Slow Wave Research Articles

Evaluation of Sleep EEG Changes in Paediatric Patients with Language Dysfunction: A Follow Up Study

Abstract Background Several case reports and studies have described an association between sleep epileptiform discharges and language dysfunctions. This has been partly confirmed in studies that have investigated the effect of this epileptiform discharges on neurocognitive function. Objectives To screen for sleep-potentiated epileptiform discharges in children with language dysfunction (language delay or regression) and to evaluate the effect of treatment of these epileptiform discharges on language dysfunction. Methods The study was conducted on 93 children with language delay or language regression. Patients were recruited from the pediatric neurology clinic, pediatric outpatient clinic, phoniatrics outpatient clinic and the inpatient neurology ward at the Ain Shams University Children’s hospital, Cairo, Egypt in the period between February 2020 and November 2021. A 90- minute sleep electroencephalography, intelligence quotient level and language age were done for all patients included in the study. Children who had an active electroencephalography with uncontrolled clinical seizures or persistently epileptogenic activity without clinical seizures received treatment according to type of activity then after 6 months they were subjected to follow up electroencephalographyand assessment of intelligence quotient level and language age. Results The enrolled patients were divided into two groups: Group (1) including 28 (30%) patients with either or both of epileptogenic activity and clinical seizures and group (2) including 65 (70%) patients without either epileptogenic activity or clinicalseizures. We found 24 (85.7 %) children in group 1 had clinical seizures with median age of onset 2.5 years (range from 1-8 years). Further in the first group, 21 (85.7 %) of children showed presence ofepileptogenic activity with 10 (47.6 %) of children showed spike and slow wave, 6 (28.6 %) showed sharp wave, 3 (14.3 %) showed continuous spike and wave during slow wave sleep (CSWS), 2 (9.5 %) children showed sharp and slow wave. In our study, levetiracetam was given as first line treatment in patients with active seizures. An add-on therapy was given in patients who were not controlled on one antiepileptic drug. A follow up 90 minutes sleep electroencephalography was done and showed a highly significant reduction in epileptogenic activity with a p value of < 0.001. A follow up language test and intelligence quotient level score were done and showed a highly significant improvement with p value of (0.001 and 0.009) respectively. Conclusion Epileptiform activities with or without epilepsy in children may alter normal language function. Treatment of these epileptogenic activity affect improvement of this language dysfunction. Trial registration: ClinicalTrials.gov I.D: NCT05487521.

Benign epileptiform variants in EEG: A comprehensive study of 3000 patients

BackgroundThe analysis of EEG demands expertise and keen observation to distinguish epileptiform discharges from benign epileptiform variants (BEVs), a frequent source of erroneous interpretation. The prevalence of BEVs varies based on geographical, racial, and ethnic characteristics. However, most data on BEVs originates from Western populations, and additional studies on different cohorts would enrich the existing literature. MethodsWe reviewed EEGs from our institutional database to study the prevalence of benign epileptiform variants and analyzed their frequency, topography, and other characteristics. Additionally, we investigated the co-existence of epileptiform discharges with BEVs. ResultsWe identified 296 patients with BEVs after reviewing 3000 EEGs (9.9%). The most common BEV was small sharp spikes (SSS), observed in 114 patients (3.8%). Wicket waves, 6 Hz spike and slow wave, 14 and 6 Hz positive bursts, and Rhythmic Temporal Theta of Drowsiness (RTTD) were identified in 67 (2.2%), 40 (1.3%), 39 (1.3%), and 35 (1.16%) patients, respectively and one patient with Subclinical Rhythmic EEG Discharges in Adults (SREDA). Additionally, we observed the co-existence of epileptiform discharges with BEVs, most commonly with SSS (27.8%). ConclusionsThe present study is a large study with 3000 EEGs to describe the BEV characteristics. BEVs were seen in 9.9% of patients, BSSS being the most common. There were minor differences in frequency, gender or age distribution compared to existing literature. We demonstrated the co-existence of epileptiform discharges. Morphological characteristics remain the cornerstone in recognising BEVs. EEG readers need to be aware of features of BEVs to avoid wrongly interpretation.

Neotectonics of the Barents Sea shelf eastern part: seismicity, faults and impact of the Atlantic-Arctic Rift System

distribution with the fault network defined from seismic data, and kinematic characteristics of seismic activity spatial migration are obtained. It is shown that seismic events recorded by the Norwegian NORSAR regional network within the Russian part of the Barents Sea shelf are grouped into linear clusters along shear kinematics faults. The fault network displaces Mesozoic seismic complexes and reaches the bottom surface, displacing quaternary deposits, which clearly indicates the modern age of displacements along which linear clusters of weak seismicity are grouped. The calculation of the total seismic moment in the space-time dimension showed the presence of seismic activity migration along short fragments of faults on the shelf with velocities from 10.5 to 25.7 km/year. There has been a surge in general activity in the shelf area since 2012. A comparison of the temporal evolution of seismic activity on the shelf with fragments of the Atlantic-Arctic Rift system suggests that it is the effect of tectonic deformation waves triggered along the geodynamically active intraplate boundary and propagating to the shelf at a speed of 20–22 km/year. Migration rates with speeds up to 77 km/year are less likely. There is a possibility that the increase in the intensity of seismic activity on the shelf after 2012 is not an emission from the effects of a slow deformation wave, but the result of a direct trigger effect on the shelf from the structures of the Knipovich and Gakkel ridges.

Decomposing the multiple encoding benefit in visual long-term memory: Primary contributions by the number of encoding opportunities.

Although access to the seemingly infinite capacity of our visual long-term memory (VLTM) can be restricted by visual working memory (VWM) capacity at encoding and retrieval, access can be improved with repeated encoding. This leads to the multiple encoding benefit (MEB), the finding that VLTM performance improves as the number of opportunities to encode the same information increases over time. However, as the number of encoding opportunities increases, so do other factors such as the number of identical encoded VWM representations and chances to engage in successful retrieval during each opportunity. Thus, across two experiments, we disentangled the contributions of each of these factors to the MEB by having participants encode a varying number of identical objects across multiple encoding opportunities. Along with behavioural data, we also examined two established EEG correlates that track the number of maintained VWM representations, namely the posterior alpha suppression and the negative slow wave. Here, we identified that the primary mechanism behind the MEB was the number of encoding opportunities. That is, recognition memory performance was higher following an increase in the number of encoding opportunities, and this could not be attributed solely to an increase in the number of encoded VWM representations or successful retrieval. Our results thus contribute to the understanding of the fundamental mechanisms behind the influence of VWM on VLTM encoding.

Modeling the Propagation of Slow Magnetoacoustic Waves in a Multistranded Coronal Loop

We study the propagation properties of slow magnetoacoustic waves in a multithermal coronal loop using a 3D MHD model, for the first time. A bundle of 33 vertical cylinders, each of 100 km radius, randomly distributed over a circular region of radius 1 Mm, is considered to represent the coronal loop. The slow waves are driven by perturbing the vertical velocity (v z ) at the base of the loop. We apply forward modeling to the simulation results to generate synthetic images in the coronal channels of the Solar Dynamics Observatory/Atmospheric Imaging Assembly. Furthermore, we add appropriate data noise to enable direct comparison with the real observations. It is found that the synthetic images at the instrument resolution show noncospatial features in different temperature channels in agreement with previous observations. Time–distance maps are constructed from the synthetic data to study the propagation properties. The results indicate that the oscillations are only visible in specific channels, depending on the temperature range of the plasma existing within the loop. Additionally, the propagation speed of slow waves is also found to be sensitive to the available temperature range. Overall, we propose that the cross-field thermal properties of coronal structures can be inferred using a combination of numerical simulations and observations of slow magnetoacoustic waves.

The timing of sleep spindles is modulated by the respiratory cycle in humans

ObjectiveCoupling of sleep spindles with cortical slow waves and hippocampus sharp-waves ripples is crucial for sleep-related memory consolidation. Recent literature evidenced that nasal respiration modulates neural activity in large-scale brain networks. In rodents, this respiratory drive strongly varies according to vigilance states. Whether sleep oscillations are also respiration-modulated in humans remains open. In this work, we investigated the influence of breathing on sleep spindles during non-rapid-eye-movement sleep in humans. MethodsFull night polysomnography of twenty healthy participants were analysed. Spindles and slow waves were automatically detected during N2 and N3 stages. Spindle-related sigma power as well as spindle and slow waves events were analysed according to the respiratory phase. ResultsWe found a significant coupling between both slow and fast spindles and the respiration cycle, with enhanced sigma activity and occurrence probability of spindles during the middle part of the expiration phase. A different coupling was observed for slow waves negative peaks which were rather distributed around the two respiration phase transitions. ConclusionOur findings suggest that breathing cycle influences the dynamics of brain activity during non-rapid-eye-movement sleep. SignificanceThis coupling may enable sleep spindles to synchronize with other sleep oscillations and facilitate information transfer between distributed brain networks.

The timing of sleep spindles is modulated by the respiratory cycle in humans

ObjectiveCoupling of sleep spindles with cortical slow waves and hippocampus sharp-waves ripples is crucial for sleep-related memory consolidation. Recent literature evidenced that nasal respiration modulates neural activity in large-scale brain networks. In rodents, this respiratory drive strongly varies according to vigilance states. Whether sleep oscillations are also respiration-modulated in humans remains open. In this work, we investigated the influence of breathing on sleep spindles during non-rapid-eye-movement sleep in humans. MethodsFull night polysomnography of twenty healthy participants were analysed. Spindles and slow waves were automatically detected during N2 and N3 stages. Spindle-related sigma power as well as spindle and slow waves events were analysed according to the respiratory phase. ResultsWe found a significant coupling between both slow and fast spindles and the respiration cycle, with enhanced sigma activity and occurrence probability of spindles during the middle part of the expiration phase. A different coupling was observed for slow waves negative peaks which were rather distributed around the two respiration phase transitions. ConclusionOur findings suggest that breathing cycle influences the dynamics of brain activity during non-rapid-eye-movement sleep. SignificanceThis coupling may enable sleep spindles to synchronize with other sleep oscillations and facilitate information transfer between distributed brain networks.

Changes in slow-wave sleep characteristics in Parkinson's disease patients with mild-moderate depression

IntroductionDepression and sleep disturbances are commonly seen non-motor symptoms in patients with Parkinson's disease (PD). This study used polysomnography to examine the relationship between mild-moderate depression in PD and sleep characteristics, particularly slow wave activities (SWA). Methods59 PD patients were split into two groups: nd-PD (n = 27) (patients with PD without depression) and d-PD (n = 32) (patients with PD with mild-moderate depression). Their clinical features, polysomnography parameters, and demographics were evaluated. Early and late sleep SWA spectrum densities and overnight SWA decline in different brain regions were particularly analyzed. ResultsNon-rapid eye movement 3 (N3) sleep duration and percentage were greater in the d-PD group. N3 percentage was linked to depression (p = 0.014). During late sleep, higher SWA (0.5–4Hz) in the frontal and central regions, higher low-SWA (0.5–2Hz) in the whole brain, central and occipital regions, and higher high-SWA (2–4Hz) in the frontal region was observed in the d-PD group. During early sleep, there was also higher low-SWA (0.5–2Hz) in the occipital region. Patients in d-PD group exhibited reduced overnight high-SWA (2–4Hz) decline (Δhigh-SWA) in the whole brain and occipital regions. Δhigh-SWA(2–4Hz) in the occipital region were associated with depression (p = 0.049). ConclusionPD patients with mild-moderate depression have impaired slow wave sleep, exhibiting as increased N3 sleep, SWA, and reduced overnight SWA decline. This implies that synaptic strength reduction during sleep and impaired synaptic homeostasis regulation may be associated with depression in PD. Reduced overnight high-SWA decline in the occipital region may serve as a novel electrophysiological biomarker for indicating depression in PD.

Local neuronal sleep after stroke: The role of cortical bistability in brain reorganization

BackgroundAcute cerebral ischemia triggers a number of cellular mechanisms not only leading to excitotoxic cell death but also to enhanced neuroplasticity, facilitating neuronal reorganization and functional recovery. ObjectiveTransferring these cellular mechanisms to neurophysiological correlates adaptable to patients is crucial to promote recovery post-stroke. The combination of TMS and EEG constitutes a promising readout of neuronal network activity in stroke patients. MethodsWe used the combination of TMS and EEG to investigate the development of local signal processing and global network alterations in 40 stroke patients with motor deficits alongside neural reorganization from the acute to the chronic phase. ResultsWe show that the TMS-EEG response reflects information about reorganization and signal alterations associated with persistent motor deficits throughout the entire post-stroke period. In the early post-stroke phase and in a subgroup of patients with severe motor deficits, TMS applied to the lesioned motor cortex evoked a sleep-like slow wave response associated with a cortical off-period, a manifestation of cortical bistability, as well as a rapid disruption of the TMS-induced formation of causal network effects. Mechanistically, these phenomena were linked to lesions affecting ascending activating brainstem fibers. Of note, slow waves invariably vanished in the chronic phase, but were highly indicative of a poor functional outcome. ConclusionIn summary, we found evidence that transient effects of sleep-like slow waves and cortical bistability within ipsilesional M1 resulting in excessive inhibition may interfere with functional reorganization, leading to a less favorable functional outcome post-stroke, pointing to a new therapeutic target to improve recovery of function.

Whole-brain model replicates sleep-like slow-wave dynamics generated by stroke lesions

Focal brain injuries, such as stroke, cause local structural damage as well as alteration of neuronal activity in distant brain regions. Experimental evidence suggests that one of these changes is the appearance of sleep-like slow waves in the otherwise awake individual. This pattern is prominent in areas surrounding the damaged region and can extend to connected brain regions in a way consistent with the individual's specific long-range connectivity patterns. In this paper we present a generative whole-brain model based on (f)MRI data that, in combination with the disconnection mask associated with a given patient, explains the effects of the sleep-like slow waves originated in the vicinity of the lesion area on the distant brain activity. Our model reveals new aspects of their interaction, being able to reproduce functional connectivity patterns of stroke patients and offering a detailed, causal understanding of how stroke-related effects, in particular slow waves, spread throughout the brain. The presented findings demonstrate that the model effectively captures the links between stroke occurrences, sleep-like slow waves, and their subsequent spread across the human brain.

Localizing Quasiperiodic Pulsations in Hard X-Ray, Microwave, and Lyα Emissions of an X6.4 Flare

We report the simultaneous observations of quasiperiodic pulsations (QPPs) in wavelengths of hard X-ray (HXR), microwave, Lyα, and ultraviolet (UV) emissions during the impulsive phase of an X6.4 flare on 2024 February 22 (SOL2024-02-22T22:08). The X6.4 flare shows three repetitive and successive pulsations in HXR and microwave wavebands, and they have an extremely large modulation depth. The onset of flare QPPs is almost simultaneous with the start of magnetic cancellation between positive and negative fields. The wavelet power spectra suggest the presence of double periods, which are centered at ∼200 and ∼95 s, respectively. The long-period QPP can also be detected in Lyα and UV wavebands at the flare area, and it could be observed in the adjacent sunspot. Our observations indicate that the flare QPPs are most likely triggered by accelerated electrons that are associated with periodic magnetic reconnections. The long period at ∼200 s is probably modulated by the slow magnetoacoustic wave originating from the neighboring sunspot, while the short period at ∼95 s could be regarded as its second harmonic mode.

Inhibition of EZH2 Reduces Aging-Related Decline in Interstitial Cells of Cajal of the Mouse Stomach

Restricted gastric motor functions contribute to aging-associated under-nutrition, sarcopenia, and frailty. We previously identified a decline in interstitial cells of Cajal (ICC, gastrointestinal pacemaker and neuromodulator cells) and their stem cells (ICC-SC) as a key factor of gastric aging. Altered functionality of the histone methyltransferase enhancer of zeste homolog 2 (EZH2) is central to organismal aging. Here, we investigated the role of EZH2 in the aging-related loss of ICC/ICC-SC. klotho mice, a model of accelerated aging, were treated with the most clinically advanced EZH2 inhibitor, EPZ6438 (tazemetostat; 160 mg/kg i.p. BID for 3 weeks). Gastric ICC were analyzed by western blotting (WB) and immunohistochemistry. ICC and ICC-SC were quantified by flow cytometry. Gastric slow wave activity was assessed by intracellular electrophysiology. Ezh2 was deactivated in ICC by treating KitcreERT2/+;Ezh2fl/fl mice with tamoxifen. TRP53, a key mediator of aging-related ICC loss, was induced with nutlin 3a in gastric muscle organotypic cultures and an ICC-SC line. In klotho mice, EPZ6438 treatment mitigated the decline in the ICC growth factor KIT ligand/stem cell factor and gastric ICC. EPZ6438 also improved gastric slow wave activity and mitigated the reduced food intake and impaired body weight gain characteristic of this strain. Conditional genomic deletion of Ezh2 in Kit-expressing cells also prevented ICC loss. In organotypic cultures and ICC-SC, EZH2 inhibition prevented the aging-like effects of TRP53 stabilization on ICC/ICC-SC. Inhibition of EZH2 with EPZ6438 mitigates aging-related ICC/ICC-SC loss and gastric motor dysfunction, improving slow wave activity and food intake in klotho mice.

The stability of slow-wave sleep and EEG oscillations across two consecutive nights of laboratory polysomnography in cognitively normal older adults.

Laboratory polysomnography provides gold-standard measures of sleep physiology, but multi-night investigations are resource intensive. We assessed the night-to-night stability via reproducibility metrics for sleep macrostructure and electroencephalography oscillations in a group of cognitively normal adults attending two consecutive polysomnographies. Electroencephalographies were analysed using an automatic algorithm for detection of slow-wave activity, spindle and K-complex densities. Average differences between nights for sleep macrostructure, electroencephalography oscillations and sleep apnea severity were assessed, and test-retest reliability was determined using two-way intraclass correlations. Agreement was calculated using the smallest real differences between nights for all measures. Night 2 polysomnographies showed significantly greater time in bed, total sleep time (6.3 hr versus 6.8 hr, p < 0.001) and percentage of rapid eye movement sleep (17.5 versus 19.7, p < 0.001). Intraclass correlations were low for total sleep time, percentage of rapid eye movement sleep and sleep efficiency, moderate for percentage of slow-wave sleep and percentage of non-rapid eye movement 2 sleep, good for slow-wave activity and K-complex densities, and excellent for spindles and apnea-hypopnea index with hypopneas defined according to 4% oxygen desaturation criteria only. The smallest real difference values were proportionally high for most sleep macrostructure measures, indicating moderate agreement, and proportionally lower for most electroencephalography microstructure variables. Slow waves, K-complexes, spindles and apnea severity indices are highly reproducible across two consecutive nights of polysomnography. In contrast, sleep macrostructure measures all demonstrated poor reproducibility as indicated by low intraclass correlation values and moderate agreement. Although there were average differences in percentage of rapid eye movement sleep and total sleep time, these were numerically small and perhaps functionally or clinically less significant. One night of in-laboratory polysomnography is enough to provide stable, reproducible estimates of an individual's sleep concerning measures of slow-wave activity, spindles, K-complex densities and apnea severity.

Neocortical long-range inhibition promotes cortical synchrony and sleep.

Behavioral states such as sleep and wake are highly correlated with specific patterns of rhythmic activity in the cortex. During low arousal states such as slow wave sleep, the cortex is synchronized and dominated by low frequency rhythms coordinated across multiple regions. Although recent evidence suggests that GABAergic inhibitory neurons are key players in cortical state modulation, the in vivo circuit mechanisms coordinating synchronized activity among local and distant neocortical networks are not well understood. Here, we show that somatostatin and chondrolectin co-expressing cells (Sst-Chodl cells), a sparse and unique class of neocortical inhibitory neurons, are selectively active during low arousal states and are largely silent during periods of high arousal. In contrast to other neocortical inhibitory neurons, we show these neurons have long-range axons that project across neocortical areas. Activation of Sst-Chodl cells is sufficient to promote synchronized cortical states characteristic of low arousal, with increased spike co-firing and low frequency brain rhythms, and to alter behavioral states by promoting sleep. Contrary to the prevailing belief that sleep is exclusively driven by subcortical mechanisms, our findings reveal that these long-range inhibitory neurons not only track changes in behavioral state but are sufficient to induce both sleep-like cortical states and sleep behavior, establishing a crucial circuit component in regulating behavioral states.

Dispersion control and radiation based on glide-symmetric spoof surface plasmon polaritons

Glide symmetry transmission line (TL) is a highly symmetric TL with characteristics such as reduced frequency dispersion and merged passband. The dispersion characteristics and field distribution of single-layer and double-layer spoof surface plasmon polaritons (SSPPs) unit with glide symmetry are studied in this paper. It is found that the double layer structure with stronger slow wave effect is more suitable for frequency scanning radiation with higher scanning rates. Thus, T-shaped glide symmetric double-layer unit is proposed. Such unit exhibits stronger field confinement and higher degrees of freedom in modulating dispersion characteristics. Besides the basic transmission characteristic, additional radiation characteristic based on such T-shaped glide symmetric double-layer units performs well with continuously beam scanning in a large frequency and angle range. Experimental results agree well with numerical simulations, demonstrating the superior performance of T-shaped glide symmetric double-layer SSPPs. The radiation method of such T-shaped glide symmetric double layer SSPPs can be applied to antenna design, which is conductive to the development of highly compact plasmonic integrated circuits and systems.

An E-plane loaded sine waveguide for G-band traveling wave tube

A new slow wave structure (SWS), named E-plane loaded sine waveguide (EPLSW) SWS is proposed for the development of G-band traveling wave tubes (TWTs). The structure, derived from the sine waveguide (SW) SWS, features staggered rectangular gratings on the two E-planes, intersecting with the sine-shaped gratings. The natural electron beam tunnel lies between these gratings. The EPLSW-SWS offers improved characteristics compared to the conventional SW-SWS. High-frequency simulation studies reveal that the passband of the EPLSW-SWS extends by more than 33 GHz over the SW-SWS under identical dispersion conditions. Additionally, the interaction impedance of EPLSW-SWS surpasses that of the SW-SWS in the frequency range of 195–255 GHz. Further analysis through particle-in-cell (PIC) results presents that when operating at 19.5 kV and 145 mA for the sheet beam current, it attains a maximum saturated power of 132.7W and a 3 dB bandwidth exceeding 50 GHz.

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.

Exploring the local field potential signal from the subthalamic nucleus for phase-targeted auditory stimulation in Parkinson's disease

BackgroundEnhancing slow waves, the electrophysiological (EEG) manifestation of non-rapid eye movement (NREM) sleep, could potentially benefit patients with Parkinson's disease (PD) by improving sleep quality and slowing disease progression. Phase-targeted auditory stimulation (PTAS) is an approach to enhance slow waves, which are detected in real-time in the surface EEG signal. ObjectiveWe aimed to test whether the local-field potential of the subthalamic nucleus (STN-LFP) can be used to detect frontal slow waves and assess the electrophysiological changes related to PTAS. MethodsWe recruited patients diagnosed with PD and undergoing Percept™ PC neurostimulator (Medtronic) implantation for deep brain stimulation of STN (STN-DBS) in a two-step surgery. Patients underwent three full-night recordings, including one between-surgeries recording and two during rehabilitation, one with DBS+ (on) and one with DBS- (off). Surface EEG and STN-LFP signals from Percept PC were recorded simultaneously, and PTAS was applied during sleep in all three recording sessions. ResultsOur results show that during NREM sleep, slow waves of the cortex and STN are time-locked. PTAS application resulted in power and coherence changes, which can be detected in STN-LFP. ConclusionOur findings suggest the feasibility of implementing PTAS using solely STN-LFP signal for slow wave detection, thus without a need for an external EEG device alongside the implanted neurostimulator. Moreover, we propose options for more efficient STN-LFP signal preprocessing, including different referencing and filtering to enhance the reliability of cortical slow wave detection in STN-LFP recordings.

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.

Impaired Hippocampal Reactivation Preceding Robust Aβ Deposition in a Model of Alzheimer's Disease.

Current therapeutic strategies for Alzheimer's disease (AD) target amyloid-beta (Aβ) fibrils and high molecular weight protofibrils associated with plaques, but other bioactive species may directly contribute to neural systems failure in AD. Employing hippocampal electrophysiological recordings and dynamic calcium imaging across the sleep-wake cycle in young mice expressing human Aβ and Aβ oligomers, we reveal marked impairments of hippocampal function long before amyloid plaques predominate. In slow wave sleep (SWS), Aβ increased the proportion of hypoactive cells and reduced place-cell reactivation. During awake behavior, Aβ impaired theta-gamma phase-amplitude coupling (PAC) and drove excessive synchronization of place cell calcium fluctuations with hippocampal theta. Remarkably, the on-line impairment of hippocampal theta-gamma PAC correlated with the SWS impairment of place-cell reactivation. Together, these results identify toxic effects of Aβ on memory encoding and consolidation processes before robust plaque deposition and support targeting soluble Aβ-related species to treat and prevent AD.