Slow Wave Research Articles

Daytime dexmedetomidine sedation with closed-loop acoustic stimulation alters slow wave sleep homeostasis in healthy adults

BackgroundThe alpha-2 adrenergic agonist dexmedetomidine induces EEG patterns resembling those of non-rapid eye movement (NREM) sleep. Fulfilment of slow wave sleep (SWS) homeostatic needs would address the assumption that dexmedetomidine induces functional biomimetic sleep states. MethodsIn-home sleep EEG recordings were obtained from 13 healthy participants before and after dexmedetomidine sedation. Dexmedetomidine target-controlled infusions and closed-loop acoustic stimulation were implemented to induce and enhance EEG slow waves, respectively. EEG recordings during sedation and sleep were staged using modified American Academy of Sleep Medicine criteria. Slow wave activity (EEG power from 0.5 to 4 Hz) was computed for NREM stage 2 (N2) and NREM stage 3 (N3/SWS) epochs, with the aggregate partitioned into quintiles by time. The first slow wave activity quintile served as a surrogate for slow wave pressure, and the difference between the first and fifth quintiles as a measure of slow wave pressure dissipation. ResultsCompared with pre-sedation sleep, post-sedation sleep showed reduced N3 duration (mean difference of −17.1 min, 95% confidence interval −30.0 to −8.2, P=0.015). Dissipation of slow wave pressure was reduced (P=0.02). Changes in combined durations of N2 and N3 between pre- and post-sedation sleep correlated with total dexmedetomidine dose, (r=−0.61, P=0.03). ConclusionsDaytime dexmedetomidine sedation and closed-loop acoustic stimulation targeting EEG slow waves reduced N3/SWS duration and measures of slow wave pressure dissipation on the post-sedation night in healthy young adults. Thus, the paired intervention induces sleep-like states that fulfil certain homeostatic NREM sleep needs in healthy young adults. Clinical trial registrationClinicalTrials.gov NCT04206059.

High-energy pacing inhibits slow-wave dysrhythmias in the small intestine.

The motility of the gastrointestinal tract is coordinated in part by rhythmic slow waves, and disrupted slow-wave patterns are linked to functional motility disorders. At present, there are no treatment strategies that primarily target slow-wave activity. This study assessed the use of pacing to suppress glucagon-induced slow-wave dysrhythmias in the small intestine. Slow waves in the jejunum were mapped in vivo using a high-resolution surface-contact electrode array in pigs (n = 7). Glucagon was intravenously administered to induce hyperglycemia. Slow-wave propagation patterns were categorized into antegrade, retrograde, collision, pacemaker, and uncoupled activity. Slow-wave characteristics such as period, amplitude, and speed were also quantified. Postglucagon infusion, pacing was applied at 4 mA and 8 mA and the resulting slow waves were quantified spatiotemporally. Antegrade propagation was dominant throughout all stages with a prevalence of 55 ± 38% at baseline. However, glucagon infusion resulted in a substantial and significant increase in uncoupled slow waves from 10 ± 8% to 30 ± 12% (P = 0.004) without significantly altering the prevalence of other slow-wave patterns. Slow-wave frequency, amplitude, and speed remained unchanged. Pacing, particularly at 8 mA, significantly suppressed dysrhythmic slow-wave patterns and achieved more effective spatial entrainment (85%) compared with 4 mA (46%, P = 0.039). This study defined the effect of glucagon on jejunal slow waves and identified uncoupling as a key dysrhythmia signature. Pacing effectively entrained rhythmic activity and suppressed dysrhythmias, highlighting the potential of pacing for gastrointestinal disorders associated with slow-wave abnormalities.NEW & NOTEWORTHY Glucagon was infused in pigs to induce hyperglycemia and the resulting slow-wave response in the intact jejunum was defined in high resolution for the first time. Subsequently, with pacing, the glucagon-induced dysrhythmias were suppressed and spatially entrained for the first time with a success rate of 85%. The ability to suppress slow-wave dysrhythmias through pacing is promising in treating motility disorders that are associated with intestinal dysrhythmias.

Electromechanical Coupling and Anatomy of the In-Vivo Gastroduodenal Junction.

Few biomarkers support diagnosis and treatment of disorders of gut-brain interaction (DGBI), although gastroduodenal junction (GDJ) electromechanical coupling is a target for novel interventions. Rhythmic 'slow waves', generated by interstitial cells of Cajal (ICC), and myogenic 'spikes' are bioelectrical mechanisms underpinning motility. In this study, simultaneous in-vivo high-resolution electrophysiological and impedance planimetry measurements were paired with immunohistochemistry to elucidate GDJ electromechanical coupling. Following ethical approval, the GDJ of anaesthetized pigs (N=12) was exposed. Anatomically-specific, high-resolution electrode arrays (256 electrodes) were applied to the serosa. EndoFLIP catheters (16 electrodes; Medtronic, MN, USA) were positioned luminally to estimate diameter. Post-mortem tissue samples were stained with Masson's trichrome and Ano1 to quantify musculature and ICC. Electrical mapping captured slow-waves (N=512) and spikes (N=1071). Contractions paralleled electrical patterns. Localized slow waves and spikes preceded rhythmic contractions of the antrum, and non-rhythmic contractions of the duodenum. Slow-wave and spike amplitudes were correlated in the antrum (r=0.74, p<0.001) and duodenum (r=0.42, p<0.001). Slow-wave and contractile amplitudes were correlated in the antrum (r=0.48, p<0.001) and duodenum (r=0.35, p<0.001). Distinct longitudinal and circular muscle layers of the antrum and duodenum had a total thickness of (2.8 ± 0.9) mm and (0.4 ± 0.1) mm, respectively. At the pylorus, muscle layers merged and thickened to (3.5 ± 1.6) mm. Pyloric myenteric ICC covered less area (1.5 ± 1.1 %) compared to the antrum (4.2 ± 3.0 %) and duodenum (5.3 ± 2.8 %). Further characterization of electromechanical coupling and ICC biopsies may generate DGBI biomarkers.

Case Report: EEG Picture in a Patient with Post-Stroke Epilepsy

Introduction: Epilepsy is a chronic brain disorder that affects people all over the world. Seizures are the most common neurologic symptom in stroke patients. Approximately 10% of all stroke patients have experienced seizures, and post-stroke seizures generally begin several years after the stroke. Case Illustration: A male patient, 55 years old, Balinese, Kinan, came to the emergency room of Prof. Dr. I.G.N.G. Ngoerah General Hospital with complaints of seizures. The first seizure occurred on December 19, 2021, with a pattern of glancing at the left eye then, followed by full-body twitching, which lasted approximately 5 minutes and stopped on its own. The patient said that before the seizure, the patient was well conscious; during the seizure, the patient was unconscious, and after the seizure, the patient regained consciousness as before the seizure. Then, the seizure repeated the next day (December 20, 2021) with the same pattern and duration, but the patient was not taken for treatment. On physical examination, the patient was alert with vital signs and general physical examination within normal limits. Neurologic examination revealed no focal neurologic deficits. Electroencephalography (EEG) examination showed intermittent slow activity in the left and right fronto-centro-occipital areas. Computed tomography scan (CT-Scan) examination of the head without contrast revealed a hypodense image in the right temporo-parietal lobe. The patient then received anti-epileptic drug (OAE) therapy, OAE therapy given Phenytoin 200 mg every 12 hours intra-orally, Folic Acid 1 mg every 24 hours intra-orally, and anti-platelet and anti-hypertension continued. Discussion: Post-stroke seizure (PSS) is an episode of convulsion that occurs either single or multiple after a stroke, which is thought to be due to irreversible or reversible brain damage. At the same time, post-stroke epilepsy is convulsions after a stroke that occur at least two revivals without provocation with a distance between revivals of more than 24 hours. PSS classification is divided into early post-stroke seizure, where seizures occur onset two weeks early post-stroke, and late (delayed) post-stroke seizure if seizures occur onset after two weeks post-stroke. Post-stroke seizures' most common electroencephalography (EEG) waves are generalized slow waves, focal slowing, focal sharp and slow waves, and periodic lateralized epileptiform discharges (PLEDs). However, 5.1% of patients have normal EEG. The administration of anti-convulsants to prevent recurrent seizures is recommended by the European Guidelines of The European Stroke Organization. In comparison, prophylaxis is not recommended for patients with post-stroke. Keywords: Post-stroke Epilepsy, Stroke, Electroencephalography

Exact Nonlinear Decomposition of Ideal-MHD Waves Using Eigenenergies

In this paper, we introduce a new method for exact decomposition of propagating, nonlinear magnetohydrodynamic (MHD) disturbances into their component eigenenergies associated with the familiar slow, Alfvén, and fast wave eigenmodes, and the entropy and field-divergence pseudoeigenmodes. First, the mathematical formalism is introduced, where it is illustrated how the ideal-MHD eigensystem can be used to construct a decomposition of the time variation of the total energy density into contributions from the eigenmodes. The decomposition method is then demonstrated by applying it to the output of three separate nonlinear MHD simulations. The analysis of the simulations confirms that the component wave modes of a composite wavefield are uniquely identified by the method. The slow, Alfvén, and fast energy densities are shown to evolve in exactly the way expected from comparison with known linear solutions and nonlinear properties, including processes such as mode conversion. Along the way, some potential pitfalls for the numerical implementation of the decomposition method are identified and discussed. We conclude that the exact, nonlinear decomposition method introduced is a powerful and promising tool for understanding the nature of the decomposition of MHD waves as well as analyzing and interpreting the output of dynamic MHD simulations.

Does Targeted Memory Reactivation during SWS and REM sleep have differential effects on mnemonic discrimination and generalization?

Targeted memory reactivation (TMR), or the presentation of learning-related cues during sleep, has been shown to benefit memory consolidation for specific memory traces when applied during non-rapid eye movement (NREM) sleep. Prior studies suggest that TMR during REM sleep may play a role in memory generalization processes, but evidence remains scarce. We tested the hypothesis that TMR exerts a differential effect on distinct mnemonic processes as a function of the sleep state (REM vs. NREM) in which TMR is delivered. Mnemonic discrimination and generalization of semantic categories were investigated using an adapted version of the Mnemonic Similarity Task, before and after sleep. Forty-eight participants encoded pictures from eight semantic categories, each associated with a sound. In the pre-sleep immediate test, they had to discriminate "old" (targets) from "similar" (lures) or "new" (foils) pictures. During sleep, half of the sounds were replayed in slow wave sleep (SWS) or REM sleep. Recognition, discrimination, and generalization memory indices were tested in the morning. These indices did not differ between SWS and REM TMR groups or reactivated and non-reactivated item categories. Additional results suggest a positive effect of TMR on performance for highly similar items mostly relying on mnemonic discrimination processes. During sleep, EEG activity after cue presentation increased in the delta-theta and sigma band in the SWS group, and in the beta band in the REM TMR group. These results do not support the hypothesis of a differential processing of novel memory traces when TMR is administered in distinctive physiological sleep states.

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

Rapid eye movement sleep (REM), also referred to as paradoxical sleep for the striking resemblance of its electroencephalogram (EEG) to the one observed in wakefulness, is characterized by the occurrence of transient events such as limb twitches or facial and rapid eye movements. Here, we investigated the local activity of the primary somatosensory or barrel cortex (S1) in naturally sleeping head-fixed male mice during REM. Through local field potential (LFP) recordings, we uncovered local appearances of spindle waves in the barrel cortex during REM concomitant with strong delta power, challenging the view of a wakefulness-like activity in REM. We further performed extra- and intracellular recordings of thalamic cells in head-fixed mice. Our data show high frequency thalamic bursts of spikes and subthreshold spindle oscillations in about half of the neurons of the ventral posterior medial nucleus which further confirmed the thalamic origin of local cortical spindles in S1 in REM. Cortical spindle oscillations were suppressed, while thalamus spike firing increased, associated with rapid mouse whisker movements and S1 cortical activity transitioned to an activated state. During REM, sensory thalamus and barrel cortex therefore alternate between high (wake-like) and low (non-REM sleep-like) activation states, potentially providing a neuronal substrate for mnemonic processes occurring during this paradoxical sleep stage.Significance Statement Mammalian sleep includes slow wave sleep, or non-rapid eye movement sleep (NREM), and the subsequent REM sleep (REM). At the EEG global level, cortical activity during REM sleep has long been believed to share some similarities with awake cortical activity. The well-defined mouse whisker system offers the unique opportunity to precisely investigate cortical and thalamic dynamics during wakefulness and REM. Combining local field potential (LFP) recordings in primary somatosensory cortex, with single-unit neuronal recordings in its associated thalamic nucleus, we found that during REM, sensory thalamus and barrel cortex alternate between high (wake-like) and low (non-REM sleep-like) activation states, potentially providing a neuronal substrate for mnemonic processes occurring during this paradoxical sleep stage.

Overcoming traps and pitfalls leading to misinterpretation of normal EEG variants and variation of the background activity.

Normal EEG variants, especially the epileptiform variants, can be challenging to interpret because they often have sharp contours and may be confused with "epileptic" interictal activities. However, they can be recognized by the fact that "most spikes or sharp wave discharges of clinical import are followed by a slow wave or a series of slow deflections" (Maulsby, 1971).If there is no wave after the spike, electroencephalographers should be suspicious of artifacts and normal EEG variants. Most normal EEG variants display a single rhythm with the same frequency within the pattern and the morphology remains stable throughout the entire EEG recording with repetition of the same pattern. In case of doubt or difficulties with a standard EEG, it is recommended to undergo an EEG that includes sleep stages with or without sleep deprivation. Finally, epileptiform is an ambiguous term corresponding to an electroencephalographic trait. Epileptiform does not imply a pathological condition, including epilepsy. The clinical context remains the most paramount in the diagnosis of epilepsy. In this article, we propose a set of rules and guidelines to identify normal EEG variants in EEG tracings and normal variation of the background activity. It is not easy to accurately assign a specific/precise name to all EEG activity, but with an orderly approach to EEG that involves using a set of criteria, nonepileptic activity can be identified.

Real‐Time Observation of Slowed Charge Density Wave Dynamics in Thinned 1T‐TaS2

AbstractTransient electrical pulsing is used to investigate the slowed charge density wave (CDW) kinetics of 1T‐TaS2. These measurements distinguish a fast response of the material, consistent with the onset of self‐heating, from much slower transients that occur on timescales orders of magnitude longer than this. The latter variations appear consistent with slow configurational changes in the CDW, which, due to the thin nature of the 1T‐TaS2, can be distinguished from the much faster dynamics of Joule heating. Experiments in which the cooling of the material is interrupted, demonstrate the possibility of “programming” it in different, strongly nonequilibrium, CDW phases. Collectively, the results point to the existence of a complex free‐energy space for the thinned material, whose multi‐valley structure and hidden metastable states govern the resulting thermal and field‐driven dynamics. Crucially, this work demonstrates that while the CDW dynamics in this material may have a thermal character, the timescales associated with these motions can be very different from those on which self‐heating occurs. This discovery will be important for efforts to implement active devices that utilize the CDW states of thinned 1T‐TaS2.

The Role of Astrocytes in Migraine with Cortical Spreading Depression: Protagonists or Bystanders? A Narrative Review.

Cortical spreading depression (CSD) is a slow wave of cortical depolarization closely associated with migraines with an aura. Previously, it was thought that CSD depolarization was mainly driven by neurons, with characteristic changes in neuronal swelling and increased extracellular potassium (K+) and glutamate. However, the role of astrocytes, a member of the neurovascular unit, in migraine with CSD has recently received increasing attention. In the early stages of CSD, astrocytes provide neurons with energy support and clear K+ and glutamate from synaptic gaps. However, in the late stages of CSD, astrocytes release large amounts of lactic acid to exacerbate hypoxia when the energy demand exceeds the astrocytes' compensatory capacity. Astrocyte endfoot swelling is a characteristic of CSD, and neurons are not similarly altered. It is primarily due to K+ influx and abnormally active calcium (Ca2+) signaling. Aquaporin 4 (AQP-4) only mediates K+ influx and has little role as an aquaporin. Astrocytes endfoot swelling causes perivascular space closure, slowing the glymphatic system flow and exacerbating neuroinflammation, leading to persistent CSD. Astrocytes are double-edged swords in migraine with CSD and may be potential targets for CSD interventions.

Multi-night acoustic stimulation is associated with better sleep, amyloid dynamics, and memory in older adults with cognitive impairment.

Sleep is a potential early, modifiable risk factor for cognitive decline and dementia. Impaired slow wave sleep (SWS) is pronounced in individuals with cognitive impairment (CI). Cognitive decline and impairments of SWS are bi-directionally linked in a vicious cycle. SWS can be enhanced non-invasively using phase-locked acoustic stimulation (PLAS), potentially breaking this vicious cycle. Eighteen healthy older adults (HC, agemean±sd, 68.3 ± 5.1) and 16 older adults (agemean±sd, 71.9 ± 3.9) with CI (Montreal Cognitive Assessment ≤ 25) underwent one baseline (sham-PLAS) night and three consecutive stimulation nights (real-PLAS). EEG responses and blood-plasma amyloid beta Aβ42/Aβ40 ratio were measured pre- and post-intervention, as was episodic memory. The latter was again evaluated 1week and 3months after the intervention. In both groups, PLAS induced a significant electrophysiological response in both voltage- and time-frequency analyses, and memory performance improved in association with the magnitude of this response. In the CI group, both electrophysiological and associated memory effects were delayed compared to the healthy group. After 3 intervention nights, electrophysiological response to PLAS was no longer different between CI and HC groups. Only in the CI sample, stronger electrophysiological responses were significantly associated with improving post-intervention Aβ42/Aβ40 ratios. PLAS seems to improve SWS electrophysiology, memory, and amyloid dynamics in older adults with CI. However, effects on memory require more time to unfold compared to healthy older adults. This indicates that PLAS may become a potential tool to ameliorate cognitive decline, but longer interventions are necessary to compensate for declining brain integrity. This study was pre-registered (clinicaltrials.gov: NCT04277104).

Sleep, Sleepiness, and Memory

Abstract Objective To evaluate the relationship between sleep and sleepiness with memory complaints. Materials and Methods Patients who were submitted to polysomnography between May and September of 2022 and answered the prospective and retrospective memory questionnaire and the Epworth sleepiness scale were included, respectively. Data were entered into an Excel spreadsheet and converted to a file compatible with the SPSS software. Results The sample consisted of 98 subjects, 62.2% male, mean age of 45.9 years, 73.4% overweight, 54.1% with comorbidities, and 51% with excessive sleepiness. There was a significant difference in sleep efficiency, respiratory disturbance index (RDI), slow wave sleep (SWS), and rapid eye movement (REM) sleep for the group with comorbidities; in latency to sleep and SWS between genders; and in RDI for the body mass index group. No correlation between RDI and memory could be identified, but there were statistically significant correlations between REM and sleep efficiency; RDI and REM sleep; RDI and SWS; SWS and sleep efficiency; and sleep efficiency and latency to sleep onset. Older adults performed better on memory tests when total sleep time (TST) is longer than 5 hours and excessive daytime sleepiness is related to complaints of prospective, retrospective, and total memory. Conclusion Elderly people with TST longer than 5 hours have a better memory. Although a correlation between RDI and memory was not observed, a correlation between excessive daytime sleepiness—one of the main symptoms of patients with sleep disorders—and memory was.

“Counting sheep PSG”: EEGLAB-compatible open-source matlab software for signal processing, visualization, event marking and staging of polysomnographic data

BackgroundProgress in advancing sleep research employing polysomnography (PSG) has been negatively impacted by the limited availability of widely available, open-source sleep-specific analysis tools. New methodHere, we introduce Counting Sheep PSG, an EEGLAB-compatible software for signal processing, visualization, event marking and manual sleep stage scoring of PSG data for MATLAB. ResultsKey features include: (1) signal processing tools including bad channel interpolation, down-sampling, re-referencing, filtering, independent component analysis, artifact subspace reconstruction, and power spectral analysis, (2) customizable display of polysomnographic data and hypnogram, (3) event marking mode including manual sleep stage scoring, (4) automatic event detections including movement artifact, sleep spindles, slow waves and eye movements, and (5) export of main descriptive sleep architecture statistics, event statistics and publication-ready hypnogram. Comparison with existing methodsCounting Sheep PSG was built on the foundation created by sleepSMG (https://sleepsmg.sourceforge.net/). The scope and functionalities of the current software have made significant advancements in terms of EEGLAB integration/compatibility, preprocessing, artifact correction, event detection, functionality and ease of use. By comparison, commercial software can be costly and utilize proprietary data formats and algorithms, thereby restricting the ability to distribute and share data and analysis results. ConclusionsThe field of sleep research remains shackled by an industry that resists standardization, prevents interoperability, builds-in planned obsolescence, maintains proprietary black-box data formats and analysis approaches. This presents a major challenge for the field of sleep research. The need for free, open-source software that can read open-format data is essential for scientific advancement to be made in the field.

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.

A model of umbral oscillations inherited from subphotospheric fast-body modes

Recently, complex horizontal patterns of umbral oscillations have been reported, but their physical nature and origin are still not fully understood. Here we show that the two-dimensional patterns of umbral oscillations of slow waves are inherited from the subphotospheric fast-body modes. Using a simple analytic model, we successfully reproduced the temporal evolution of oscillation patterns with a finite number of fast-body modes. In this model, the radial apparent propagation of the pattern is associated with the appropriate combination of the amplitudes in radial modes. We also find that the oscillation patterns are dependent on the oscillation period. This result indicates that there is a cutoff radial mode, which is a unique characteristic of the model of fast-body modes. In principle, both internal and external sources can excite these fast-body modes and produce horizontal patterns of umbral oscillations.

Microglial TNFα controls daily changes in synaptic GABAARs and sleep slow waves.

Microglia sense the changes in their environment. How microglia actively translate these changes into suitable cues to adapt brain physiology is unknown. We reveal an activity-dependent regulation of cortical inhibitory synapses by microglia, driven by purinergic signaling acting on P2RX7 and mediated by microglia-derived TNFα. We demonstrate that sleep induces microglia-dependent synaptic enrichment of GABAARs in a manner dependent on microglial TNFα and P2RX7. We further show that microglia-specific depletion of TNFα alters slow waves during NREM sleep and blunt memory consolidation in sleep-dependent learning tasks. Together, our results reveal that microglia orchestrate sleep-intrinsic plasticity of synaptic GABAARs, sculpt sleep slow waves, and support memory consolidation.

Transmission of slow waves in Masimo O3 near infrared spectroscopy measures

IntroductionCerebral autoregulation (CA) dysfunction is a key complication following brain injury. CA assessment using near-infrared spectroscopy (NIRS) offers a promising alternative to the current non-invasive standard, cerebral blood flow velocity (CBFV) measured with transcranial Doppler. Research questionCan autoregulatory slow waves (frequency range 0.005–0.05 Hz) associated with spontaneous and induced changes in ABP in healthy volunteers be detected by parameters measured with the Masimo O3 NIRS device? MethodsABP, CBFV and Masimo O3 parameters were measured in 10 healthy volunteers at baseline and during ABP oscillations induced by squat/stand manoeuvres. Transmission of slow waves was assessed with power spectral density and coherence analysis in NIRS signals and compared to that of CBFV. ResultsAt baseline, slow waves were detected with sufficient power that substantially exceeded the signals’ measurement resolution in all parameters except cerebral oxygen saturation. During ABP oscillations in the 0.033 Hz range (induced by squat/stand), the power of slow waves increased in all parameters in a similar pattern, with total (cHb) and oxygenated (O2Hb) haemoglobin concentrations most closely mirroring CBFV (median standardised power [first-third quartile], baseline vs squat/stand: CBFV 0.35 [0.28–0.42] vs 0.50 [0.45–0.62], O2Hb 0.47 [0.33–0.68] vs 0.61 [0.59–0.69]). Coherence with ABP increased for both CBFV and NIRS measures from low at baseline (<0.4) to high during induced changes (>0.8). ConclusionSpontaneous fluctuations in ABP can be observed in analysed Masimo O3 metrics to a varying degree. The clinical utility of Masimo O3 signals in CA assessment requires further investigation in brain injury patients.

Gyrofluid simulations of turbulence and reconnection in space plasmas

A Hamiltonian two-field gyrofluid model is used to investigate the dynamics of an electron-ion collisionless plasma subject to a strong ambient magnetic field, within a spectral range extending from the magnetohydrodynamic (MHD) scales to the electron skin depth. This model isolates Alfvén, Kinetic Alfvén and Inertial Kinetic Alfvén waves that play a central role in space plasmas, and extends standard reduced fluid models to broader ranges of the plasma parameters. Recent numerical results are reviewed, including (i) the reconnection-mediated MHD turbulence developing from the collision of counter-propagating Alfvén wave packets, (ii) the specific features of the cascade dynamics in strongly imbalanced turbulence, including a possible link between the existence of a spectral transition range and the presence of co-propagating wave interactions at sub-ion scales, for which new simulations are reported, (iii) the influence of the ion-to-electron temperature ratio in two-dimensional collisionless magnetic reconnection. The role of electron finite Larmor radius corrections is pointed out and the extension of the present model to a four-field gyrofluid model is discussed. Such an extended model accurately describes electron finite Larmor radius effects at small or moderate values of the electron beta parameter, and also retains the coupling to slow magnetosonic waves.

Nocturnal Heart Rate Response to Spontaneous Arousals Following Sleep Restriction

Short sleep duration is associated with future cardiovascular disease including hypertension, especially in females, but mechanistic evidence is largely lacking. Experimental sleep restriction has been shown to cause short sleep-mediated tachycardia and reduced heart rate variability, indicative of autonomic cardiac instability, in some but not all studies. Heart rate (HR) response to spontaneous cortical arousals can be regarded as an index of autonomic cardiac control given its characteristic temporal pattern. Whether the HR response to cortical arousals is altered during experimental sleep restriction remains unknown. We hypothesized that sleep restriction would result in augmented HR reactivity to spontaneous arousals, and that this response would be more marked in females. We studied 19 young, healthy subjects (eight females, age: 23.5 ± 5 years, body mass index [BMI]: 24.5 ± 3.6 kg/m2). In a randomized, crossover design, participants were tested during a normal sleep (NS, 9 hr sleep opportunity) or sleep restriction (SR, 4 hr sleep opportunity) study arm. Each 16-day study visit consisted of a 4-day study acclimation phase, 9-day experimental sleep perturbation segment, followed by a 3-day recovery period. An overnight polysomnography (PSG) study was conducted on study days 2, 5 and 11 (at baseline and after 1 and 7 days of restricted versus control sleep). A registered PSG technician provided sleep staging and spontaneous arousal scoring, which was confirmed by an investigator with sleep expertise (IMG). For each identified spontaneous arousal, the HR change was quantified for 30 cardiac cycles post-arousal onset and compared to a pre-arousal baseline (average HR 5 – 10 cardiac cycles prior to arousal). An arousal was considered valid for analysis if at least one minute of stage N2 or rapid eye movement (REM) sleep occurred following sleep stage transition and was at least 30 seconds apart from other sleep disturbance-related events (e.g., limb movement, apneic event, etc.). Given low prevalence of slow wave sleep (SWS) arousals, arousals occurring in that sleep stage were excluded from present analysis. Statistical analysis, including repeated measures ANOVA (RMANOVA, p &lt; 0.05) with condition and time (cardiac cycles) as within-subjects factors and sex as the between-subjects factor, was conducted to compare the beat-to-beat HR response to arousal between study conditions. Additionally, average and peak HR responses to spontaneous arousals were compared via RMANOVA with condition and time (study days) as within-subjects and sex as between-subjects factors. HR response to spontaneous arousal in stage two and REM sleep was similar between NS and SR on study day 5 or day 11 (condition × time: p = 0.943, 0.865). Secondary analysis of average and peak HR responsiveness to spontaneous arousals in stage two and REM sleep between conditions and study days was also not statistically different (condition × time: p = 0.193, 0.185). Last, no significant sex differences were detected across comparisons (condition × time × sex: p &gt; 0.05 for all). These findings suggest that a 9-day sleep restriction paradigm may not alter cardiac autonomic function in otherwise healthy adults. Future work is warranted to determine whether these results extend to individuals with established cardiovascular risk factors or cardiovascular disease. Support: NIH T32-DK007013, R01-114676, and CTSA grant UL1-TR002377. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Spatiotemporal EEG dynamics of the sleep onset process in preadolescence

BackgroundDuring preadolescence the sleep electroencephalography undergoes massive qualitative and quantitative modifications. Despite these relevant age-related peculiarities, the specific EEG pattern of the wake-sleep transition in preadolescence has not been exhaustively described. MethodsThe aim of the present study is to characterize regional and temporal electrophysiological features of the sleep onset (SO) process in a group of 23 preadolescents (9–14 years) and to compare the topographical pattern of slow wave activity and delta/beta ratio of preadolescents with the EEG pattern of young adults. ResultsResults showed in preadolescence the same dynamics known for adults, but with peculiarities in the delta and beta activity, likely associated with developmental cerebral modifications: the delta power showed a widespread increase during the SO with central maxima, and the lower bins of the beta activity showed a power increase after SO. Compared to adults, preadolescents during the SO exhibited higher delta power only in the slowest bins of the band: before SO slow delta activity was higher in prefrontal, frontal and occipital areas in preadolescents, and, after SO the younger group had higher slow delta activity in occipital areas. In preadolescents delta/beta ratio was higher in more posterior areas both before and after the wake-sleep transition and, after SO, preadolescents showed also a lower delta/beta ratio in frontal areas, compared to adults. ConclusionResults point to a general higher homeostatic drive for the developing areas, consistently with plastic-related maturational modifications, that physiologically occur during preadolescence.