without rapid eye movement sleep without atonia and controls and their relationship to measures of motor and cognitive function. Thirty-eight individuals with mild-to-moderate Parkinson’s disease and 21 matched control subjects underwent ultra-high field MRI (7 T), quantitative motor assessments of gait and bradykinesia and neuropsychological testing. The Parkinson’s disease cohort was separated post hoc into those with and without elevated chin or leg muscle activity during rapid eye movement sleep based on polysomnography findings. Fractional anisotropy was significantly higher, and diffusivity significantly lower, in regions of the corpus callosum, projection and association white matter pathways in the Parkinson’s group with normal rapid eye movement sleep muscle tone compared with controls, and in a subset of pathways relative to the Parkinson’s disease group with rapid eye movement sleep without atonia. The Parkinson’s disease group with elevated rapid eye movement sleep muscle tone showed significant impairments in the gait and upper arm speed compared with controls and significantly worse scores in specific cognitive domains (executive function, visuospatial memory) compared with the Parkinson’s disease group with normal rapid eye movement sleep muscle tone. Regression analyses showed that gait speed and step length in the Parkinson’s disease cohort were predicted by measures of fractional anisotropy of the anterior corona radiata, whereas elbow flexion velocity was predicted by fractional anisotropy of the superior corona radiata. Visuospatial memory task performance was predicted by the radial diffusivity of the posterior corona radiata. These findings show that people with mild-to-moderate severity of Parkinson’s disease who have normal muscle tone during rapid eye movement sleep demonstrate compensatory-like adaptations in axonal microstructure that are associated with preserved motor and cognitive function, but these adaptations are reduced or absent in those with increased rapid eye movement sleep motor tone.

Neuroimaging of rapid eye movement sleep behavior disorder and its relation to Parkinson's disease

Abstract: Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by polysomnography‐confirmed REM sleep without atonia and dream‐enacting behaviors. This disorder is considered a prodromal syndrome of alpha‐synucleinopathies like Parkinson's disease (PD), where it affects more than 50% of PD patients. The underlying pathology of RBD has been generally understood to involve the pontine nuclei within the brainstem. However, the complete pathophysiology beyond the brainstem remains unclear as does its relationship with PD pathology. Therefore, this review aims to survey the neuroimaging literature involving PET, SPECT, and MR imaging techniques to provide an updated understanding of the neuro‐chemical, structural, and functional changes in both RBD and PD patients comorbid with RBD. This review found neuroimaging evidence that indicate alterations to the dopaminergic and cholinergic system, blood perfusion, and glucose metabolism in both RBD patients and PD patients with RBD. Beyond the brainstem, structural and functional changes were found to involve the nigrostriatal system, limbic system, and the cortex—suggesting that RBD is a multi‐systemic neurodegenerative process. Future investigations are encouraged to follow RBD patients longitudinally using multimodal imaging techniques to enhance our understanding of this parasomnia disorder. Uncovering which individuals are most likely to develop an alpha‐synuclein disorder in the prodromal phase will improve patient outcomes and potentially aid in the development of novel treatments for patients affected by RBD.

Automatic analysis of muscular activity in the flexor digitorum superficialis muscles: a fast screening method for rapid eye movement sleep without atonia

Abstract: Abstract Study objectives To identify a fast and reliable method for rapid eye movement (REM) sleep without atonia (RWA) quantification. Methods We analyzed 36 video-polysomnographies (v-PSGs) of isolated REM sleep behavior disorder (iRBD) patients and 35 controls’ v-PSGs. Patients diagnosed with RBD had: i) RWA, quantified with a reference method, i.e. automatic and artifact-corrected 3-s Sleep Innsbruck Barcelona (SINBAR) index in REM sleep periods (RSPs, i.e. manually selected portions of REM sleep); and ii) v-PSG-documented RBD behaviors. We quantified RWA with other (semi)-automated methods requiring less human intervention than the reference one: the indices proposed by the SINBAR group (the 3-s and 30-s phasic flexor digitorum superficialis (FDS), phasic/”any”/tonic mentalis), and the REM atonia, short and long muscle activity indices (in mentalis/submentalis/FDS muscles). They were calculated in whole REM sleep (i.e. REM sleep scored following international guidelines), in RSPs, with and without manual artifact correction. Area under curves (AUC) discriminating iRBD from controls were computed. Using published cut-offs, the indices’ sensitivity and specificity for iRBD identification were calculated. Apnea-hypopnea index in REM sleep (AHIREM) was considered in the analyses. Results RWA indices from FDS muscles alone had the highest AUCs and all of them had 100% sensitivity. Without manual RSP selection and artifact correction, the “30-s phasic FDS” and the “FDS long muscle activity” had the highest specificity (85%) with AHIREM < 15/h. RWA indices were less reliable when AHIREM≥15/h. Conclusions If AHIREM<15/h, FDS muscular activity in whole REM sleep and without artifact correction is fast and reliable to rule out RWA.

Impaired Ocular Tracking and Cortical Atrophy in Idiopathic Rapid Eye Movement Sleep Behavior Disorder

Abstract: Idiopathic rapid eye movement sleep behavior disorder (iRBD) is a prodromal stage of synucleinopathies. Patients with synucleinopathies frequently display eye movement abnormalities. However, whether patients with iRBD have eye movement abnormalities remains unknown.

Isolated dream‐enactment behaviours as a prodromal hallmark of rapid eye movement sleep behaviour disorder

Abstract: Recurrent dream-enactment behaviours (DEB) and rapid eye movement (REM) sleep without atonia (RSWA) are two diagnostic hallmarks of REM sleep behaviour disorder (RBD), a specific prodrome of α-synucleinopathy. Whilst isolated RSWA (without DEB) was suggested as a prodrome of RBD, the implication of ‘isolated’ recurrent DEB remains under-investigated. In this cross-sectional study, we sought to investigate neurodegenerative markers amongst the first-degree relatives (FDRs, aged >40 years) of patients with RBD who underwent clinical assessment for DEB, neurodegenerative markers, and video-polysomnography assessment. Isolated recurrent DEB was defined as: (i) three or more episodes of DEB, (ii) had a DEB episode in the past 1 year, and (iii) subthreshold RSWA. We identified 29 FDRs (mean [SD] age 53.4 [8.3] years, 55.2% male) with isolated recurrent DEB and 98 age and sex-matched FDRs as controls. Isolated DEB was associated with nightmare (27.6% versus 11.2%, p = 0.02), and the DEB group had a higher rate of current smoking (27.6% versus 3.1%, p = 0.006), type 2 diabetes mellitus (24.1% versus 10.2%, p = 0.003), anxiety disorder (24.1% versus 11.2%, p = 0.02), and constipation (hard lump of stool, 31.0% versus 7.1%, p < 0.001) than the control group. The present findings revealed that family relatives of patients with RBD with isolated recurrent DEB have increased risk of RBD and neurodegenerative features, which adds to the emerging data that isolated DEB is a prodromal feature of RBD and α-synucleinopathy neurodegeneration.

Regional variation in cholinergic terminal activity determines the non-uniform occurrence of cortical slow-wave activity during REM sleep

Abstract: Sleep consists of two basic stages: non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. NREM sleep is characterized by slow high-amplitude cortical EEG signals, while REM sleep is characterized desynchronized cortical rhythms. While, until recently, it has been widely believed that cortical activity during REM sleep is globally desynchronized, recent electrophysiological studies showed slow waves (SW) in some cortical areas during REM sleep. Electrophysiological techniques, however, have been unable to resolve the regional structure of these activities, due to relatively sparse sampling. We mapped functional gradients in cortical activity during REM sleep using mesoscale imaging in mice, and observed local SW patterns occurring mainly in somatomotor and auditory cortical regions, with minimum presence within the default mode network. The role of the cholinergic system in local desynchronization during REM sleep was also explored by calcium imaging of cholinergic terminal activity within the mouse cortex. Terminal activity was weaker in regions exhibiting SW activity more frequently during REM sleep. We also analyzed Allen Mouse Brain Connectivity dataset and found that these regions have weaker cholinergic projections from the basal forebrain.

Relationship between Substantia Nigra Neuromelanin Imaging and Dual Alpha-Synuclein Labeling of Labial Minor in Salivary Glands in Isolated Rapid Eye Movement Sleep Behavior Disorder and Parkinson’s Disease

Abstract: We investigated the presence of misfolded alpha-Synuclein (α-Syn) in minor salivary gland biopsies in relation to substantia nigra pars compacta (SNc) damage measured using magnetic resonance imaging in patients with isolated rapid eye movement sleep behavior disorder (iRBD) and Parkinson’s disease (PD) as compared to healthy controls. Sixty-one participants (27 PD, 16 iRBD, and 18 controls) underwent a minor salivary gland biopsy and were scanned using a 3 Tesla MRI. Deposits of α-Syn were found in 15 (55.6%) PD, 7 (43.8%) iRBD, and 7 (38.9%) controls using the anti-aggregated α-Syn clone 5G4 antibody and in 4 (14.8%) PD, 3 (18.8%) iRBD and no control using the purified mouse anti-α-Syn clone 42 antibody. The SNc damages obtained using neuromelanin-sensitive imaging did not differ between the participants with versus without α-Syn deposits (irrespective of the antibodies and the disease group). Our study indicated that the α-Syn detection in minor salivary gland biopsies lacks sensitivity and specificity and does not correlate with the SNc damage, suggesting that it cannot be used as a predictive or effective biomarker for PD.

Cerebrospinal Fluid TNF-α and Orexin in Patients With Parkinson's Disease and Rapid Eye Movement Sleep Behavior Disorder

Abstract: Background Parkinson's disease (PD) pathological changes begin before motor symptoms appear. Rapid eye movement sleep behavior disorder (RBD) has the highest specificity and predictive value of any marker of prodromal PD. Tumor necrosis factor α (TNF-α) plays a part in the pathology of PD and disease conversion in isolated RBD (iRBD). TNF can also directly impair the hypocretin system in mice in vivo. As a result, we intend to investigate the effect of TNF-α on orexin levels in PD patients with RBD. Method Participants were recruited from the Department of Neurology of Xuanwu Hospital, Capital Medical University to engage in assessments on motor symptoms, sleep, cognition, etc. Then we collected blood and cerebrospinal fluid of all patients and 10 controls' cerebrospinal fluid. The levels of TNF-α in the serum and cerebrospinal fluid, as well as the level of orexin in the cerebrospinal fluid, were measured in the patients. Results The difference in TNF- levels in cerebrospinal fluid and serum between the three groups were not statistically significant. The levels of orexin in the three groups were not significantly lower than in the control group. UPDRS-III scores were significantly higher in the PD+RBD and PD-RBD groups than in the iRBD group. There was no statistically significant difference in H-Y stages, PSQI, or ESS scores between the PD+RBD and PD-RBD groups. Conclusion Our findings suggest that TNF-α may not have a significant effect on the orexinergic system in patients with Parkinson's disease and iRBD. As a result, it is necessary to investigate the changes in TNF-α and orexin levels in different disease stages and to enlarge the sample size to determine whether TNF-α affects the function of the orexin system, which may be related to the occurrence of RBD and disease progression in Parkinson's disease.

Focal Epilepsy Impacts Rapid Eye Movement Sleep Microstructure.

Abstract: STUDY OBJECTIVES Whereas there is plenty of evidence on the influence of epileptic activity on non-rapid eye movement (NREM) sleep macro- and micro-structure, data on the impact of epilepsy on rapid eye movement (REM) sleep remains sparse. Using high-density electroencephalography (HD-EEG), we assessed global and focal disturbances of sawtooth waves (STW) as cortically generated sleep oscillations of REM sleep in patients with focal epilepsy. METHODS Twenty-two patients with drug-resistant focal epilepsy (13 females; mean age, 32.6±10.7 years; 12 temporal lobe epilepsy) and 12 healthy controls (3 females; 24.0±3.2 years) underwent combined overnight HD-EEG and polysomnography. STW rate, duration, frequency, power, spatial extent, IED rates and sleep homeostatic properties were analysed. RESULTS STW rate and duration were reduced in patients with focal epilepsy compared to healthy controls (rate: 0.64/min±0.46 vs. 1.12/min±0.41, p=0.005, d=-0.98; duration: 3.60s±0.76 vs. 4.57±1.00, p=0.003, d=-1.01). Not surprisingly given the fronto-central maximum of STW, the reductions were driven by extratemporal lobe epilepsy patients (rate: 0.45/min±0.31 vs. 1.12/min±0.41, p=0.0004, d=-1.35; duration: 3.49s±0.92 vs. 4.57±1.00, p=0.017, d=-0.99) and more pronounced in the first vs. the last sleep cycle (rate: d=-0.90 vs. d=-0.62, duration: d=-1.01 vs. d=-0.80). There was no regional decrease of STWs in the region with the epileptic focus vs. the contralateral side (all ps>0.5). CONCLUSION Patients with focal epilepsy and in particular extratemporal lobe epilepsy show a global reduction of STW activity in REM sleep. This may suggest that epilepsy impacts cortically generated sleep oscillations even in REM sleep when epileptic activity is low.

Polysomnography in humans and animal models

Abstract: Sleep is one of the great mysteries of life. We spend a third of our life sleeping without awareness of the outside world. Part of this time, during dreams, we have a bizarre cognitive activity disconnected from reality and guided by internal stimuli. In the last 70 years, as a result of basic research, there has been a remarkable increase in the knowledge of the physiology of sleep. Some of this knowledge has been transferred to the medical practice, where about 80 different sleep disturbances have been described. In most mammals (including humans) and birds, two sleep states can be readily distinguished: rapid eye movement sleep and nonrapid eye movement sleep. Polysomnography (PSG) is the basic tool used to recognize and characterize these behavioral states, and to explore brain activity during sleep. In the present work, we present a brief review of the main PSG procedures and data analysis in clinical and humans research settings, as well as in animal models.

Temperature-robust rapid eye movement and slow wave sleep in the lizard Laudakia vulgaris

Abstract: During sleep our brain switches between two starkly different brain states - slow wave sleep (SWS) and rapid eye movement (REM) sleep. While this two-state sleep pattern is abundant across birds and mammals, its existence in other vertebrates is not universally accepted, its evolutionary emergence is unclear and it is undetermined whether it is a fundamental property of vertebrate brains or an adaptation specific to homeotherms. To address these questions, we conducted electrophysiological recordings in the Agamid lizard, Laudakia vulgaris during sleep. We found clear signatures of two-state sleep that resemble the mammalian and avian sleep patterns. These states switched periodically throughout the night with a cycle of ~90 seconds and were remarkably similar to the states previously reported in Pogona vitticeps. Interestingly, in contrast to the high temperature sensitivity of mammalian states, state switches were robust to large variations in temperature. We also found that breathing rate, micro-movements and eye movements were locked to the REM state as they are in mammals. Collectively, these findings suggest that two-state sleep is abundant across the agamid family, shares physiological similarity to mammalian sleep, and can be maintain in poikilothems, increasing the probability that it existed in the cold-blooded ancestor of amniotes.

Predictors of rapid eye movement sleep behavior disorder in patients with Parkinson’s disease based on random forest and decision tree

Abstract: Background and objectives Sleep disorders related to Parkinson’s disease (PD) have recently attracted increasing attention, but there are few clinical reports on the correlation of Parkinson’s disease patients with rapid eye movement (REM) sleep behavior disorder (RBD). Therefore, this study conducted a cognitive function examination for Parkinson’s disease patients and discussed the application effect of three algorithms in the screening of influencing factors and risk prediction effects. Methods Three algorithms (logistic regression, machine learning-based regression trees and random forest) were used to establish a prediction model for PD-RBD patients, and the application effects of the three algorithms in the screening of influencing factors and the risk prediction of PD-RBD were discussed. Results The subjects included 169 patients with Parkinson’s disease (Parkinson’s disease with RBD [PD-RBD] = 69 subjects; Parkinson’s disease without RBD [PD-nRBD] = 100 subjects). This study compared the predictive performance of RF, decision tree and logistic regression, selected a final model with the best model performance and proposed the importance of variables in the final model. After the analysis, the accuracy of RF (83.05%) was better than that of the other models (decision tree = 75.10%, logistic regression = 71.62%). PQSI, Scopa-AUT score, MoCA score, MMSE score, AGE, LEDD, PD-course, UPDRS total score, ESS score, NMSQ, disease type, RLSRS, HAMD, UPDRS III and PDOnsetage are the main variables for predicting RBD, along with increased weight. Among them, PQSI is the most important factor. The prediction model of Parkinson’s disease RBD that was established in this study will help in screening out predictive factors and in providing a reference for the prognosis and preventive treatment of PD-RBD patients. Conclusions The random forest model had good performance in the prediction and evaluation of PD-RBD influencing factors and was superior to decision tree and traditional logistic regression models in many aspects, which can provide a reference for the prognosis and preventive treatment of PD-RBD patients.

Impaired Brain Information Transmission Efficiency and Flexibility in Parkinson's Disease and Rapid Eye Movement Sleep Behavior Disorder: Evidence from Functional Connectivity and Functional Dynamics

Abstract: Parkinson's disease (PD) is a common neurodegenerative disorder. Rapid eye movement sleep behavior disorder (RBD) is one of the prodromal symptoms of PD. Studies have shown that brain information transmission is affected in PD patients. Consequently, we hypothesized that brain information transmission is impaired in RBD and PD. To prove our hypothesis, we performed functional connectivity (FC) and functional dynamics analysis of three aspects—based on the whole brain, within the resting-state network (RSN), and the interaction between RSNs—using normal control (NC) (n = 21), RBD (n = 24), and PD (n = 45) resting-state functional magnetic resonance imaging (rs-fMRI) data sets. Furthermore, we tested the explanatory power of FC and functional dynamics for the clinical features. Our results found that the global functional dynamics and FC of RBD and PD were impaired. Within RSN, the impairment concentrated in the visual network (VIS) and sensorimotor network (SMN), and the impaired degree of SMN in RBD was higher than that in PD. On the interaction between RSNs, RBD showed a widespread decrease, and PD showed a focal decrease which concentrated in SMN and VIS. Finally, we proved FC and functional dynamics were related to clinical features. These differences confirmed that brain information transmission efficiency and flexibility are impaired in RBD and PD, and these impairments are associated with the clinical features of patients.