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Introduction: Attentional control is crucial in the development and maintenance of anxiety disorders. Understanding the underlying mechanisms of attentional control can help to shed light on the neuropathological processes in anxiety disorders (ANX). Quantitative electroencephalography (QEEG) offers a cost-effective, noninvasive method for examining the neuropathological mechanisms of mental disorders. Methods: In this study, 67 patients with ANX and 45 healthy controls (HC) were recruited. EEG recordings were obtained for 5 minutes in an eyes-closed condition. QEEG was employed to evaluate the mechanisms of attentional control in ANX. Results: Neurophysiological measures indicated that anxiety patients exhibited a more frontal topographic pattern of theta/beta ratio (TBR) compared to HC. Additionally, a significant decrease in temporal beta power was observed in the ANX group. Correlation analysis revealed that decreased beta power and increased TBR were significant association between attentional control deficits in ANX. Discussion: These findings provide electrophysiological evidence of impaired attentional control processing in anxiety patients, characterized by decreased temporal beta power and increased frontal TBR. Temporal beta power and frontal TBR may serve as promising biomarkers for attentional control in ANX. [ABSTRACT FROM AUTHOR]

Age is a primary risk factor for Parkinson's disease (PD); however, the effects of aging on the Parkinsonian brain remain poorly understood, particularly for deep brain structures. We investigated intraoperative micro‐electrode recordings from the subthalamic nucleus (STN) of PD patients aged between 42 and 76 years. Age was associated with decreased oscillatory beta power and non‐oscillatory high‐frequency power, independent of PD‐related variables. Single unit firing and burst rates were also reduced, whereas the coefficient of variation and the structure of burst activity were unchanged. Phase synchronization (debiased weighed phase lag index [dWPLI]) between sites was pronounced in the beta band between electrodes in the superficial STN but was unaffected by age. Our results show that aging is associated with reduced neuronal activity without changes to its temporal structure. We speculate that the loss of activity in the STN may mediate the relationship between PD and age. [ABSTRACT FROM AUTHOR]

Background/Objectives: Sports-related concussions are a main cause of cognitive dysfunction and somatic complaints, particularly in youth. While the majority of concussion symptoms resolve within one week, cognitive effects may persist. In this study, we sought to study changes to cognition within this acute time frame. Methods: In this current study, we use an established swine model of traumatic brain injury (TBI) to study the effects of single and repeated head rotations on resting-state electroencephalography (rs-EEG) in awake piglets in the acute (within 7 days) time period after injury. We studied both healthy and experimental groups to (1) establish healthy reference ranges (RRs; N = 23) for one-minute rs-EEG in awake piglets, (2) compare the effects of single (N = 12) and repeated head rotations (N = 13) on rs-EEG, and (3) examine the acute time course (pre-injury and days 1, 4, and 7 post-injury) in animals administered single and repeated head rotations. EEG data were Fourier transformed, and total (1–30 Hz) and relative power in the alpha (8–12 Hz), beta (16.5–25 Hz), delta (1–4 Hz), and theta (4–7.5 Hz) bands were analyzed. Results: Total power and relative alpha, beta, delta, and theta power were consistent measures across days in healthy animals. We found a significant and transient increase in relative alpha power after repeated injury on day 1 in all regions and a rise above the healthy RR in the frontal and left temporal regions. Conclusions: Future studies will expand the study duration to investigate and inform clinical prognoses from acute measurements of rs-EEG. [ABSTRACT FROM AUTHOR]

During natural behavior, an action often needs to be suddenly stopped in response to an unexpected sensory input—referred to as reactive stopping. Reactive stopping has been mostly investigated in humans, which led to hypotheses about the involvement of different brain structures, in particular the hyperdirect pathway. Here, we directly investigate the contribution and interaction of two key regions of the hyperdirect pathway, the orbitofrontal cortex (OFC) and subthalamic nucleus (STN), using dual-area, multielectrode recordings in male rats performing a stop-signal task. In this task, rats have to initiate movement to a go-signal, and occasionally stop their movement to the go-signal side after a stop-signal, presented at various stop-signal delays. Both the OFC and STN show near-simultaneous field potential reductions in the beta frequency range (12–30 Hz) compared with the period preceding the go-signal and the movement period. These transient reductions (∼200 ms) only happen during reactive stopping, which is when the stop-signal was received after action initiation, and are well timed after stop-signal onset and before the estimated time of stopping. Phase synchronization analysis also showed a transient attenuation of synchronization between the OFC and STN in the beta range during reactive stopping. The present results provide the first direct quantification of local neural oscillatory activity in the OFC and STN and interareal synchronization specifically timed during reactive stopping. [ABSTRACT FROM AUTHOR]

IntroductionAttentional control is crucial in the development and maintenance of anxiety disorders. Understanding the underlying mechanisms of attentional control can help to shed light on the neuropathological processes in anxiety disorders (ANX). Quantitative electroencephalography (QEEG) offers a cost-effective, noninvasive method for examining the neuropathological mechanisms of mental disorders.MethodsIn this study, 67 patients with ANX and 45 healthy controls (HC) were recruited. EEG recordings were obtained for 5 minutes in an eyes-closed condition. QEEG was employed to evaluate the mechanisms of attentional control in ANX.ResultsNeurophysiological measures indicated that anxiety patients exhibited a more frontal topographic pattern of theta/beta ratio (TBR) compared to HC. Additionally, a significant decrease in temporal beta power was observed in the ANX group. Correlation analysis revealed that decreased beta power and increased TBR were significant association between attentional control deficits in ANX.DiscussionThese findings provide electrophysiological evidence of impaired attentional control processing in anxiety patients, characterized by decreased temporal beta power and increased frontal TBR. Temporal beta power and frontal TBR may serve as promising biomarkers for attentional control in ANX.

Parkinson’s Disease (PD) is characterized by the temporary alleviation of motor symptoms following electrode implantation (or nucleus destruction), known as the microlesion effect (MLE). Electrophysiological studies have explored different PD stages, but understanding electrophysiological characteristics during the MLE period remains unclear. The objective was to examine the characteristics of local field potential (LFP) signals in the subthalamic nucleus (STN) during the hyperacute period following implantation (within 2 days) and 1 month post-implantation. 15 patients diagnosed with PD were enrolled in this observational study, with seven simultaneous recordings of bilateral STN-LFP signals using wireless sensing technology from an implantable pulse generator. Recordings were made in both on and off medication states over 1 month after implantation. We used a method to parameterize the neuronal power spectrum to separate periodic oscillatory and aperiodic components effectively. Our results showed that beta power exhibited a significant increase in the off medication state 1 month after implantation, compared to the postoperative hyperacute period. Notably, this elevation was effectively attenuated by levodopa administration. Furthermore, both the exponents and offsets displayed a decrease at 1 month postoperatively when compared to the hyperacute postoperative period. Remarkably, levodopa medication exerted a modulatory effect on these aperiodic parameters, restoring them back to levels observed during the hyperacute period. Our findings suggest that both periodic and aperiodic components partially capture distinct electrophysiological characteristics during the MLE. It is crucial to adequately evaluate such discrepancies when exploring the mechanisms of MLE and optimizing adaptive stimulus protocols. [ABSTRACT FROM AUTHOR]

Background/Objectives: Sports-related concussions are a main cause of cognitive dysfunction and somatic complaints, particularly in youth. While the majority of concussion symptoms resolve within one week, cognitive effects may persist. In this study, we sought to study changes to cognition within this acute time frame. Methods: In this current study, we use an established swine model of traumatic brain injury (TBI) to study the effects of single and repeated head rotations on resting-state electroencephalography (rs-EEG) in awake piglets in the acute (within 7 days) time period after injury. We studied both healthy and experimental groups to (1) establish healthy reference ranges (RRs; N = 23) for one-minute rs-EEG in awake piglets, (2) compare the effects of single (N = 12) and repeated head rotations (N = 13) on rs-EEG, and (3) examine the acute time course (pre-injury and days 1, 4, and 7 post-injury) in animals administered single and repeated head rotations. EEG data were Fourier transformed, and total (1–30 Hz) and relative power in the alpha (8–12 Hz), beta (16.5–25 Hz), delta (1–4 Hz), and theta (4–7.5 Hz) bands were analyzed. Results: Total power and relative alpha, beta, delta, and theta power were consistent measures across days in healthy animals. We found a significant and transient increase in relative alpha power after repeated injury on day 1 in all regions and a rise above the healthy RR in the frontal and left temporal regions. Conclusions: Future studies will expand the study duration to investigate and inform clinical prognoses from acute measurements of rs-EEG.

Background: Subthalamic nucleus deep brain stimulation (STN-DBS) is an effective treatment for advanced Parkinson's disease (PD). Clinical outcomes after DBS can be limited by poor programming, which remains a clinically driven, lengthy and iterative process. Electrophysiological recordings in PD patients undergoing STN-DBS have shown an association between STN spectral power in the beta frequency band (beta power) and the severity of clinical symptoms. New commercially-available DBS devices now enable the recording of STN beta oscillations in chronically-implanted PD patients, thereby allowing investigation into the use of beta power as a biomarker for DBS programming. Objective: To determine the potential advantages of beta-guided DBS programming over clinically and image-guided programming in terms of clinical efficacy and programming time. Methods: We conducted a randomized, blinded, three-arm, crossover clinical trial in eight Parkinson's patients with STN-DBS who were evaluated three months after DBS surgery. We compared clinical efficacy and time required for each DBS programming paradigm, as well as DBS parameters and total energy delivered between the three strategies (beta-, clinically- and image-guided). Results: All three programming methods showed similar clinical efficacy, but the time needed for programming was significantly shorter for beta- and image-guided programming compared to clinically-guided programming (p

Subthalamic nucleus (STN) beta-triggered adaptive deep brain stimulation (ADBS) has been shown to provide clinical improvement comparable to conventional continuous DBS (CDBS) with less energy delivered to the brain and less stimulation induced side effects. However, several questions remain unanswered. First, there is a normal physiological reduction of STN beta band power just prior to and during voluntary movement. ADBS systems will therefore reduce or cease stimulation during movement in people with Parkinson's disease and could therefore compromise motor performance compared to CDBS. Second, beta power was smoothed and estimated over a time period of 400 ms in most previous ADBS studies, but a shorter smoothing period could have the advantage of being more sensitive to changes in beta power, which could enhance motor performance. In this study, we addressed these two questions by evaluating the effectiveness of STN beta-triggered ADBS using a standard 400 ms and a shorter 200 ms smoothing window during reaching movements. Results from 13 people with Parkinson's disease showed that reducing the smoothing window for quantifying beta did lead to shortened beta burst durations by increasing the number of beta bursts shorter than 200 ms and more frequent switching on/off of the stimulator but had no behavioural effects. Both ADBS and CDBS improved motor performance to an equivalent extent compared to no DBS. Secondary analysis revealed that there were independent effects of a decrease in beta power and an increase in gamma power in predicting faster movement speed, while a decrease in beta event related desynchronization (ERD) predicted quicker movement initiation. CDBS suppressed both beta and gamma more than ADBS, whereas beta ERD was reduced to a similar level during CDBS and ADBS compared with no DBS, which together explained the achieved similar performance improvement in reaching movements during CDBS and ADBS. In addition, ADBS significantly improved tremor compared with no DBS but was not as effective as CDBS. These results suggest that STN beta-triggered ADBS is effective in improving motor performance during reaching movements in people with Parkinson's disease, and that shortening of the smoothing window does not result in any additional behavioural benefit. When developing ADBS systems for Parkinson's disease, it might not be necessary to track very fast beta dynamics; combining beta, gamma, and information from motor decoding might be more beneficial with additional biomarkers needed for optimal treatment of tremor. [ABSTRACT FROM AUTHOR]

ObjectiveParoxysmal epileptiform abnormalities on electroencephalography (EEG) are the hallmark of epilepsies, but it is uncertain to what extent epilepsy and background EEG oscillations share neurobiological underpinnings. Here, we aimed to assess the genetic correlation between epilepsy and background EEG oscillations.MethodsConfounding factors, including the heterogeneous etiology of epilepsies and medication effects, hamper studies on background brain activity in people with epilepsy. To overcome this limitation, we compared genetic data from a genome-wide association study (GWAS) on epilepsy (n = 12 803 people with epilepsy and 24 218 controls) with that from a GWAS on background EEG (n = 8425 subjects without epilepsy), in which background EEG oscillation power was quantified in four different frequency bands: alpha, beta, delta, and theta. We replicated our findings in an independent epilepsy replication dataset (n = 4851 people with epilepsy and 20 428 controls). To assess the genetic overlap between these phenotypes, we performed genetic correlation analyses using linkage disequilibrium score regression, polygenic risk scores, and Mendelian randomization analyses.ResultsOur analyses show strong genetic correlations of genetic generalized epilepsy (GGE) with background EEG oscillations, primarily in the beta frequency band. Furthermore, we show that subjects with higher beta and theta polygenic risk scores have a significantly higher risk of having generalized epilepsy. Mendelian randomization analyses suggest a causal effect of GGE genetic liability on beta oscillations.SignificanceOur results point to shared biological mechanisms underlying background EEG oscillations and the susceptibility for GGE, opening avenues to investigate the clinical utility of background EEG oscillations in the diagnostic workup of epilepsy.

There remains some debate about whether beta power effects observed during sentence comprehension reflect ongoing syntactic unification operations (beta‐syntax hypothesis), or instead reflect maintenance or updating of the sentence‐level representation (beta‐maintenance hypothesis). In this study, we used magnetoencephalography to investigate beta power neural dynamics while participants read relative clause sentences that were initially ambiguous between a subject‐ or an object‐relative reading. An additional condition included a grammatical violation at the disambiguation point in the relative clause sentences. The beta‐maintenance hypothesis predicts a decrease in beta power at the disambiguation point for unexpected (and less preferred) object‐relative clause sentences and grammatical violations, as both signal a need to update the sentence‐level representation. While the beta‐syntax hypothesis also predicts a beta power decrease for grammatical violations due to a disruption of syntactic unification operations, it instead predicts an increase in beta power for the object‐relative clause condition because syntactic unification at the point of disambiguation becomes more demanding. We observed decreased beta power for both the agreement violation and object‐relative clause conditions in typical left hemisphere language regions, which provides compelling support for the beta‐maintenance hypothesis. Mid‐frontal theta power effects were also present for grammatical violations and object‐relative clause sentences, suggesting that violations and unexpected sentence interpretations are registered as conflicts by the brain's domain‐general error detection system. Our research adjudicates in favour of the hypothesis that MEG beta power dynamics in the brain's language network observed during sentence comprehension reflect the encoding of information into working memory. We also show that less preferred object relative clause sentences are treated similarly to sentences containing outright grammatical violations by the brain's domain‐general error detection system, as reflected in increased mid‐frontal theta power. [ABSTRACT FROM AUTHOR]

Subthalamic nucleus deep brain stimulation (STN-DBS) is an effective treatment for advanced Parkinson's disease (PD). Clinical outcomes after DBS can be limited by poor programming, which remains a clinically driven, lengthy and iterative process. Electrophysiological recordings in PD patients undergoing STN-DBS have shown an association between STN spectral power in the beta frequency band (beta power) and the severity of clinical symptoms. New commercially-available DBS devices now enable the recording of STN beta oscillations in chronically-implanted PD patients, thereby allowing investigation into the use of beta power as a biomarker for DBS programming. To determine the potential advantages of beta-guided DBS programming over clinically and image-guided programming in terms of clinical efficacy and programming time. We conducted a randomized, blinded, three-arm, crossover clinical trial in eight Parkinson's patients with STN-DBS who were evaluated three months after DBS surgery. We compared clinical efficacy and time required for each DBS programming paradigm, as well as DBS parameters and total energy delivered between the three strategies (beta-, clinically- and image-guided). All three programming methods showed similar clinical efficacy, but the time needed for programming was significantly shorter for beta- and image-guided programming compared to clinically-guided programming (p < 0.001). Beta-guided programming may be a useful and more efficient approach to DBS programming in Parkinson's patients with STN-DBS. It takes significantly less time to program than traditional clinically-based programming, while providing similar symptom control. In addition, it is readily available within the clinical DBS programmer, making it a valuable tool for improving current clinical practice. • Beta-Guided programming is an innovative approach that may streamline the programming process for PD patients with STN DBS. • While preliminary findings from our study suggest that Beta Titration may potentially mitigate STN overstimulation and enhance symptom control, • Our results demonstrate that beta-guided programming significantly reduces programming time, suggesting it could be efficiently integrated into routine clinical practice using a commercially available patient programmer. [ABSTRACT FROM AUTHOR]

Aging is a key risk factor for the development of Parkinson’s disease (PD). PD is characterized by excessive synchrony of beta oscillations (13–30 Hz) in the basal ganglia thalamo-cortical network. However, cortical beta power is not reliably elevated in individuals with PD. Here, we sought to disentangle how resting cortical beta power compares in younger controls, older controls, and individuals with PD using scalp electroencephalogram (EEG) and a novel approach for quantifying beta power. Specifically, we used a Gaussian model to determine if sensorimotor beta power distinguishes these groups. In addition, we looked at the distribution of beta power across the entire cortex. Our findings showed that Gaussian-modeled beta power does not differentiate individuals with PD (on medication) from healthy younger or older controls in sensorimotor cortex. However, beta power (and not theta or alpha) was higher in healthy older versus younger controls. This effect was most pronounced in regions near sensorimotor cortex including the frontal and parietal areas [P < 0.05, false discovery rate (FDR) corrected]. In addition, the bandwidth of the periodic beta was also higher in healthy older than young individuals in parietal regions. Finally, the aperiodic component, specifically the exponent of the signal, was higher (steeper) in younger controls than in individuals with PD in the right parietal-occipital region (P < 0.05, FDR corrected), possibly reflecting differences in neuronal spiking. Our findings suggest that cortical Gaussian beta power is possibly modulated by age and could be further explored in longitudinal studies to determine whether sensorimotor beta increases with increasing age. NEW & NOTEWORTHY Altered sensorimotor beta activity has been shown to be a feature in aging and PD. Using a novel approach, we clarify that resting sensorimotor beta power does not distinguish subjects with PD from healthy younger and older controls. However, beta power was higher in older compared with younger controls in central sensorimotor, frontal, and parietal regions. These results provide a clearer picture of sensorimotor beta power, demonstrating that it is elevated in aging but not PD. [ABSTRACT FROM AUTHOR]

Objective: Assessment of electroencephalographic (EEG) activity in depression has provided insights into neural profiles of the illness. However, there is limited understanding on how symptom severity and risk factors, such as childhood adversity, influence EEG features. Methods: Eyes-closed EEG was acquired in N = 28 depressed individuals being treated in a tertiary psychiatric setting. Absolute alpha, beta, theta, and delta power and inter-/intra-hemispheric coherence were examined. Relations between the Montgomery-Åsberg Depression Scale (MADRS) and Adverse Childhood Experience (ACE) Questionnaire and EEG features were assessed. Results: Individuals in the high (MADRS≥30) versus lower (MADRS ≤ 29) symptom severity group exhibited greater overall beta power, and lower Fp 1 -Fp 2 delta and theta coherence. Those with high (≥3) versus lower (≤2) ACE scores exhibited greater T 7 -T 8 beta coherence. Lowest F 3 -F 4 beta coherence was observed in those with high ACE/high depression severity. A negative correlation existed between F 8 -P 8 alpha coherence and symptom severity. Conclusions: Those with higher depression severity exhibit increased beta power, possibly reflecting a hyper-vigilant state . Depression severity and ACE history may produce subtle alterations in frontal delta/theta and temporal/frontal beta coherence regions. Significance: This is the first study to examine the neural impact of depression severity and ACE-assessed childhood trauma in depressed individuals receiving treatment in a tertiary setting, accounting for the clinical reality of the prevalence of their co-occurrence., Competing Interests: Declaration of Conflicting InterestsThe author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: Dr P. Blier was in receipt of a Tier 1 Canada Research Chair and an Endowed Chair from the Royal’s Institute of Mental Health Research (IMHR) and has received research support or speaker honoraria from or served as a consultant to, Allergan, Bristol-Myers Squibb, Janssen, Lundbeck, Otsuka, Pierre Fabre Médicaments, Pfizer, Shire, and Takeda. The other authors have no other not conflicts of interest to disclose.

Human self-motion perception largely relies on the integration of the visual, vestibular and proprioceptive systems. Much behavioral research has been conducted in order to understand this integration process; however, little is known about the online processes in humans during self-motion perception. Of the few studies to physically move human participants with full-body motion while recording the brain, most have used EEG due to its relative mobility. Past research provides evidence that multisensory self-motion perception elicits theta, alpha, and beta oscillations. It is important, however, to understand the individual contribution of each sense to fully understand how these oscillatory frequencies contribute to self-motion perception. To our knowledge, there has yet to be a study that directly compares the EEG correlates of visual self-motion with a no-motion physical input, versus physical-self motion with a no-motion visual input. We recorded event-related spectral power within a motion simulator controlled by a MOOG Stewart platform. Participants were given a visual or physical stimulus and made heading direction judgments. Compared to physical-only trials, visual-only trials produced earlier theta ERS and alpha ERD early in the trial, and more robust beta ERS late in the trial. We suggest beta-band power is likely associated with the process of visual-vestibular weighting. Moreover, within the right motor area, we found differences in theta power associated with left versus right headings. Theta ERS in the right motor area appears to be associated with heading processing for both the visual and vestibular systems but is minimally affected by multisensory weighting.

Bilateral salpingo-oophorectomy (BSO; removal of ovaries and fallopian tubes) prior to age 48 is associated with elevated risk for both Alzheimer's disease (AD) and sleep disorders such as insomnia and sleep apnea. In early midlife, individuals with BSO show reduced hippocampal volume, function, and hippocampal-dependent verbal episodic memory performance associated with changes in sleep. It is unknown whether BSO affects fine-grained sleep measurements (sleep microarchitecture) and how these changes might relate to hippocampal-dependent memory. We recruited thirty-six early midlife participants with BSO. Seventeen of these participants were taking 17β-estradiol therapy (BSO+ET) and 19 had never taken ET (BSO). Twenty age-matched control participants with intact ovaries (AMC) were also included. Overnight at-home polysomnography recordings were collected, along with subjective sleep quality and hot flash frequency. Multivariate Partial Least Squares (PLS) analysis was used to assess how sleep varied between groups. Compared to AMC, BSO without ET was associated with significantly decreased time spent in non-rapid eye movement (NREM) stage 2 sleep as well as increased NREM stage 2 and 3 beta power, NREM stage 2 delta power, and spindle power and maximum amplitude. Increased spindle maximum amplitude was negatively correlated with verbal episodic memory performance. Decreased sleep latency, increased sleep efficiency, and increased time spent in rapid eye movement sleep were observed for BSO+ET. Findings suggest there is an association between ovarian hormone loss and sleep microarchitecture, which may contribute to poorer cognitive outcomes and be ameliorated by ET. • Ovarian removal is linked to less time spent in NREM stage 2 sleep. • Ovarian removal is linked to increased beta and delta power. • Ovarian removal is linked to increased spindle amplitude and power. • Higher spindle amplitude is linked to poorer verbal episodic memory. • 17β-estradiol therapy may improve some aspects of sleep macroarchitecture. [ABSTRACT FROM AUTHOR]

Jae Myeong Kang,1,2,* Seo-Eun Cho,2,* Kyoung-Sae Na,2 Seung-Gul Kang1,2 1Sleep Medicine Center, Gil Medical Center, Gachon University College of Medicine, Incheon, Republic of Korea; 2Department of Psychiatry, Gil Medical Center, Gachon University College of Medicine, Incheon, Republic of Korea*These authors contributed equally to this workCorrespondence: Seung-Gul KangDepartment of Psychiatry, Gil Medical Center, Gachon University, College of Medicine, 21, Namdong-daero 774 Beon-gil, Namdong-gu, Incheon, 21565, Republic of KoreaTel +82 32-458-2818Email kangsg@gachon.ac.krPurpose: Previous spectral analysis studies on obstructive sleep apnea (OSA) involved small samples, and the results were inconsistent. We performed a spectral analysis of sleep EEG based on different severities of OSA using the Sleep Heart Health Study data. This study aimed to determine the difference in EEG spectral power during sleep in the non-OSA group and with different severities of OSA in the general population.Patients and Methods: The participants (n = 5,804) underwent polysomnography, and they were classified into non-OSA, mild OSA, moderate OSA, and severe OSA groups. The fast Fourier transformation was used to compute the EEG power spectrum for total sleep duration within contiguous 30-second epochs of sleep. The EEG spectral powers of the groups were compared using 4,493 participants after adjusting potential confounding factors that could affect sleep EEG.Results: The power spectra differed significantly among the groups for all frequency bands (p corr < 0.001). We found that the quantitative EEG spectral powers in the beta and sigma bands of total sleep differed (p corr < 0.001) among the participants in the non-OSA group and with different severities of OSA, controlling for covariates. The beta power was higher and the sigma power was lower in the OSA groups than in the non-OSA group. The beta power decreased in the order of severe OSA, moderate OSA, mild OSA, and non-OSA.Conclusion: This study suggests that there are differences between the microstructures of PSG-derived sleep EEG of non-OSA participants and those with different severities of OSA.Keywords: sleep EEG, spectral power, polysomnography, OSA, beta power, sigma power

Introduction Power spectral analysis is the most common method of quantitative electroencephalogram (qEEG) techniques and enables investigation of the microstructure of insomnia. Previous spectral analysis studies on insomnia have shown inconsistent results due to their heterogeneity and small sample sizes. Objectives We compared the difference of electroencephalogram (EEG) spectral power during sleep among participants without insomnia, insomniacs with no hypnotic use, hypnotic users with no insomnia complaints, and hypnotic users with insomnia complaints. Methods We used the Sleep Heart Health Study data, which is large sample size and has good quality control. The fast Fourier transformation was used to calculate the EEG power spectrum for total sleep duration within contiguous 30-second epochs of sleep. For 1,985 participants, EEG spectral power was compared among the groups while adjusting for potential confounding factors that could affect sleep EEG. Results The power spectra during total sleep differed significantly among the groups in all frequency bands (p corr < 0.001). We found that quantitative EEG spectral power in the beta and sigma bands of total sleep differed (p corr < 0.001) between participants without insomnia and hypnotic users with insomnia complaints after controlling for potential confounders. The higher beta and sigma power were found in the hypnotic users with insomnia complaints than in the non-insomnia participants. Conclusions This study suggests differences in the microstructures of polysomnography-derived sleep EEG between the insomnia groups. Disclosure No significant relationships.

Despite the clinical and financial burden of Parkinson's disease (PD), there is no standardized, reliable biomarker to diagnose and track PD progression. Instead, PD is primarily assessed using subjective clinical rating scales and patient self-report. Such approaches can be imprecise, hindering diagnosis and disease monitoring. An objective biomarker would be beneficial for clinical care, refining diagnosis, and treatment. Due to widespread electrophysiological abnormalities both within and between brain structures in PD, development of electrophysiologic biomarkers may be feasible. Basal ganglia recordings acquired with neurosurgical approaches have revealed elevated power in the beta frequency range (13–30 Hz) in PD, suggesting that beta power could be a putative PD biomarker. However, there are limitations to the use of beta power as a biomarker. Recent advances in analytic approaches have led to novel methods to quantify oscillatory synchrony in the beta frequency range. Here we describe some of these novel approaches in the context of PD and explore how they may serve as electrophysiological biomarkers. These novel signatures include (1) interactions between beta phase and broadband (> 50 Hz, "gamma") amplitude (i.e., phase amplitude coupling, PAC), (2) asymmetries in waveform shape, (3) beta coherence, and (4) beta "bursts." Development of a robust, reliable, and readily accessible electrophysiologic biomarker would represent a major step towards more precise and personalized care in PD. [ABSTRACT FROM AUTHOR]

Late-life depression (LLD) is a debilitating condition that is associated with poor response to antidepressant medications and deficits in cognitive performance. Nicotinic cholinergic stimulation has emerged as a potentially effective candidate to improve cognitive performance in patients with cognitive impairment. Previous studies of nicotinic stimulation in animal models and human populations with cognitive impairment led to examining potential cognitive and mood effects of nicotinic stimulation in older adults with LLD. We report results from a pilot study of transdermal nicotine in LLD testing whether nicotine treatment would enhance cognitive performance and mood. The study used electroencephalography (EEG) recordings as a tool to test for potential mechanisms underlying the effect of nicotine. Eight non-smoking participants with LLD completed EEG recordings at baseline and after 12 weeks of transdermal nicotine treatment (NCT02816138). Nicotine augmentation treatment was associated with improved performance on an auditory oddball task. Analysis of event-related oscillations showed that nicotine treatment was associated with reduced beta desynchronization at week 12 for both standard and target trials. The change in beta power on standard trials was also correlated with improvement in mood symptoms. This pilot study provides preliminary evidence for the impact of nicotine in modulating cortical activity and improving mood in depressed older adults and shows the utility of using EEG as a marker of functional engagement in nicotinic interventions in clinical geriatric patients. [ABSTRACT FROM AUTHOR]

Late-life depression (LLD) is a debilitating condition that is associated with poor response to antidepressant medications and deficits in cognitive performance. Nicotinic cholinergic stimulation has emerged as a potentially effective candidate to improve cognitive performance in patients with cognitive impairment. Previous studies of nicotinic stimulation in animal models and human populations with cognitive impairment led to examining potential cognitive and mood effects of nicotinic stimulation in older adults with LLD. We report results from a pilot study of transdermal nicotine in LLD testing whether nicotine treatment would enhance cognitive performance and mood. The study used electroencephalography (EEG) recordings as a tool to test for potential mechanisms underlying the effect of nicotine. Eight non-smoking participants with LLD completed EEG recordings at baseline and after 12 weeks of transdermal nicotine treatment (NCT02816138). Nicotine augmentation treatment was associated with improved performance on an auditory oddball task. Analysis of event-related oscillations showed that nicotine treatment was associated with reduced beta desynchronization at week 12 for both standard and target trials. The change in beta power on standard trials was also correlated with improvement in mood symptoms. This pilot study provides preliminary evidence for the impact of nicotine in modulating cortical activity and improving mood in depressed older adults and shows the utility of using EEG as a marker of functional engagement in nicotinic interventions in clinical geriatric patients.

Sleep disturbances are common in post-traumatic stress disorder (PTSD), although which sleep microarchitectural characteristics reliably classify those with and without PTSD remains equivocal. Here, we investigated sleep microarchitectural differences (i.e., spectral power, spindle activity) in trauma-exposed individuals that met (n = 45) or did not meet (n = 52) criteria for PTSD and how these differences relate to post-traumatic and related psychopathological symptoms. Using ecologically-relevant home sleep polysomnography recordings, we show that individuals with PTSD exhibit decreased beta spectral power during NREM sleep and increased fast sleep spindle peak frequencies. Contrary to prior reports, spectral power in the beta frequency range (20.31–29.88 Hz) was associated with reduced PTSD symptoms, reduced depression, anxiety and stress and greater subjective ability to regulate emotions. Increased fast frequency spindle activity was not associated with individual differences in psychopathology. Our findings may suggest an adaptive role for beta power during sleep in individuals exposed to a trauma, potentially conferring resilience. Further, we add to a growing body of evidence that spindle activity may be an important biomarker for studying PTSD pathophysiology.

Clinically deployed deep brain stimulation (DBS) for the treatment of Parkinson’s disease operates in an open loop with fixed stimulation parameters, and this may result in high energy consumption and suboptimal therapy. The objective of this manuscript is to establish, through simulation in a computational model, a closed-loop control system that can automatically adjust the stimulation parameters to recover normal activity in model neurons. Exaggerated beta band activity is recognized as a hallmark of Parkinson’s disease and beta band activity in model neurons of the globus pallidus internus (GPi) was used as the feedback signal to control DBS of the GPi. Traditional proportional controller and proportional-integral controller were not effective in eliminating the error between the target level of beta power and the beta power under Parkinsonian conditions. To overcome the difficulties in tuning the controller parameters and improve tracking performance in the case of changes in the plant, a supervisory control algorithm was implemented by introducing a Radial Basis Function (RBF) network to build the inverse model of the plant. Simulation results show the successful tracking of target beta power in the presence of changes in Parkinsonian state as well as during dynamic changes in the target level of beta power. Our computational study suggests the feasibility of the RBF network-driven supervisory control algorithm for real-time modulation of DBS parameters for the treatment of Parkinson’s disease.

• Two awake, unanesthetized macaque monkeys were used as experimental subjects. • rTMS of either 1 Hz or 10 Hz was applied to the MI in a daily session. • Resting-state ECoGs in the MI and MEPs were recorded before and after rTMS application. • ECoG beta-band power and MEP amplitude significantly decreased after 1-Hz rTMS. • ECoG high-gamma band power and MEP amplitude significantly increased after 10-Hz rTMS. Repetitive transcranial magnetic stimulation (rTMS) is now widely used as a means of neuromodulation, but the details of the mechanisms by which rTMS works remain unclarified. As a step forward to unveiling the neural phenomena occurring underneath the TMS coil, we conducted an electrophysiological study using awake and unanesthetized monkeys with subdural electrocorticogram (ECoG) electrodes implanted over the primary motor cortex (MI). We evaluated the effects of low-frequency (1 Hz) and high-frequency (10 Hz) rTMS on the resting-state ECoG signals in the stimulated MI, as well as the motor evoked potentials (MEPs) in the contralateral hand. Following the 1-Hz rTMS application, the ECoG beta band power and the MEP amplitude were significantly decreased. Following the 10-Hz rTMS application, the ECoG high-gamma power and the MEP amplitude significantly increased. Given that beta and high-gamma activities in the ECoG reflect the synchronous firing and the firing frequency of cell assemblies, respectively, in local neural circuits, these results suggest that low-frequency rTMS inhibits neural activity by desynchronizing the firing activity of local circuits, whereas high-frequency rTMS facilitates neural activity by increasing the firing rate of cell assemblies in the local circuits. [ABSTRACT FROM AUTHOR]

Clinically deployed deep brain stimulation (DBS) for the treatment of Parkinson's disease operates in an open loop with fixed stimulation parameters, and this may result in high energy consumption and suboptimal therapy. The objective of this manuscript is to establish, through simulation in a computational model, a closed-loop control system that can automatically adjust the stimulation parameters to recover normal activity in model neurons. Exaggerated beta band activity is recognized as a hallmark of Parkinson's disease and beta band activity in model neurons of the globus pallidus internus (GPi) was used as the feedback signal to control DBS of the GPi. Traditional proportional controller and proportional-integral controller were not effective in eliminating the error between the target level of beta power and the beta power under Parkinsonian conditions. To overcome the difficulties in tuning the controller parameters and improve tracking performance in the case of changes in the plant, a supervisory control algorithm was implemented by introducing a Radial Basis Function (RBF) network to build the inverse model of the plant. Simulation results show the successful tracking of target beta power in the presence of changes in Parkinsonian state as well as during dynamic changes in the target level of beta power. Our computational study suggests the feasibility of the RBF network-driven supervisory control algorithm for real-time modulation of DBS parameters for the treatment of Parkinson's disease. [ABSTRACT FROM AUTHOR]

• Assessed conflict monitoring on two novel picture-word interference tasks. • Tasks examined conflict monitoring across animal and object categories. • Conflict effects observed in both tasks. • Task differences observed between animals and objects. • Task performance related to performance on standard measures of cognitive control. Conflict monitoring has been studied extensively using experimental paradigms that manipulate perceptual dimensions of stimuli and responses. The picture-word interference (PWI) task has historically been used to examine semantic conflict, but primarily for the purpose of examining lexical retrieval. In this study, we utilized two novel PWI tasks to assess conflict monitoring in the context of semantic conflict. Participants included nineteen young adults (14F, age = 20.79 ± 3.14) who completed two tasks: Animals and Objects. Task and conflict effects were assessed by examining behavioral (reaction time and accuracy) and neurophysiological (oscillations in theta, alpha, and beta band) measures. Results revealed conflict effects within both tasks, but the pattern of findings differed across the two semantic categories. Participants were slower to respond to unmatched versus matched trials on the Objects task only and were less accurate responding to matched versus unmatched trials in the Animals task only. We also observed task differences, with participants responding more accurately on conflict trials for Animals compared to Objects. Differences in neural oscillations were observed, including between-task differences in low beta oscillations and within-task differences in theta, alpha, and low beta. We also observed significant correlations between task performance and standard measures of cognitive control. This work provides new insights into conflict monitoring, highlighting the importance of examining conflict across different semantic categories, especially in the context of animacy. The findings serve as a benchmark to assess conflict monitoring using PWI tasks across populations of varying cognitive ability. [ABSTRACT FROM AUTHOR]

Beta power suppression in the basal ganglia is stronger during movements that require high force levels and high movement effort but it has been difficult to dissociate the two. We recorded scalp EEG and basal ganglia local field potentials in Parkinson's disease patients (11 STN, 7 GPi) ON and OFF dopaminergic medication while they performed a visually-guided force matching task using a pen on a force-sensitive graphics tablet. Force adjustments were accompanied by beta power suppression irrespective of whether the force was increased or reduced. Before the adjustment was completed, beta activity returned. High beta power was specifically associated with slowing of the force adjustment. ON medication, the peak force rate was faster and cortico-basal ganglia beta phase coupling was more readily modulated. In particular, phase decoupling was stronger during faster adjustments. The results suggest that beta power in the basal ganglia does not covary with force per se, but rather with a related factor, the absolute force rate, or a more general concept of movement effort. The results also highlight that beta activity reappears during stabilization of isometric contractions, and that dopamine-related suppression of cortico-basal ganglia beta coupling is linked to faster force adjustments.

Background. Cue-reactivity as a characteristic symptom of substance use disorders (SUD) is highly context dependent. Paradigms with high context validity need to be established for the investigation of underlying neurobiological mechanisms. While craving can be assessed by self-report as one aspect of cue-reactivity (CR), the assessment of biological measures such as the autonomous response and EEG promises a holistic perspective including CR at an automatized level. In a multimodal approach, smoking cue exposure (CE) effects on heart rate variability (HRV), EEG frequency power, and craving as well as their interrelation were assessed. This pilot study focused on the validity of CR measurements in a naturalistic CE paradigm. Methods. EEG frequency power, HRV, and craving were assessed during resting state (RS) and smoking CE in smokers (n = 14) and nonsmoking controls (n = 10) to investigate the psychophysiological and subjective reactions to CE. Results. Increased beta power was found only in smokers during CE compared to the control condition. There was an inverse correlation of beta power and maximum craving. Likewise, HRV correlated negatively with maximum smoking urges in smokers immediately after the measurements, without differentiation between CE and control condition. Conclusion. The increased beta power in smokers during CE is discussed as increased inhibitory control related to reduced craving in smokers. Furthermore, increased craving during CE seems to be associated to decreased vagal activity. The multimodal measurements during the CE showed ecological validity to be fundamental for CE assessment in clinical populations to evaluate its predictive value., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background: Although the association of human temperament and preference has been studied previously, few investigations have examined cerebral cortical activation to assess brain dynamics associated with the motivation to engage in performance. The present study adopted a personality and cognitive neuroscience approach to investigate if participation in ballroom dancing is associated with sensation-seeking temperament and elevated cerebral cortical arousal during freely chosen musical recall. Methods: Preferred tempo, indicated by tapping speed during melodic recall, and a measure of fundamental disposition or temperament were assessed in 70 ballroom dancers and 71 nondancers. All participants completed a trait personality inventory (i.e., the Chen Huichang 60 Temperaments Inventory) to determine four primary types: choleric, sanguine, phlegmatic and melancholic. Participants separately recalled their favorite musical piece and tapped to it with their index finger for 40 beats using a computer keyboard. A subset of 59 participants (29 ballroom dancers and 30 nondancers) also repeated the same tapping task while electroencephalographic (EEG) activity was recorded. Results: The results revealed that the dancers were more extraverted, indicative of a heightened need for arousal, exhibited a preference for faster musical tempo, and exhibited elevated EEG beta power during the musical recall task relative to nondancers. Paradoxically, dancers also showed elevated introversion (i.e., melancholic score) relative to nondancers, which can be resolved by consideration of interactional personality theory if one assumes reasonably that dance performance environment is perceived in a stimulating manner. Conclusion: The results are generally consistent with arousal theory, and suggest that ballroom dancers seek elevated stimulation and, thereby, choose to engage with active and energetic rhythmic auditory stimulation, thus providing the nervous system with the requisite stimulation for desired arousal. These results also suggest an underlying predisposition for engagement in ballroom dance and support the gravitational hypothesis, which propose that personality traits and perception lead to the motivation to engage in specific forms of human performance. [ABSTRACT FROM AUTHOR]

In Parkinson's disease (PD), pathologically high levels of beta activity (12-30 Hz) reflect specific symptomatology and normalize with pharmacological or surgical intervention. Although beta characterization in the subthalamic nucleus (STN) of PD patients undergoing deep brain stimulation (DBS) has now been translated into adaptive DBS paradigms, a limited number of studies have characterized beta power in the globus pallidus internus (GPi), an equally effective DBS target. Our objective was to compare beta power in the STN and GPi during rest and movement in people with PD undergoing DBS. Thirty-seven human female and male participants completed a simple behavioral experiment consisting of periods of rest and button presses, leading to local field potential recordings from 19 (15 participants) STN and 26 (22 participants) GPi nuclei. We examined overall beta power as well as beta time-domain dynamics (i.e., beta bursts). We found higher beta power during rest and movement in the GPi, which also had more beta desynchronization during movement. Beta power was positively associated with bradykinesia and rigidity severity; however, these clinical associations were present only in the GPi cohort. With regards to beta dynamics, bursts were similar in duration and frequency in the GPi and STN, but GPi bursts were stronger and correlated to bradykinesia-rigidity severity. Beta dynamics therefore differ across basal ganglia nuclei. Relative to the STN, beta power in the GPi may be readily detected, modulates more with movement, and relates more to clinical impairment. Together, this could point to the GPi as a potentially effective target for beta-based adaptive DBS. [ABSTRACT FROM AUTHOR]

Background and Aims: Pathological high amplitude of beta oscillations is thought as the underlying mechanism of motor symptoms in Parkinson's disease (PD), in particular with regard to bradykinesia. In addition, abnormality in a neurophysiological phenomenon labeled sensory attenuation has been found in patients with PD. The current study explored the hypothesis that the abnormal sensory attenuation has a causal link with the typical abnormality in beta oscillations in PD.Methods: The study tested sixteen right-handed patients with a diagnosis of PD and 22 healthy participants, which were matched by age and gender. Somatosensory evoked potentials were elicited through electrical stimulation of the median nerve at the wrist. Electrical activity was recorded at the scalp using a 128 channels EEG. Somatosensory evoked potentials were recorded in 2 conditions: at rest and at the onset of a voluntary movement, which was a self-paced abduction movement of the right thumb.Results: Healthy participants showed a reduction of the N20-P25 amplitude at the onset of the right thumb abduction compared to the rest condition (P < 0.05). When patients were OFF medication, they showed mild reduction of the N20-P25 component at movement onset (P < 0.05). On the contrary, they did show greater attenuation of the N20-P25 component at the onset of movement compared to the rest condition when ON medication (P < 0.05). There was no significant evidence of a link between the degree of sensory attenuation and the change in beta oscillations in our cohort of patients.Conclusion: These results confirmed a significant link between dopaminergic modulation and sensory attenuation. However, the sensory attenuation and beta oscillations were found as two independent phenomena.

Background and Aims: Pathological high amplitude of beta oscillations is thought as the underlying mechanism of motor symptoms in Parkinson's disease (PD), in particular with regard to bradykinesia. In addition, abnormality in a neurophysiological phenomenon labeled sensory attenuation has been found in patients with PD. The current study explored the hypothesis that the abnormal sensory attenuation has a causal link with the typical abnormality in beta oscillations in PD. Methods: The study tested sixteen right-handed patients with a diagnosis of PD and 22 healthy participants, which were matched by age and gender. Somatosensory evoked potentials were elicited through electrical stimulation of the median nerve at the wrist. Electrical activity was recorded at the scalp using a 128 channels EEG. Somatosensory evoked potentials were recorded in 2 conditions: at rest and at the onset of a voluntary movement, which was a self-paced abduction movement of the right thumb. Results: Healthy participants showed a reduction of the N20-P25 amplitude at the onset of the right thumb abduction compared to the rest condition (P < 0.05). When patients were OFF medication, they showed mild reduction of the N20-P25 component at movement onset (P < 0.05). On the contrary, they did show greater attenuation of the N20-P25 component at the onset of movement compared to the rest condition when ON medication (P < 0.05). There was no significant evidence of a link between the degree of sensory attenuation and the change in beta oscillations in our cohort of patients. Conclusion: These results confirmed a significant link between dopaminergic modulation and sensory attenuation. However, the sensory attenuation and beta oscillations were found as two independent phenomena. [ABSTRACT FROM AUTHOR]

Abstract Introduction The aim of this study was to build a random forest classifier to improve the diagnostic accuracy in differentiating dementia with Lewy bodies (DLB) from Alzheimer's disease (AD) and to quantify the relevance of multimodal diagnostic measures, with a focus on electroencephalography (EEG). Methods A total of 66 DLB, 66 AD patients, and 66 controls were selected from the Amsterdam Dementia Cohort. Quantitative EEG (qEEG) measures were combined with clinical, neuropsychological, visual EEG, neuroimaging, and cerebrospinal fluid data. Variable importance scores were calculated per diagnostic variable. Results For discrimination between DLB and AD, the diagnostic accuracy of the classifier was 87%. Beta power was identified as the single‐most important discriminating variable. qEEG increased the accuracy of the other multimodal diagnostic data with almost 10%. Discussion Quantitative EEG has a higher discriminating value than the combination of the other multimodal variables in the differentiation between DLB and AD.

Highlights • Beta band EEG power predicts baseball batting performance. • Demonstrates use of mobile EEG. • Provides insight in performance prediction. • Beta power reflective of the "sports zone". Abstract Mental state prior to sports skill execution is related to subsequent performance. For example, relationships between pre-performance electroencephalogram (EEG) power and subsequent movement outcomes in golf putting, pistol shooting, and basketball free throw shooting have been previously reported. With that said, the existing body of research examining the pre-performance EEG – performance relationship has been focused on the execution of internally as opposed to externally-paced motor skills. Given that the execution of internally and externally-paced movements are dependent on different neural pathways, in the present study we examined whether or not pre-performance EEG power predicted ensuing performance of an externally-paced motor skill – baseball batting. Sixty-seven baseball players had EEG data recorded for 120 s prior to batting practice. Performance was assessed by three expert coaches and the accuracy of coach performance ratings was verified via Generalizability Theory. An analysis of our data revealed an inverse relationship between frontal EEG power in the beta range and subsequent batting performance - reduced beta power was associated with better batting performance whereas increased beta power was associated with worse batting performance. Our results are in line with prior research that has demonstrated a relationship between increased EEG power in the beta range and the subsequent commitment of motor errors in addition to the aforementioned work examining pre-performance EEG and the execution of internally-paced motor skills. [ABSTRACT FROM AUTHOR]

Aim The Sewol ferry capsizing accident on South Korea's southern coast resulted in the death of 304 people, and serious bereavement problems for their families. Electroencephalography (EEG) beta frequency is associated with psychiatric symptoms, such as insomnia. The aim of this study was to investigate the relation between frontal beta power, psychological symptoms, and insomnia in the bereaved families. Methods Eighty-four family members of the Sewol ferry victims (32 men and 52 women) were recruited and their EEG was compared with that of 25 (13 men and 12 women) healthy controls. A two-channel EEG device was used to measure cortical activity in the frontal lobe. Symptom severity of insomnia, post-traumatic stress disorder, complicated grief, and anxiety were evaluated. Results The bereaved families showed a higher frontal beta power than healthy controls. Subgroup analysis showed that frontal beta power was lower in the individuals with severe insomnia than in those with normal sleep. There was a significant inverse correlation between frontal beta power and insomnia symptom in the bereaved families. Conclusion This study suggests that increased beta power, reflecting the psychopathology in the bereaved families of the Sewol ferry disaster, may be a compensatory mechanism that follows complex trauma. Frontal beta power could be a potential marker indicating the severity of sleep disturbances. Our results suggest that sleep disturbance is an important symptom in family members of the Sewol ferry disaster's victims, which may be screened by EEG beta power. [ABSTRACT FROM AUTHOR]

Background: Memory deficits are dominant in dementia and are positively correlated with electroencephalographic (EEG) beta power. EEG beta power can predict the progression of Alzheimer´s (AD) as early as at the stage of mild cognitive impairment (MCI) and could possibly be used as surrogate marker for memory impairment. The objective of this study is to analyze the relationship between frontal and parietal EEG beta power and memory-test outcome. Frontal and parietal beta power is analyzed for a resting state and an eyes-closed backward counting condition and related to memory impairment parameters.Methods: A total of 28 right-handed female geriatric patients (mean age = 80.6) participated voluntarily in this study. Beta 1 (12.9-19.2 Hz) and beta 2 (19.2-32.4 Hz) EEG power at F3, F4, Fz, P3, P4, and Pz are correlated with immediate wordlist recall, delayed wordlist recall, recognition of learned words, and delayed figure recall. For classification between impaired and intact memory, we calculated a binary logistic regression model with memory impairment as a dependent variable and beta 2 power as an independent variable.Results: We found significant positive correlations between frontal and parietal beta power and delayed memory recall. A significant correlation (Bonferroni correction, p < 0.05) was found at F4 beta 2 during backward counting. The binary logistic regression model with F4 beta 2 power during the counting condition as a predictor yielded a sensitivity of 76.9% (95% CI) and a specificity of 73.3% (95% CI) for classifying patients into "verbal-memory impaired" and "intact."Conclusions: EEG beta 2 power recorded during a backward counting condition with eyes closed can be used as surrogate marker for verbal memory impairment in geriatric patients. Antidepressant treatment was correlated with EEG data in resting state but not in counting condition. Further studies are necessary to verify the results of this pilot study. [ABSTRACT FROM AUTHOR]

Enhanced beta-band activity recorded in patients suffering from Parkinson's Disease (PD) has been described as a potential physiomarker for disease severity. Beta power is suppressed by Levodopa intake and STN deep brain stimulation (DBS) and correlates with disease severity across patients. The aim of the present study was to explore the promising signature of the physiomarker in the spatial domain. Based on local field potential data acquired from 54 patients undergoing STN-DBS, power values within alpha, beta, low beta, and high beta bands were calculated. Values were projected into common stereotactic space after DBS lead localization. Recorded beta power values were significantly higher at posterior and dorsal lead positions, as well as in active compared with inactive pairs. The peak of activity in the beta band was situated within the sensorimotor functional zone of the nucleus. In contrast, higher alpha activity was found in a more ventromedial region, potentially corresponding to associative or premotor functional zones of the STN. Beta and alpha-power peaks were then used as seeds in a fiber tracking experiment. Here, the beta-site received more input from primary motor cortex whereas the alphasite was more strongly connected to premotor and prefrontal areas. The results summarize predominant spatial locations of frequency signatures recorded in STN-DBS patients in a probabilistic fashion. The site of predominant beta-activity may serve as an electrophysiologically determined target for optimal outcome in STN-DBS for PD in the future. [ABSTRACT FROM AUTHOR]

The failure to retain memory for extinguished fear plays a major role in the maintenance of posttraumatic stress disorder (PTSD), with successful extinction recall necessary for symptom reduction. Disturbed sleep, a hallmark symptom of PTSD, impairs fear extinction recall. However, our understanding of the electrophysiological mechanisms underpinning sleep's role in extinction retention remains underdetermined. We examined the relationship between the microarchitecture of sleep and extinction recall in healthy humans (n = 71, both male and females included) and a pilot study in individuals with PTSD (n = 12). Participants underwent a fear conditioning and extinction protocol over 2 days, with sleep recording occurring between conditioning and extinction. Twenty-four hours after extinction learning, participants underwent extinction recall. Power spectral density (PSD) was computed for pre- and post-extinction learning sleep. Increased beta-band PSD (~17-26 Hz) during pre-extinction learning sleep was associated with worse extinction recall in healthy participants (r = 0.41, p = .004). Beta PSD was highly stable across three nights of sleep (intraclass correlation coefficients > 0.92). Results suggest beta-band PSD is specifically implicated in difficulties recalling extinguished fear., (© The Author(s) 2023. Published by Oxford University Press on behalf of Sleep Research Society.)

Walking on two legs is inherently unstable. Still, we humans perform remarkable well at it, mostly without falling. To gain more understanding of the role of the brain in controlling gait stability we measured brain activity using electro-encephalography (EEG) during stabilized and normal walking.Subjects walked on a treadmill in two conditions, each lasting 10 minutes; normal, and while being laterally stabilized by elastic cords. Kinematics of trunk and feet, electro-myography (EMG) of neck muscles, as well as 64-channel EEG were recorded. To assess gait stability the local divergence exponent, step width, and trunk range of motion were calculated from the kinematic data. We used independent component analysis to remove movement, EMG, and eyeblink artifacts from the EEG, after which dynamic imaging of coherent sources beamformers were determined to identify cortical sources that showed a significant difference between conditions. Stabilized walking led to a significant increase in gait stability, i.e. lower local divergence exponents. Beamforming analysis of the beta band activity revealed significant sources in bilateral pre-motor cortices. Projection of sensor data on these sources showed a significant difference only in the left premotor area, with higher beta power during stabilized walking, specifically around push-off, although only significant around contralateral push-off. It appears that even during steady gait the cortex is involved in the control of stability.