Increase In Slow Wave Activity Research Articles

Lateral Habenula Glutamatergic Neurons Modulate Isoflurane Anesthesia in Mice.

Since their introduction in the 1840s, one of the largest mysteries of modern anesthesia are how general anesthetics create the state of reversible loss of consciousness. Increasing researchers have shown that neural pathways that regulate endogenous sleep–wake systems are also involved in general anesthesia. Recently, the Lateral Habenula (LHb) was considered as a hot spot for both natural sleep–wake and propofol-induced sedation; however, the role of the LHb and related pathways in the isoflurane-induced unconsciousness has yet to be identified. Here, using real-time calcium fiber photometry recordings in vivo, we found that isoflurane reversibly increased the activity of LHb glutamatergic neurons. Then, we selectively ablated LHb glutamatergic neurons in Vglut2-cre mice, which caused a longer induction time and less recovery time along with a decrease in delta-band power in mice under isoflurane anesthesia. Furthermore, using a chemogenetic approach to specifically activate LHb glutamatergic neurons shortened the induction time and prolonged the recovery time in mice under isoflurane anesthesia with an increase in delta-band power. In contrast, chemogenetic inhibition of LHb glutamatergic neurons was very similar to the effects of selective lesions of LHb glutamatergic neurons. Finally, optogenetic activation of LHb glutamatergic neurons or the synaptic terminals of LHb glutamatergic neurons in the rostromedial tegmental nucleus (RMTg) produced a hypnosis-promoting effect in isoflurane anesthesia with an increase in slow wave activity. Our results suggest that LHb glutamatergic neurons and pathway are vital in modulating isoflurane anesthesia.

Electrophysiological signatures of acute systemic lipopolysaccharide-induced inflammation: potential implications for delirium science

BackgroundNovel preventive therapies are needed for postoperative delirium, which especially affects older patients. A mouse model is presented that captures inflammation-associated cortical slow wave activity (SWA) observed in patients, allowing exploration of the mechanistic role of prostaglandin-adenosine signalling. MethodsEEG and cortical cytokine measurements (interleukin 6, monocyte chemoattractant protein-1) were obtained from adult and aged mice. Behaviour, SWA, and functional connectivity were assayed before and after systemic administration of lipopolysaccharide (LPS)+piroxicam (cyclooxygenase inhibitor) or LPS+caffeine (adenosine receptor antagonist). To avoid the confounder of inflammation-driven changes in movement which alter SWA and connectivity, electrophysiological recordings were classified as occurring during quiescence or movement, and propensity score matching was used to match distributions of movement magnitude between baseline and post-LPS administration. ResultsLPS produces increases in cortical cytokines and behavioural quiescence. In movement-matched data, LPS produces increases in SWA (likelihood-ratio test: χ2(4)=21.51, P<0.001), but not connectivity (χ2(4)=6.39, P=0.17). Increases in SWA associate with interleukin 6 (P<0.001) and monocyte chemoattractant protein-1 (P=0.001) and are suppressed by piroxicam (P<0.001) and caffeine (P=0.046). Aged animals compared with adult animals show similar LPS-induced SWA during movement, but exaggerated cytokine response and increased SWA during quiescence. ConclusionsCytokine-SWA correlations during wakefulness are consistent with observations in patients with delirium. Absence of connectivity effects after accounting for movement changes suggests decreased connectivity in patients is a biomarker of hypoactivity. Exaggerated effects in quiescent aged animals are consistent with increased hypoactive delirium in older patients. Prostaglandin-adenosine signalling may link inflammation to neural changes and hence delirium.

Acoustic enhancement of slow wave sleep on consecutive nights improves alertness and attention in chronically short sleepers

IntroductionChronic sleep restriction has been linked to occupational errors and motor vehicle crashes. Enhancing slow wave sleep may alleviate some of the cognitive deficits associated with chronic sleep restriction. However, the extent to which acoustic stimulation of slow wave activity (SWA) may improve alertness and attention is not well established, particularly with respect to consecutive nights of exposure. MethodsTwenty-five healthy adults (32.9 ± 8.2 years; 16 female) who self-restricted their sleep during workdays participated in a randomized, double-blind, cross-over study. Participants wore an automated acoustic stimulation device for two consecutive nights. Acoustic tones (50 ms long) were delivered on the up-phase of the slow wave first and then at constant 1-s inter-tone-intervals once N3 was identified (STIM), until an arousal or shift to another sleep stage occurred, or at inaudible decibels during equivalent stimulation periods (SHAM). Subjective alertness/fatigue (KSS, Samn-Perelli) was assessed across both days, and objective measures of alertness (MSLT) and attention (PVT) were assessed after two nights of stimulation. ResultsAfter one night of acoustic stimulation, increased slow wave energy was observed in 68% of participants, with an average significant increase of 17.7% (p = 0.01), while Night 2 was associated with a 22.2% increase in SWA (p = 0.08). SWE was highly stable across the two nights of STIM (ICC 0.93, p < 0.001), and around half (56%) of participants were consistently classified as responders (11/25) or non-responders (3/25). Daytime testing showed that participants felt more alert and awake following each night of acoustic stimulation (p < 0.05), with improved objective attention across the day following two nights of acoustic stimulation. DiscussionConsecutive nights of acoustic stimulation enhanced SWA on both nights, and improved next day alertness and attention. Given large individual differences, we highlight the need to examine both the long-term effects of stimulation, and to identify inter-individual differences in acoustic stimulation response. Our findings suggest that the use of an acoustic device to enhance slow wave sleep may alleviate some of the deficits in alertness and attention typically associated with sleep restriction.

Modulating overnight memory consolidation by acoustic stimulation during slow-wave sleep: a systematic review and meta-analysis.

The low-frequency high-amplitude oscillations of slow-wave sleep (SWS) are considered to promote the consolidation of episodic memory. Previous research suggests that sleep slow waves can be entrained and enhanced by presenting short acoustic stimuli to the up-states of endogenous waves. Several studies have investigated the effects of these increases in slow-wave activity on overnight memory consolidation, with inconsistent results. The aim of this meta-analysis was to evaluate the accumulated evidence connecting acoustic stimulation during sleep to episodic memory consolidation. A systematic literature search was conducted in October 2020 using PubMed, Web of Science, and PsycInfo. The main study inclusion criteria were the application of acoustic slow wave enhancement in healthy participants and an assessment of pre- and post-sleep episodic memory performance. Effect sizes were pooled using a random-effects model. A total of 10 primary studies with 11 experiments and 177 participants were included. Results showed a combined effect size (Hedges' g) of 0.25 (p = 0.07). Subgroup models based on young adults (n = 8), phase-locked stimulation approaches (n = 8), and their combination (n = 6) showed combined effect sizes of 0.31 (p = 0.051), 0.36 (p = 0.047), and 0.44 (p = 0.01), respectively. There was no indication of publication bias or bias in individual studies. Acoustic enhancement of SWS tends to increase the overnight consolidation of episodic memory but effects remain small and-with the exception of subgroup models-at trend levels. Currently, the evidence is not sufficient to recommend the use of commercially available devices.

Mind-wandering Is Accompanied by Both Local Sleep and Enhanced Processes of Spatial Attention Allocation.

Mind-wandering (MW) is a subjective, cognitive phenomenon, in which thoughts move away from the task toward an internal train of thoughts, possibly during phases of neuronal sleep-like activity (local sleep, LS). MW decreases cortical processing of external stimuli and is assumed to decouple attention from the external world. Here, we directly tested how indicators of LS, cortical processing, and attentional selection change in a pop-out visual search task during phases of MW. Participants’ brain activity was recorded using magnetoencephalography, MW was assessed via self-report using randomly interspersed probes. As expected, the performance decreased under MW. Consistent with the occurrence of LS, MW was accompanied by a decrease in high-frequency activity (HFA, 80–150 Hz) and an increase in slow wave activity (SWA, 1–6 Hz). In contrast, visual attentional selection as indexed by the N2pc component was enhanced during MW with the N2pc amplitude being directly linked to participants’ performance. This observation clearly contradicts accounts of attentional decoupling that would predict a decrease in attention-related responses to external stimuli during MW. Together, our results suggest that MW occurs during phases of LS with processes of attentional target selection being upregulated, potentially to compensate for the mental distraction during MW.

Local Sleep Slow-Wave Activity Colocalizes With the Ictal Symptomatogenic Zone in a Patient With Reflex Epilepsy: A High-Density EEG Study.

Background: Slow-wave activity (SWA) during non-rapid eye movement (NREM) sleep reflects synaptic potentiation during preceding wakefulness. Epileptic activity may induce increases in state-dependent SWA in human brains, therefore, localization of SWA may prove useful in the presurgical workup of epileptic patients. We analyzed high-density electroencephalography (HDEEG) data across vigilance states from a reflex epilepsy patient with a clearly localizable ictal symptomatogenic zone to provide a proof-of-concept for the testability of this hypothesis.Methods: Overnight HDEEG recordings were obtained in the patient during REM sleep, NREM sleep, wakefulness, and during a right facial motor seizure then compared to 10 controls. After preprocessing, SWA (i.e., delta power; 1–4 Hz) was calculated at each channel. Scalp level and source reconstruction analyses were computed. We assessed for statistical differences in maximum SWA between the patient and controls within REM sleep, NREM sleep, wakefulness, and seizure. Then, we completed an identical statistical comparison after first subtracting intrasubject REM sleep SWA from that of NREM sleep, wakefulness, and seizure SWA.Results: The topographical analysis revealed greater left hemispheric SWA in the patient vs. controls in all vigilance states except REM sleep (which showed a right hemispheric maximum). Source space analysis revealed increased SWA in the left inferior frontal cortex during NREM sleep and wakefulness. Ictal data displayed poor source-space localization. Comparing each state to REM sleep enhanced localization accuracy; the most clearly localizing results were observed when subtracting REM sleep from wakefulness.Conclusion: State-dependent SWA during NREM sleep and wakefulness may help to identify aspects of the potential epileptogenic zone. Future work in larger cohorts may assess the clinical value of sleep SWA to help presurgical planning.

Electroencephalography quantitative indicators of patients with bilateral vocal fold paralysis

Treatment of patients with bilateral vocal fold paralyses remains a complicated task. Study of central mechanisms of realization of larynx functions in case of stenosis is of interest. By electro­encephalography method (EEG) patients with bilateral vocal fold paralysis were examined: 55 patients without surgical treatment (group I), and 51 patients who had unilateral chordoarytenoidotomy (group II). All the patients showed changes in percentage content of the α - and β-rhythms and Δ- and θ-rhythms ("slow" waves). The group II patients demonstrated more pronounced rhythms, as compared with the control group. During the background recording, in group I the increase in the percentage content of the Δ-rhythms in frontal and parietal directions up to 28.2±2.3 and 29.2±2.4%, was seen, the group II patients showed the increase in Δ-activity up to 32.2±2.8 and 35.4±2.9% in frontal, temporal and parietal directions accordingly. Besides, the group II patients proved to have an increasing of β-rhythms activity in all the directions, as compared to the control group, as well as an increasing of θ-rhythms in temporal and parietal directions. Herewith, the increase of θ-rhythms in temporal directions up to 21.4±2.2%, was much higher as compared to group I data 16.5±1.3%. Besides, all the patients showed decrease in α-rhythms amplitude. So, the redistribution of electroencephalography rhythms in the way of α-range fluctuation decrease and increase of slow wave activity (θ- и Δ- waves), as well as α-rhythms amplitude decrease in patients having vocal fold motor disorders testify to the prevailing influence of subcortical structures on the bioelectrical brain activity and facts of nervous processes depletion in brain, including chronic hypoxia of patients suffering from larynx stenosis of paralytic origin.

0669 The Effects Of Continuous Positive Airway Pressure Therapy In Moderate To Severe Obstructive Sleep Apnea: A High-density EEG Study

Abstract Introduction A previous high-density electroencephalography (EEG) investigation in asymptomatic OSA showed regional deficits in sleep EEG power particularly slow wave activity (SWA) during NREM sleep in the parietal region. It is unclear whether treatment with CPAP can reverse local sleep EEG abnormalities in OSA, and whether any recovery is related to improvement in sleep-dependent memory consolidation. Methods Fifteen male participants (age 50.4±6.5yrs, AHI 51.7±23.5/h) with moderate-severe OSA (AHI&amp;gt;15/h) underwent overnight polysomnography with 256-channel high-density EEG at baseline and following 3 months of CPAP therapy. A word paired associates declarative memory task was administered before and after sleep. After artefact removal, spectral analysis was performed for all channels. Topographical power maps were calculated for standard frequency ranges for NREM sleep (164 channels within a 0.57 radius from the vertex). Maps were compared using both absolute and normalized power (z-scores computed for each subject) and differences between baseline and treatment were determined by statistical nonparametric mapping. Results In 11 CPAP compliant patients (intolerant of CPAP [n=3]/high-density EEG [n=1]), analysis of polysomnographic variables showed that total sleep time did not differ but N1 (baseline vs. treatment: 66.9 vs. 39.5 mins,p=0.008) and N2 (195.0 vs. 150.6 mins,p=0.002) sleep was lower and N3 (89.8 vs. 128.7 mins,p=0.003) was higher after CPAP. Topographic analysis of high-density EEG data revealed a regional increase in SWA (1-4.5Hz) EEG power during N3 sleep in a cluster of electrodes overlying the centro-parietal cortex (cluster mean t-value=2.87,p=0.02). The change in overnight declarative memory consolidation (% recognition) after CPAP was significantly correlated with the change in slow spindle frequency activity in frontal regions (cluster mean r=0.875,p=0.003). Conclusion CPAP treatment may enhance localised deficits in sleep EEG activity in OSA, and specific regional recovery may translate to memory improvements in the short-term. These data also highlight the potential for long-term therapeutic effects on cognitive outcomes in OSA. Support

Dietary natural cocoa ameliorates disrupted circadian rhythms in locomotor activity and sleep-wake cycles in mice with chronic sleep disorders caused by psychophysiological stress.

Cocoa contains many chemical compounds that affect the physiological functions of experimental animals and humans. The present study used a mouse model characterized by disrupted circadian rhythms of locomotor activity and sleep-wake cycles to determine whether natural cocoa improves chronic sleep disorders (CSDs) induced by psychophysiological stress. Mice were fed a high-fat, high-sucrose diet supplemented with 2.0% natural cocoa and stressed for 30 d to induce CSDs. Dietary cocoa restored the amplitude reduction of day-night activity rhythms by improving reduced nocturnal wheel-running activities during CSDs. Electroencephalography revealed that dietary cocoa significantly ameliorated CSD-induced increases in wakefulness during the first half of the inactive phase and in nonrapid eye movement sleep during the first half of the active phase. The attenuation of circadian rapid eye movement sleep rhythms and increased electroencephalography slow-wave activity (a marker of nonrapid eye movement sleep intensity) induced by CSDs improved in mice supplemented with cocoa. Dietary cocoa notably did not affect wheel-running activity rhythms or sleep-wake cycles under normal conditions. Dietary cocoa significantly increased the hypothalamic mRNA expression of Hspa1 a that encodes HSP70 and is associated with sleep regulation. Furthermore, Hspa1 a expression was not induced by CSDs in mice supplemented with cocoa. These findings suggest that dietary cocoa exerts beneficial effects on insomnia and circadian sleep disorders induced by psychophysiological stress.

An increase in sleep slow waves predicts better working memory performance in healthy individuals

Sleep is imperative for brain health and well-being, and restorative sleep is associated with better cognitive functioning. Increasing evidence indicates that electrophysiological measures of sleep, especially slow wave activity (SWA), regulate the consolidation of motor and perceptual procedural memory. In contrast, the role of sleep EEG and SWA in modulating executive functions, including working memory (WM), has been far less characterized. Here, we investigated across-night changes in sleep EEG that may ameliorate WM performance. Participants (N = 25, M = 100%) underwent two consecutive nights with high-density EEG, along with N-back tasks, which were administered at three time points the day before and after the second night of sleep. Non-rapid eye movement sleep EEG power spectra, power topography, as well as several slow-wave parameters were computed and compared across nights. Improvers on the 1-back, but not non-improvers, showed a significant increase in SWA as well as in down slope and negative peak amplitude, in a fronto-parietal region, and these parameters increases predicted better WM performance. Overall, these findings show that slow-wave sleep has a beneficial effect on WM and that it can occur in the adult brain even after minimal training. This is especially relevant, when considering that WM and other executive function cognitive deficits are present in several neuropsychiatric disorders, and that slow-wave enhancing interventions can improve cognition, thus providing novel insights and treatment strategies for these patients.

Evaluation of brain bioelectrical activity during xenon-oxygen mixture inhalation

Xenon is an inert gas used like inhalational anesthetic during different surgeries, including high-risk operations and for pain treatment caused by different factors. If concentration of the gas is less than 50 %, or the duration of the procedure is very short, no consciousness depression occurs. 20 healthy persons from 22 to 30 years old were undergone xenon/oxygen inhalation with concentration 70/30 % respectively for 3 minutes. Electroencephalography (EEG) was recorded before, during and 30 minutes later the procedure. For the data processing spectral analysis was used. Statistical analysis was performed by Wilcoxon and Page tests. As a result, significant increase in slow wave activity and reduction in alpha-rhythm activity were observed during and after the procedure as well as repartition of activity zones in brain similar to physiological sleep. This fact may be used in conduction of treatment and diagnostics procedures.

Pathophysiology of corticobasal degeneration: Insights from neurophysiological studies

BackgroundSeveral studies have applied electrophysiological techniques to physiologically characterize corticobasal degeneration (CBD). MethodsWe performed a systematic literature search of these studies and reviewed all 25 identified articles. ResultsConventional electroencephalography (EEG) is usually normal even in the late stages of disease. Quantitative EEG (qEEG) with spectral analysis revealed mainly lateralized abnormalities, such as an increase of slow wave activity and occasionally the occurrence of sharp waves, and a significant increase of coherence between left parietal-right premotor areas. CBD patients generally have long latency reflexes (LLR) with shorter latencies than in the classic cortical reflex myoclonus observed in progressive myoclonic epilepsy. The somatosensory evoked potentials (SEPs) showed reduced amplitude of the N20–P25 component. These abnormalities may reflect dysfunction of sensory projections to the motor cortex, while the localized parietal cortical damage is thought to be a pivotal factor for the absence of giant SEPs in these patients. Transcranial magnetic stimulation (TMS) revealed asymmetric intracortical disinhibition and asymmetric maps organization; an impaired transcallosal pathways function correlates with the atrophy of the corpus callosum. These findings suggest a pathologic hyperexcitability of the motor cortex, due to a loss of inhibitory input from the sensory cortex. ConclusionsNeurophysiological techniques, in combination with neuroimaging studies, may shed light on the pathophysiological mechanisms of CBD. A better understanding of the disease processes may help clinicians to make a more accurate and early diagnosis. TMS, SEP, LLR, and co-evaluation of EEG and EMG can aid the in differentiation between CBD and other parkinsonism syndromes.

EEG Frequency Characteristics in Healthy Advanced Elderly

Abstract. Changes in electroencephalographic (EEG) activity over the course of the normal aging process demonstrate that elderly individuals exhibit an increase in slow wave activity. In this study, we reexamined findings that EEG activity in healthy elderly individuals aged over 85 years (range 85–94) was the same or different compared to individuals younger than 84 years (range 65–84). We performed EEG frequency analysis to investigate the characteristics of resting state frequency components in a cross-sectional study. In individuals aged 85 and older, the dominant frequency component demonstrated a significant shift toward the slower alpha frequency in the left temporal and occipital regions. However, among the oldest individuals, a spectral peak appeared at 9.0–10.0 Hz, and power curves at peak frequency exhibited a sharp rise. Interestingly, healthy individuals older than 85 did not exhibit an appreciable change in EEG, suggesting that “slowing” is not a characteristic sign of aging.

Response to chronic sleep restriction, extension, and subsequent total sleep deprivation in humans: adaptation or preserved sleep homeostasis?

Sleep is regulated by a homeostatic process which in the two-process model of human sleep regulation is represented by electroencephalogram slow-wave activity (SWA). Many studies of acute manipulation of wake duration have confirmed the precise homeostatic regulation of SWA in rodents and humans. However, some chronic sleep restriction studies in rodents show that the sleep homeostatic response, as indexed by SWA, is absent or diminishes suggesting adaptation occurs. Here, we investigate the response to 7 days of sleep restriction (6 hr time in bed) and extension (10 hr time in bed) as well as the response to subsequent total sleep deprivation in 35 healthy participants in a cross-over design. The homeostatic response was quantified by analyzing sleep structure and SWA measures. Sleep restriction resulted primarily in a reduction of rapid eye movement (REM) sleep. SWA and accumulated SWA (slow-wave energy, SWE) were not much affected by sleep extension/restriction. The SWA responses did not diminish significantly in the course of the intervention and did not deviate significantly from the predictions of the two-process model. The response to total sleep deprivation consisted of an increase in SWA and rise rate of SWA and SWE and did not differ between the two conditions. The data show that changes in sleep duration within an ecologically relevant range have a marked effect on REM sleep and that SWA responds in accordance with predictions based on a saturating exponential increase during wake and an exponential decline in sleep of homeostatic sleep pressure during both chronic sleep restriction and extension.

The rostromedial tegmental nucleus is essential for non-rapid eye movement sleep.

The rostromedial tegmental nucleus (RMTg), also called the GABAergic tail of the ventral tegmental area, projects to the midbrain dopaminergic system, dorsal raphe nucleus, locus coeruleus, and other regions. Whether the RMTg is involved in sleep–wake regulation is unknown. In the present study, pharmacogenetic activation of rat RMTg neurons promoted non-rapid eye movement (NREM) sleep with increased slow-wave activity (SWA). Conversely, rats after neurotoxic lesions of 8 or 16 days showed decreased NREM sleep with reduced SWA at lights on. The reduced SWA persisted at least 25 days after lesions. Similarly, pharmacological and pharmacogenetic inactivation of rat RMTg neurons decreased NREM sleep. Electrophysiological experiments combined with optogenetics showed a direct inhibitory connection between the terminals of RMTg neurons and midbrain dopaminergic neurons. The bidirectional effects of the RMTg on the sleep–wake cycle were mimicked by the modulation of ventral tegmental area (VTA)/substantia nigra compacta (SNc) dopaminergic neuronal activity using a pharmacogenetic approach. Furthermore, during the 2-hour recovery period following 6-hour sleep deprivation, the amount of NREM sleep in both the lesion and control rats was significantly increased compared with baseline levels; however, only the control rats showed a significant increase in SWA compared with baseline levels. Collectively, our findings reveal an essential role of the RMTg in the promotion of NREM sleep and homeostatic regulation.

PSYCHOPHYSIOLOGICAL CHARACTERISTICS OF CHILDREN WITH AGGRESSIVE BEHAVIOR

The article presents a review of research on the problem of aggressive forms of behavior in children. Scholarly knowledge of definitions "aggression" and "aggressiveness" has being deepened and discovered. An available data analysis on dependence of the aggressiveness level on the features of the central nervous system functioning, psychological and social attitude of the individual has been carried out. The concepts of positive and negative aggression were indicated. A psychophysiological approach to aggressiveness has been considered, based on the study of the activity of various parts of the brain and characteristics of its functional status in children with aggressive behavior. Electroencephalographic markers in children with aggressive forms of behavior are appearance of cortical asymmetry associated with a slow-wave activity increase. Changes in indices of event-related potentials allow to suggest that aggressive individuals have certain cognitive impairments, in particular, problems with memory. According to the level registration of the brain constant potential, aggressive behavior leads to a significant increase in energy costs of the right hemisphere. Children with aggressive behavior are characterized by a disruption in the processing of incoming information, a hyperactive behavioral activation system and underactive behavioral inhibition system. An integrated approach in assessing the aggressiveness of children is based on interaction peculiarities of biological, psychophysiological and psychosocial factors, taking into account possibility of comorbid conditions development.

Sertindole: EEG Analysis, Tolerability, and Clinical Efficacy.

One of the common side effects of antipsychotic drugs is excessive sedation. The treatment with antipsychotics often manifests as an increase in slow wave activity in electroencephalography (EEG). The aim of this study was to analyze EEG recordings of patients treated with a non-sedative antipsychotic drug sertindole with regard to its adverse effects and clinical efficacy. EEG recordings of 45 patients (27 females, mean age 30.1±8.7 years) with schizophrenia were analyzed. EEG recordings were categorized based on abnormalities severity. The clinical efficacy was rated on the Clinical Global Impression Scale. Abnormalities from mild to moderate were found in 29% of the group. Clinical improvement was observed in 80% of patients. Sedation/daytime sleepiness was present in 7% of patients. Other side effects were prolongation of QTc (11%, severe 4%), insomnia (9%), extrapyramidal symptoms (7%), and heart palpitations (2%). Patients treated with sertindole do not show side effects similar to those found during treatment with other antipsychotic drugs. Increased slow wave activity in EEG and sedation were absent in the majority of the investigated patients.

Non-REM Sleep Instability in Children With Primary Monosymptomatic Sleep Enuresis.

Sleep enuresis is one of the most common sleep disturbances in childhood. Parental perception of deeper sleep in children with sleep enuresis is not confirmed by objective studies. However, evidence of disturbed sleep has been demonstrated by questionnaire, actigraphy, and polysomnographic studies, but no neurophysiological correlation with low arousability has been found. The goal of this study was to analyze the sleep microstructure of children with sleep enuresis using cyclic alternating pattern (CAP) analysis. Forty-nine children were recruited, 27 with enuresis (19 males and 8 females, mean age 9.78 years, 2.52 standard deviation) and 22 normal control patients (11 males and 11 females, mean age 10.7 years, 3.43 standard deviation); all subjects underwent clinical evaluation followed by a full-night polysomnographic recording. Psychiatric, neurological, respiratory, and renal diseases were excluded. No differences in sex, age, and apnea-hypopnea index were noted in the patients with enuresis and the control patients. Sleep stage architecture in children with sleep enuresis showed a decrease in percentage of stage N3 sleep. CAP analysis showed an increase in CAP rate in stage N3 sleep and in phase A1 index during stage N3 sleep in the sleep enuresis group, but also a significant reduction of A2% and A3% and of phases A2 and A3 indexes, supporting the concept of decreased arousability in patients with sleep enuresis. The decrease of phase A2 and A3 indexes in our patients might reflect the impaired arousal threshold of children with sleep enuresis. Sleep fragmentation might result in a compensatory increase of slow wave activity (indicated by the increase of CAP rate in stage N3 sleep) and may explain the higher arousal threshold (indicated by a decrease of phase A2 and A3 indexes) linked to an increased sleep pressure. The findings of this study indicate the presence of a significant disruption of sleep microstructure (CAP) in children with sleep enuresis, supporting the hypothesis of a higher arousal threshold.

What drives slow wave activity during early non-REM sleep: Learning during prior wake or effort?

What is the function of sleep in humans? One claim is that sleep consolidates learning. Slow wave activity (SWA), i.e. slow oscillations of frequency < 4 Hz, has been observed in electroencephalograms (EEG) during sleep; it increases with prior wakefulness and decreases with sleep. Studies have claimed that increase in SWA in specific regions of the sleeping brain is correlated with overnight improved performance, i.e. overnight consolidation, on a demanding motor learning task. We wondered if SWA change during sleep is attributable to overnight consolidation or to metabolic demand. Participants executed out-and-back movements to a target using a pen-like cursor with their dominant hand while the target and cursor position were displayed on a screen. They trained on three different conditions on separate nights, differing in the amount and degree of rotation between the actual hand movement direction and displayed cursor movement direction. In the no-rotation (NR) condition, there was no rotation. In the single rotation (SR) condition, the amount of rotation remained the same throughout, and performance improved both across pre-sleep training and after sleep, i.e. overnight consolidation occurred; in the random rotation (RR) condition, the amount of rotation varied randomly from trial to trial, and no overnight consolidation occurred; SR and RR were cognitively demanding. The average EEG power density of SWA for the first 30 min. of non-rapid eye movement sleep after training was computed. Both SR and RR elicited increase in SWA in the parietal region; furthermore, the topographic distribution of SWA in each was remarkably similar. No correlation was found between the overnight performance improvement on SR and the SWA change in the parietal region on measures of learning. Our results argue that regulation of SWA in early sleep is associated with high levels of cognitive effort during prior wakefulness, and not just overnight consolidation.

Intraindividual Increase of Homeostatic Sleep Pressure Across Acute and Chronic Sleep Loss: A High-Density EEG Study.

To compare intraindividually the effects of acute sleep deprivation (ASD) and chronic sleep restriction (CSR) on the homeostatic increase in slow wave activity (SWA) and to relate it to impairments in basic cognitive functioning, that is, vigilance. The increase in SWA after ASD (40 hours of wakefulness) and after CSR (seven nights with time in bed restricted to 5 hours per night) relative to baseline sleep was assessed in nine healthy, male participants (age = 18-26 years) by high-density electroencephalography. The SWA increase during the initial part of sleep was compared between the two conditions of sleep loss. The increase in SWA was related to the increase in lapses of vigilance in the psychomotor vigilance task (PVT) during the preceding days. While ASD induced a stronger increase in initial SWA than CSR, the increase was globally correlated across the two conditions in most electrodes. The increase in initial SWA was positively associated with the increase in PVT lapses. The individual homeostatic response in SWA is globally preserved across acute and chronic sleep loss, that is, individuals showing a larger increase after ASD also do so after CSR and vice versa. Furthermore, the increase in SWA is globally correlated to vigilance impairments after sleep loss over both conditions. Thus, the increase in SWA might therefore provide a physiological marker for individual differences in performance impairments after sleep loss.