Consciousness in non-REM-parasomnia episodes.

Sleepwalking and related parasomnias are thought to result from incomplete awakenings out of non-rapid eye movement (non-REM) sleep. Non-REM parasomnia behaviours have been described as unconscious and automatic, or related to vivid, dream-like conscious experiences. Similarly, some observations have suggested that patients are unresponsive during episodes, while others that they can interact with their surroundings. To better grasp and characterise the full spectrum of consciousness and environmental (dis)connection associated with behavioural episodes, 35 adult patients with non-REM sleep parasomnias were interviewed in-depth about their experiences. The level of consciousness during parasomnia episodes was reported to be variable both within and between individuals, ranging from minimal or absent consciousness and largely automatic behaviours (frequently/always present in 36% of patients) to preserved conscious experiences characterised by delusional thinking to varying degrees of specificity (65%), often about impending danger, variably formed, uni- or multisensory hallucinations (53%), impaired insight (77%), negative emotions (75%), and variable, but often pronounced, amnesia (30%). Patients described their experiences as a dream scene during which they felt awake ("awake dreaming"). The surroundings were either realistically perceived, misinterpreted (in the form of perceptual illusions or misidentifications of people), or entirely hallucinated as a function of the prevailing delusion. These observations suggest that the level of consciousness, amnesia and sensory disconnection during non-REM parasomnia episodes is variable and graded. In their full-fledged expression, non-REM parasomnia experiences feature several core features of dreams. They therefore represent a valuable model for the study of consciousness, sleep-related sensory disconnection and dreaming.

Pulse Wave Amplitude Drops Index: A Biomarker of Cardiovascular Risk in Obstructive Sleep Apnea.

Rationale: It is currently unclear which patients with obstructive sleep apnea (OSA) are at increased cardiovascular risk. Objective: To investigate the value of pulse wave amplitude drops (PWADs), reflecting sympathetic activations and vasoreactivity, as a biomarker of cardiovascular risk in OSA. Methods: PWADs were derived from pulse oximetry-based photoplethysmography signals in three prospective cohorts: HypnoLaus (N = 1,941), the Pays-de-la-Loire Sleep Cohort (PLSC; N = 6,367), and "Impact of Sleep Apnea syndrome in the evolution of Acute Coronary syndrome. Effect of intervention with CPAP" (ISAACC) (N = 692). The PWAD index was the number of PWADs (>30%) per hour during sleep. All participants were divided into subgroups according to the presence or absence of OSA (defined as ⩾15 or more events per hour or <15/h, respectively, on the apnea-hypopnea index) and the median PWAD index. Primary outcome was the incidence of composite cardiovascular events. Measurements and Main Results: Using Cox models adjusted for cardiovascular risk factors (hazard ratio; HR [95% confidence interval]), patients with a low PWAD index and OSA had a higher incidence of cardiovascular events compared with the high-PWAD and OSA group and those without OSA in the HypnoLaus cohort (HR, 2.16 [1.07-4.34], P = 0.031; and 2.35 [1.12-4.93], P = 0.024) and in the PLSC (1.36 [1.13-1.63], P = 0.001; and 1.44 [1.06-1.94], P = 0.019), respectively. In the ISAACC cohort, the low-PWAD and OSA untreated group had a higher cardiovascular event recurrence rate than that of the no-OSA group (2.03 [1.08-3.81], P = 0.028). In the PLSC and HypnoLaus cohorts, every increase of 10 events per hour in the continuous PWAD index was negatively associated with incident cardiovascular events exclusively in patients with OSA (HR, 0.85 [0.73-0.99], P = 0.031; and HR, 0.91 [0.86-0.96], P < 0.001, respectively). This association was not significant in the no-OSA group and the ISAACC cohort. Conclusions: In patients with OSA, a low PWAD index reflecting poor autonomic and vascular reactivity was independently associated with a higher cardiovascular risk.

Reconsidering sleep perception in insomnia: from misperception to mismeasurement.

So-called 'sleep misperception' refers to a phenomenon in which individuals have the impression of sleeping little or not at all despite normal objective measures of sleep. It is unknown whether this subjective-objective mismatch truly reflects an abnormal perception of sleep, or whether it results from the inability of standard sleep recording techniques to capture 'wake-like' brain activity patterns that could account for feeling awake during sleep. Here, we systematically reviewed studies reporting sleep macro- and microstructural, metabolic, and mental correlates of sleep (mis)perception. Our findings suggest that most individuals tend to accurately estimate their sleep duration measured with polysomnography (PSG). In good sleepers, feeling awake during sleep is the rule at sleep onset, remains frequent in the first non-rapid eye movement sleep cycle and almost never occurs in rapid eye movement (REM) sleep. In contrast, there are patients with insomnia who consistently underestimate their sleep duration, regardless of how long they sleep. Unlike good sleepers, they continue to feel awake after the first sleep cycle and importantly, during REM sleep. Their mental activity during sleep is also more thought-like. Initial studies based on standard PSG parameters largely failed to show consistent differences in sleep macrostructure between these patients and controls. However, recent studies assessing sleep with more refined techniques have revealed that these patients show metabolic and microstructural electroencephalography changes that likely reflect a shift towards greater cortical activation during sleep and correlate with feeling awake. We discuss the significance of these correlates and conclude with open questions and possible ways to address them.

Sleep spindles in people with schizophrenia, schizoaffective disorders or bipolar disorders: a pilot study in a general population-based cohort.

BACKGROUND: Sleep spindles have been involved in sleep stabilization and sleep-related memory mechanisms and their deficit emerged as possible biomarker in schizophrenia. However, whether this sleep phenotype is also present in other disorders that share psychotic symptoms remains unclear. To address this gap, we assessed sleep spindles in participants of a prospective population-based cohort who underwent psychiatric assessment (CoLaus|PsyCoLaus) and polysomnographic recording (HypnoLaus). METHODS: Sleep was recorded using ambulatory polysomnography in participants (N = 1037) to the PsyCoLaus study. Sleep spindle parameters were measured in people with a lifelong diagnosis of schizophrenia (SZ), schizoaffective depressive (SAD), schizoaffective manic (SAM), bipolar disorder type I (BP-I) and type II (BP-II). The associations between lifetime diagnostic status (independent variables, SZ, SAD, SAM, BPD-I, BPD-II, controls) and spindle parameters (dependent variables) including density, duration, frequency and maximum amplitude, for all (slow and fast), slow- and fast-spindle were assessed using linear mixed models. Pairwise comparisons of the different spindle parameters between the SZ group and each of the other psychiatric groups was performed using a contrast testing framework from our multiple linear mixed models. RESULTS: Our results showed a deficit in the density and duration of sleep spindles in people with SZ. They also indicated that participants with a diagnosis of SAD, SAM, BP-I and BP-II exhibited different sleep spindle phenotypes. Interestingly, spindle densities and frequencies were different in people with a history of manic symptoms (SAM, BP-I, and BP-II) from those without (SZ, SAD). CONCLUSIONS: Although carried out on a very small number of participants due to the low prevalence of these disorders in general population, this pilot study brought new elements that argued in favor of a deficit of sleep spindles density and duration in people with schizophrenia. In addition, while we could expect a gradual change in intensity of the same sleep spindle parameters through psychotic diagnoses, our results seem to indicate a more complex situation in which the frequency of sleep spindles might be more impacted by diagnoses including a history of mania or hypomania. Further studies with a larger number of participants are required to confirm these effects.

Integrity of Corpus Callosum Is Essential for theCross-Hemispheric Propagation of Sleep Slow Waves:A High-Density EEG Study in Split-Brain Patients.

The slow waves of non-rapid eye movement (NREM) sleep reflect experience-dependent plasticity and play a direct role in the restorative functions of sleep. Importantly, slow waves behave as traveling waves, and their propagation is assumed to occur through cortico-cortical white matter connections. In this light, the corpus callosum (CC) may represent the main responsible for cross-hemispheric slow-wave propagation. To verify this hypothesis, we performed overnight high-density (hd)-EEG recordings in five patients who underwent total callosotomy due to drug-resistant epilepsy (CPs; two females), in three noncallosotomized neurologic patients (NPs; two females), and in a sample of 24 healthy adult subjects (HSs; 13 females). In all CPs slow waves displayed a significantly reduced probability of cross-hemispheric propagation and a stronger inter-hemispheric asymmetry. In both CPs and HSs, the incidence of large slow waves within individual NREM epochs tended to differ across hemispheres, with a relative overall predominance of the right over the left hemisphere. The absolute magnitude of this asymmetry was greater in CPs relative to HSs. However, the CC resection had no significant effects on the distribution of slow-wave origin probability across hemispheres. The present results indicate that CC integrity is essential for the cross-hemispheric traveling of slow waves in human sleep, which is in line with the assumption of a direct relationship between white matter integrity and slow-wave propagation. Our findings also revealed a residual cross-hemispheric slow-wave propagation that may rely on alternative pathways, including cortico-subcortico-cortical loops. Finally, these data indicate that the lack of the CC does not lead to differences in slow-wave generation across brain hemispheres.SIGNIFICANCE STATEMENT The slow waves of NREM sleep behave as traveling waves, and their propagation has been suggested to reflect the integrity of white matter cortico-cortical connections. To directly assess this hypothesis, here we investigated the role of the corpus callosum in the cortical spreading of NREM slow waves through the study of a rare population of totally callosotomized patients. Our results demonstrate a causal role of the corpus callosum in the cross-hemispheric traveling of sleep slow waves. Additionally, we found that callosotomy does not affect the relative tendency of each hemisphere at generating slow waves. Incidentally, we also found that slow waves tend to originate more often in the right than in the left hemisphere in both callosotomized and healthy adult individuals.

Cortical and subcortical hemodynamic changes during sleep slow waves in human light sleep.

EEG slow waves, the hallmarks of NREM sleep are thought to be crucial for the regulation of several important processes, including learning, sensory disconnection and the removal of brain metabolic wastes. Animal research indicates that slow waves may involve complex interactions within and between cortical and subcortical structures. Conventional EEG in humans, however, has a low spatial resolution and is unable to accurately describe changes in the activity of subcortical and deep cortical structures. To overcome these limitations, here we took advantage of simultaneous EEG-fMRI recordings to map cortical and subcortical hemodynamic (BOLD) fluctuations time-locked to slow waves of light sleep. Recordings were performed in twenty healthy adults during an afternoon nap. Slow waves were associated with BOLD-signal increases in the posterior brainstem and in portions of thalamus and cerebellum characterized by preferential functional connectivity with limbic and somatomotor areas, respectively. At the cortical level, significant BOLD-signal decreases were instead found in several areas, including insula and somatomotor cortex. Specifically, a slow signal increase preceded slow-wave onset and was followed by a delayed, stronger signal decrease. Similar hemodynamic changes were found to occur at different delays across most cortical brain areas, mirroring the propagation of electrophysiological slow waves, from centro-frontal to inferior temporo-occipital cortices. Finally, we found that the amplitude of electrophysiological slow waves was positively related to the magnitude and inversely related to the delay of cortical and subcortical BOLD-signal changes. These regional patterns of brain activity are consistent with theoretical accounts of the functions of sleep slow waves.

Risk factors of excessive daytime sleepiness in a prospective population-based cohort.

Although excessive daytime sleepiness is commonly evaluated in clinical and research settings using the Epworth Sleepiness Scale, few studies have assessed the factors associated with its incidence in the general population. We prospectively investigated the predictors of incident and persistent excessive daytime sleepiness in 2,751 subjects (46.1% men, mean age 56.0 ± 9.8 years) from the CoLaus-PsyCoLaus population-based cohort (Lausanne, Switzerland) over 5 years. Participants completed the Epworth Sleepiness Scale and the Pittsburgh Sleep Quality Index, and underwent a full clinical evaluation at baseline and 5 years afterwards. Ambulatory polysomnography was performed at baseline in a sub-sample of 1,404 subjects. Among the 2,438 subjects without excessive daytime sleepiness (Epworth Sleepiness Scale ≤ 10) at baseline, the 5-year incidence of excessive daytime sleepiness was 5.1% (n = 124). Multivariate logistic regression revealed that male sex, depressive symptoms, reported poor sleep quality and moderate to severe obstructive sleep apnea were independent predictors of incident excessive daytime sleepiness, while older age, moderate coffee consumption, periodic leg movement during sleep and hypertension were independent protective factors. Stratified analysis according to sex and age showed some distinctive associations. Among the 313 patients with excessive daytime sleepiness at baseline, 137 (43.8%) had persistent excessive daytime sleepiness 5 years later. Our findings provide new insights into the predictors of incident excessive daytime sleepiness, but interventional studies are needed to understand the impact of treating these risk factors on the incidence of excessive daytime sleepiness.

Regional Delta Waves In Human Rapid Eye Movement Sleep.

Although the EEG slow wave of sleep is typically considered to be a hallmark of nonrapid eye movement (NREM) sleep, recent work in mice has shown that slow waves can also occur in REM sleep. Here, we investigated the presence and cortical distribution of negative delta (1-4 Hz) waves in human REM sleep by analyzing high-density EEG sleep recordings obtained in 28 healthy subjects. We identified two clusters of delta waves with distinctive properties: (1) a frontal-central cluster characterized by ∼2.5-3.0 Hz, relatively large, notched delta waves (so-called "sawtooth waves") that tended to occur in bursts, were associated with increased gamma activity and rapid eye movements (EMs), and upon source modeling displayed an occipital-temporal and a frontal-central component and (2) a medial-occipital cluster characterized by more isolated, slower (<2 Hz), and smaller waves that were not associated with rapid EMs, displayed a negative correlation with gamma activity, and were also found in NREM sleep. Therefore, delta waves are an integral part of REM sleep in humans and the two identified subtypes (sawtooth and medial-occipital slow waves) may reflect distinct generation mechanisms and functional roles. Sawtooth waves, which are exclusive to REM sleep, share many characteristics with ponto-geniculo-occipital waves described in animals and may represent the human equivalent or a closely related event, whereas medial-occipital slow waves appear similar to NREM sleep slow waves.SIGNIFICANCE STATEMENT The EEG slow wave is typically considered a hallmark of nonrapid eye movement (NREM) sleep, but recent work in mice has shown that it can also occur in REM sleep. By analyzing high-density EEG recordings collected in healthy adult individuals, we show that REM sleep is characterized by prominent delta waves also in humans. In particular, we identified two distinctive clusters of delta waves with different properties: a frontal-central cluster characterized by faster, activating "sawtooth waves" that share many characteristics with ponto-geniculo-occipital waves described in animals and a medial-occipital cluster containing slow waves that are more similar to NREM sleep slow waves. These findings indicate that REM sleep is a spatially and temporally heterogeneous state and may contribute to explaining its known functional and phenomenological properties.

Dreaming in NREM Sleep: A High-Density EEG Study of Slow Waves and Spindles.

Dreaming can occur in both rapid eye movement (REM) and non-REM (NREM) sleep. We recently showed that in both REM and NREM sleep, dreaming is associated with local decreases in slow wave activity (SWA) in posterior brain regions. To expand these findings, here we asked how specific features of slow waves and spindles, the hallmarks of NREM sleep, relate to dream experiences. Fourteen healthy human subjects (10 females) underwent nocturnal high-density EEG recordings combined with a serial awakening paradigm. Reports of dreaming, compared with reports of no experience, were preceded by fewer, smaller, and shallower slow waves, and faster spindles, especially in central and posterior cortical areas. We also identified a minority of very steep and large slow waves in frontal regions, which occurred on a background of reduced SWA and were associated with high-frequency power increases (local "microarousals") heralding the successful recall of dream content. These results suggest that the capacity of the brain to generate experiences during sleep is reduced in the presence of neuronal off-states in posterior and central brain regions, and that dream recall may be facilitated by the intermittent activation of arousal systems during NREM sleep.SIGNIFICANCE STATEMENT By combining high-density EEG recordings with a serial awakening paradigm in healthy subjects, we show that dreaming in non-rapid eye movement sleep occurs when slow waves in central and posterior regions are sparse, small, and shallow. We also identified a small subset of very large and steep frontal slow waves that are associated with high-frequency activity increases (local "microarousals") heralding successful recall of dream content. These results provide noninvasive measures that could represent a useful tool to infer the state of consciousness during sleep.

Visual imagery and visual perception induce similar changes in occipital slow waves of sleep.

Previous studies have shown that regional slow-wave activity (SWA) during non-rapid eye movement (NREM) sleep is modulated by prior experience and learning. Although this effect has been convincingly demonstrated for the sensorimotor domain, attempts to extend these findings to the visual system have provided mixed results. In this study we asked whether depriving subjects of external visual stimuli during daytime would lead to regional changes in slow waves during sleep and whether the degree of "internal visual stimulation" (spontaneous imagery) would influence such changes. In two 8-h sessions spaced 1 wk apart, 12 healthy volunteers either were blindfolded while listening to audiobooks or watched movies (control condition), after which their sleep was recorded with high-density EEG. We found that during NREM sleep, the number of small, local slow waves in the occipital cortex decreased after listening with blindfolding relative to movie watching in a way that depended on the degree of visual imagery subjects reported during blindfolding: subjects with low visual imagery showed a significant reduction of occipital sleep slow waves, whereas those who reported a high degree of visual imagery did not. We also found a positive relationship between the reliance on visual imagery during blindfolding and audiobook listening and the degree of correlation in sleep SWA between visual areas and language-related areas. These preliminary results demonstrate that short-term alterations in visual experience may trigger slow-wave changes in cortical visual areas. Furthermore, they suggest that plasticity-related EEG changes during sleep may reflect externally induced ("bottom up") visual experiences, as well as internally generated ("top down") processes. NEW & NOTEWORTHY Previous work has shown that slow-wave activity, a marker of sleep depth, is linked to neural plasticity in the sensorimotor cortex. We show that after short-term visual deprivation, subjects who reported little visual imagery had a reduced incidence of occipital slow waves. This effect was absent in subjects who reported strong spontaneous visual imagery. These findings suggest that visual imagery may "substitute" for visual perception and induce similar changes in non-rapid eye movement slow waves.

A potential role of hypophosphatemia for diagnosing convulsive seizures: A case-control study.

OBJECTIVE: Transient loss of consciousness (TLOC) is a common presentation in the emergency room, where patient history can usually differentiate syncope from generalized tonic-clonic (GTC) seizures. Several serum markers, such as creatine kinase and lactate, can be helpful, especially when history is unreliable. Here, we explore a potential supporting role of electrolyte plasma levels in a case-control study. METHODS: In our electroencephalographic database, we retrospectively identified consecutive episodes of loss of consciousness in adults seen over 3 years in our hospital emergency department for a case-control study. We investigated plasma levels of several electrolytes (sodium, potassium, phosphate, calcium, magnesium) at the emergency visit, as well as demographics, diagnosis, blood-sample delay time, and history of alcohol abuse. RESULTS: Of the 126 patients identified, 75 had GTC seizures and 46 had other TLOC causes. Among electrolyte levels, only hypophosphatemia was associated with GTC seizures (median = 0.79 mmol·L-1 , range = 0.34-1.37 in GTC seizures vs 0.93 mmol·L-1 , range = 0.52-1.56, P = 0.001 in TLOC). After adjusting for blood sampling delay, alcohol abuse, and other electrolyte levels, only hypophosphatemia was associated with GTC seizures, occurring in 37 (51%) of GTC seizures and 12 (22%) of other TLOC (odds ratio = 3.5, 95% confidence interval = 1.5-8.3, P = 0.003). Hypophosphatemia < 0.6 mmol·L-1 was 93% specific and 20% sensitive for GTC seizure occurrence. In follow-ups, hypophosphatemia was transitory. SIGNIFICANCE: Transient hypophosphatemia is common after GTC seizures and could represent an additional biological marker to help differentiate GTC seizures from other TLOC, especially when history is unclear. This hypothesis needs to be tested prospectively.

How do children fall asleep? A high-density EEG study of slow waves in the transition from wake to sleep.

INTRODUCTION: Slow waves, the hallmarks of non-rapid eye-movement (NREM) sleep, are thought to reflect maturational changes that occur in the cerebral cortex throughout childhood and adolescence. Recent work in adults has revealed evidence for two distinct synchronization processes involved in the generation of slow waves, which sequentially come into play in the transition to sleep. In order to understand how these two processes are affected by developmental changes, we compared slow waves between children and young adults in the falling asleep period. METHODS: The sleep onset period (starting 30s before end of alpha activity and ending at the first slow wave sequence) was extracted from 72 sleep onset high-density EEG recordings (128 electrodes) of 49 healthy subjects (age 8-25). Using an automatic slow wave detection algorithm, the number, amplitude and slope of slow waves were analyzed and compared between children (age 8-11) and young adults (age 20-25). RESULTS: Slow wave number and amplitude increased linearly in the falling asleep period in children, while in young adults, isolated high-amplitude slow waves (type I) dominated initially and numerous smaller slow waves (type II) with progressively increasing amplitude occurred later. Compared to young adults, children displayed faster increases in slow wave amplitude and number across the falling asleep period in central and posterior brain regions, respectively, and also showed larger slow waves during wakefulness immediately prior to sleep. CONCLUSIONS: Children do not display the two temporally dissociated slow wave synchronization processes in the falling asleep period observed in adults, suggesting that maturational factors underlie the temporal segregation of these two processes. Our findings provide novel perspectives for studying how sleep-related behaviors and dreaming differ between children and adults.

[Sleep-related movement disorders]. / Mouvements anormaux liés au sommeil.

Sleep is characterized, from a behavioral point of view, by a physical quiescence. However, sleep can be disrupted by movements which can occur before falling asleep, during the sleep-wake transition, or during sleep. Some of these movements may be considered quasi-physiological because they are very common in the general population and have little or no clinical impact. However, others may have an impact on sleep quality, or be associated with other neurological conditions. Patients' symptoms and complaints, the movements' description by witnesses, home video and video-polysomnographic recordings in the sleep laboratory allow to establish the diagnosis. The instauration of a treatment should be guided by clinical repercussions.

Le sommeil se caractérise, d'un point de vue comportemental, par une quiescence physique. Pourtant, il peut être perturbé par des mouvements qui peuvent survenir avant l'endormissement, lors de la transition veille-sommeil ou lors du sommeil. Certains de ces mouvements peuvent être considérés comme quasi physiologiques car ils sont très fréquents dans la population générale et ont peu ou pas de répercussions cliniques. Par contre, d'autres peuvent avoir un impact sur la qualité du sommeil ou s'associer à d'autres pathologies neurologiques. L'anamnèse du patient et des témoins de ses nuits, des enregistrements vidéo à domicile et l'enregistrement vidéo-polysomnographique au laboratoire permettent de poser le diagnostic. La nécessité ou pas d'un traitement viendra, marquée par les répercussions cliniques.

Neural and behavioral correlates of extended training during sleep deprivation in humans: evidence for local, task-specific effects.

Recent work has demonstrated that behavioral manipulations targeting specific cortical areas during prolonged wakefulness lead to a region-specific homeostatic increase in theta activity (5-9 Hz), suggesting that theta waves could represent transient neuronal OFF periods (local sleep). In awake rats, the occurrence of an OFF period in a brain area relevant for behavior results in performance errors. Here we investigated the potential relationship between local sleep events and negative behavioral outcomes in humans. Volunteers participated in two prolonged wakefulness experiments (24 h), each including 12 h of practice with either a driving simulation (DS) game or a battery of tasks based on executive functions (EFs). Multiple high-density EEG recordings were obtained during each experiment, both in quiet rest conditions and during execution of two behavioral tests, a response inhibition test and a motor test, aimed at assessing changes in impulse control and visuomotor performance, respectively. In addition, fMRI examinations obtained at 12 h intervals were used to investigate changes in inter-regional connectivity. The EF experiment was associated with a reduced efficiency in impulse control, whereas DS led to a relative impairment in visuomotor control. A specific spatial and temporal correlation was observed between EEG theta waves occurring in task-related areas and deterioration of behavioral performance. The fMRI connectivity analysis indicated that performance impairment might partially depend on a breakdown in connectivity determined by a "network overload." Present results demonstrate the existence of an association between theta waves during wakefulness and performance errors and may contribute explaining behavioral impairments under conditions of sleep deprivation/restriction.

Sleep reverts changes in human gray and white matter caused by wake-dependent training.

Learning leads to rapid microstructural changes in gray (GM) and white (WM) matter. Do these changes continue to accumulate if task training continues, and can they be reverted by sleep? We addressed these questions by combining structural and diffusion weighted MRI and high-density EEG in 16 subjects studied during the physiological sleep/wake cycle, after 12 h and 24 h of intense practice in two different tasks, and after post-training sleep. Compared to baseline wake, 12 h of training led to a decline in cortical mean diffusivity. The decrease became even more significant after 24 h of task practice combined with sleep deprivation. Prolonged practice also resulted in decreased ventricular volume and increased GM and WM subcortical volumes. All changes reverted after recovery sleep. Moreover, these structural alterations predicted cognitive performance at the individual level, suggesting that sleep's ability to counteract performance deficits is linked to its effects on the brain microstructure. The cellular mechanisms that account for the structural effects of sleep are unknown, but they may be linked to its role in promoting the production of cerebrospinal fluid and the decrease in synapse size and strength, as well as to its recently discovered ability to enhance the extracellular space and the clearance of brain metabolites.

Shared EEG correlates between non-REM parasomnia experiences and dreams.

Sleepwalking and related parasomnias result from incomplete awakenings out of non-rapid eye movement sleep. Behavioral episodes can occur without consciousness or recollection, or in relation to dream-like experiences. To understand what accounts for these differences in consciousness and recall, here we recorded parasomnia episodes with high-density electroencephalography (EEG) and interviewed participants immediately afterward about their experiences. Compared to reports of no experience (19%), reports of conscious experience (56%) were preceded by high-amplitude EEG slow waves in anterior cortical regions and activation of posterior cortical regions, similar to previously described EEG correlates of dreaming. Recall of the content of the experience (56%), compared to no recall (25%), was associated with higher EEG activation in the right medial temporal region before movement onset. Our work suggests that the EEG correlates of parasomnia experiences are similar to those reported for dreams and may thus reflect core physiological processes involved in sleep consciousness.

Sleep disturbances and incident risk of major depressive disorder in a population-based cohort.

Sleep disturbances are well-known symptoms of major depressive disorder (MDD). However, the prospective risk of MDD in the presence of sleep disturbances in a general population-based cohort is not well known. This study investigated associations between both polysomnography (PSG)-based or subjective sleep features and incident MDD. Participants representative of the general population who had never had MDD completed sleep questionnaires (n = 2000) and/or underwent PSG (n = 717). Over 8 years' follow-up, participants completed psychiatric interviews enabling the diagnosis of MDD. Survival Cox models were used to analyze associations between sleep features and MDD incidence. A higher Epworth Sleepiness Scale and presence of insomnia symptoms were significantly associated with a higher incidence of MDD (hazard ratio [HR] [95 % confidence interval (CI)]: 1.062 [1.022-1.103], p = 0.002 and 1.437 [1.064-1.940], p = 0.018, respectively). Higher density of rapid eye movements in rapid eye movement (REM) sleep was associated with a higher incidence of MDD in men (HR 1.270 [95 % CI 1.064-1.516], p = 0.008). In women, higher delta power spectral density was associated with a lower MDD incidence (HR 0.674 [95 % CI 0.463-0.981], p = 0.039). This study confirmed the associations between subjective and objective sleep features and the incidence of MDD in a large community dwelling cohort.

Dusk2Dawn: an EEGLAB plugin for automatic cleaning of whole-night sleep electroencephalogram using Artifact Subspace Reconstruction.

Whole-night sleep electroencephalogram (EEG) is plagued by several types of large-amplitude artifacts. Common approaches to remove them are fraught with issues: channel interpolation, rejection of noisy intervals, and independent component analysis are time-consuming, rely on subjective user decisions, and result in signal loss. Artifact Subspace Reconstruction (ASR) is an increasingly popular approach to rapidly and automatically clean wake EEG data. Indeed, ASR adaptively removes large-amplitude artifacts regardless of their scalp topography or consistency throughout the recording. This makes ASR, at least in theory, a highly-promising tool to clean whole-night EEG. However, ASR crucially relies on calibration against a subset of relatively clean "baseline" data. This is problematic when the baseline changes substantially over time, as in whole-night EEG data. Here we tackled this issue and, for the first time, validated ASR for cleaning sleep EEG. We demonstrate that ASR applied out-of-the-box, with the parameters recommended for wake EEG, results in the dramatic removal of slow waves. We also provide an appropriate procedure to use ASR for automatic and rapid cleaning of whole-night sleep EEG data or any long EEG recording. Our procedure is freely available in Dusk2Dawn, an open-source plugin for EEGLAB.

Effect of oxybutynin and reboxetine on obstructive sleep apnea: a randomized, placebo-controlled, double-blind, crossover trial.

STUDY OBJECTIVES: Although recent investigations combining noradrenergic and antimuscarinic drugs have shown promising short-term results to treat obstructive sleep apnea (OSA), the mid-term effect and optimal dosage remain uncertain. The present study aimed to evaluate the effect of 1 week of 5 mg oxybutynin and 6 mg reboxetine (oxy-reb) on OSA versus placebo. METHODS: We performed a randomized, placebo-controlled, double-blind, crossover trial comparing the effect of 1 week of oxy-reb versus 1 week of placebo on OSA severity. At-home polysomnography was performed at baseline and after each week of intervention. RESULTS: Fifteen participants (male 66.7%) aged 59 [44-62] years (median [interquartile range]) with a mean body mass index of 33.1 ± 6.6 kg/m2 were included. No significant difference in apnea-hypopnea index (AHI) was observed between conditions (estimated marginal means [95% confidence interval] at baseline: 39.7 [28.5-55.3]; oxy-reb: 34.5 [22.7-52.3]; placebo: 37.9 [27.1-52.9]; p = 0.652), but oxy-reb improved average oxygen desaturation (p = 0.016) and hypoxic burden (p = 0.011) and lowered sleep efficiency (p = 0.019) and rapid eye movement sleep (p = 0.002). Moreover, participants reported reduced sleep quality during the week of oxy-reb compared to the week of placebo (4.7 [3.5; 5.9] vs. 6.5 [5.5; 7.5] on a 0-10 visual analogic scale, respectively; p = 0.001). No significant differences in sleepiness, vigilance, and fatigue were observed. No serious adverse events occurred. CONCLUSIONS: Administration of oxybutynin 5 mg and reboxetine 6 mg did not improve OSA severity assessed by AHI, but did alter sleep architecture and sleep quality. Reduced average oxygen desaturation and hypoxic burden were also observed. CLINICAL TRIAL: ClinicalTrials.gov, https://clinicaltrials.gov, NCT04394143.

Objective polysomnography-based sleep features and major depressive disorder subtypes in the general population.

Insomnia and its opposite hypersomnia are part of the diagnostic criteria for major depressive disorder (MDD). However, no study has investigated whether the postulated sleep alterations in clinical subtypes of MDD are reflected in polysomnography (PSG)-derived objective sleep measures. The objective of this study was to establish associations between the melancholic, atypical and unspecified subtypes of MDD and objective PSG-based sleep features. This cross-sectional analysis included 1820 community-dwelling individuals who underwent PSG and a semi-structured psychiatric interview to elicit diagnostic criteria for MDD and its subtypes. Adjusted robust linear regression was used to assess associations between MDD subtypes and PSG-derived objective sleep measures. Current melancholic MDD was significantly associated with decreased absolute delta power and sleep efficiency and with increased wake after sleep onset. Remitted unspecified MDD was significantly associated with increased rapid eye movements density. No other significant associations were identified. Our findings reflect that some PSG-based sleep features differed in MDD subtypes compared with no MDD. The largest number of significant differences were observed for current melancholic MDD, whereas only rapid eye movements density could represent a risk factor for MDD as it was the only sleep measure that was also associated with MDD in remitted participants.