Beta Synchronization Research Articles

Long-Lasting Event-Related Beta Synchronizations of Electroencephalographic Activity in Response to Support-Surface Perturbations During Upright Stance: A Pilot Study Associating Beta Rebound and Active Monitoring in the Intermittent Postural Control.

Movement related beta band cortical oscillations, including beta rebound after execution and/or suppression of movement, have drawn attention in upper extremity motor control literature. However, fewer studies focused on beta band oscillations during postural control in upright stance. In this preliminary study, we examined beta rebound and other components of electroencephalogram (EEG) activity during perturbed upright stance to investigate supraspinal contributions to postural stabilization. Particularly, we aimed to clarify the timing and duration of beta rebound within a non-sustained, but long-lasting postural recovery process that occurs more slowly compared to upper extremities. To this end, EEG signals were acquired from nine healthy young adults in response to a brief support-surface perturbation, together with the center of pressure, the center of mass and electromyogram (EMG) activities of ankle muscles. Event-related potentials (ERPs) and event-related spectral perturbations were computed from EEG data using the perturbation-onset as a triggering event. After short-latency (<0.3 s) ERPs, our results showed a decrease in high-beta band oscillations (event-related desynchronization), which was followed by a significant increase (event-related synchronization) in the same band, as well as a decrease in theta band oscillations. Unlike during upper extremity motor tasks, the beta rebound in this case was initiated before the postural recovery was completed, and sustained for as long as 3 s with small EMG responses for the first half period, followed by no excessive EMG activities for the second half period. We speculate that those novel characteristics of beta rebound might be caused by slow postural dynamics along a stable manifold of the unstable saddle-type upright equilibrium of the postural control system without active feedback control, but with active monitoring of the postural state, in the framework of the intermittent control.

Beta synchrony for expressive language lateralizes to right hemisphere in development

A left perisylvian network is known to support language in healthy adults. Low-beta (13–23 Hz) event-related desynchrony (ERD) has been observed during verb generation, at approximately 700–1200 ms post-stimulus presentation in past studies; the signal is known to reflect increased neuronal firing and metabolic demand during language production. In contrast, concurrent beta event-related synchrony (ERS) is thought to reflect neuronal inhibition but has not been well studied in the context of language. Further, while low-beta ERD for expressive language has been found to gradually shift from bilateral in childhood to left hemispheric by early adulthood, developmental lateralization of ERS has not been established. We used magnetoencephalography to study low beta ERS lateralization in a group of children and adolescents (n = 78), aged 4 to less than 19 years, who performed covert verb generation. We found that the youngest children had bilateral ERD and ERS. By adolescence, low-beta ERD was predominantly left lateralized in perisylvian cortex (i.e., Broca’s and Wernicke’s regions), while beta ERS was predominantly right lateralized. Increasing lateralization was significantly correlated to age for both ERD (Spearman’s r = 0.45, p < 0.01) and ERS (Spearman’s r = − 0.44, p < 0.01). Interestingly, while ERD lateralized in a linear manner, ERS lateralization followed a nonlinear trajectory, suggesting distinct developmental trajectories. Implications to early-age neuroplasticity and neuronal inhibition are discussed.

Subthalamic beta-targeted neurofeedback speeds up movement initiation but increases tremor in Parkinsonian patients.

Previous studies have explored neurofeedback training for Parkinsonian patients to suppress beta oscillations in the subthalamic nucleus (STN). However, its impacts on movements and Parkinsonian tremor are unclear. We developed a neurofeedback paradigm targeting STN beta bursts and investigated whether neurofeedback training could improve motor initiation in Parkinson's disease compared to passive observation. Our task additionally allowed us to test which endogenous changes in oscillatory STN activities are associated with trial-to-trial motor performance. Neurofeedback training reduced beta synchrony and increased gamma activity within the STN, and reduced beta band coupling between the STN and motor cortex. These changes were accompanied by reduced reaction times in subsequently cued movements. However, in Parkinsonian patients with pre-existing symptoms of tremor, successful volitional beta suppression was associated with an amplification of tremor which correlated with theta band activity in STN local field potentials, suggesting an additional cross-frequency interaction between STN beta and theta activities.

Beta-Range Corticomuscular Coupling Reflects Asymmetries in Hand Movement.

Hand movement in humans is verified as asymmetries and lateralization, and two hemispheres make some distinct but complementary contributions in the control of hand movement. However, little research has been done on whether the information transfer of the motor system is different between left and right hand movement. Considering the importance of functional corticomuscular coupling (FCMC) between the motor cortex and contralateral muscle in movement assessment, this study aimed to explore the differences between left and right hand by investigating the interaction between muscle and brain activity. Here, we applied the transfer spectral entropy (TSE) algorithm to quantize the connection between electroencephalogram (EEG) over the brain scalp and electromyogram (EMG) from extensor digitorum (ED) and flexor digitorum superficialis (FDS) muscles recorded simultaneously during a gripping task. Eight healthy subjects were enrolled in this study. Results showed that left hand yielded narrower and lower beta synchronization compared to the right. Further analysis indicated coupling strength in EEG-EMG(FDS) combination was higher at beta band than that in EEG-EMG(ED) combination, and exhibited distinct differences between descending (EEG to EMG direction) and ascending (EMG to EEG direction) direction. This study presents the distinctions of beta-range FCMC between left and right hand, and confirms the importance of beta synchronization in understanding the mechanism of motor stability control. The cortex-muscle FCMC might be used as an evaluation approach to explore the difference between left and right movement system.

Beta Rebound as an Index of Temporal Integration of Somatosensory and Motor Signals.

Modulation of cortical beta rhythm (15–30 Hz) is present during preparation for and execution of voluntary movements as well as during somatosensory stimulation. A rebound in beta synchronization is observed after the end of voluntary movements as well as after somatosensory stimulation and is believed to describe the return to baseline of sensorimotor networks. However, the contribution of efferent and afferent signals to the beta rebound remains poorly understood. Here, we applied electrical median nerve stimulation (MNS) to the right side followed by transcranial magnetic stimulation (TMS) on the left primary motor cortex after either 15 or 25 ms. Because the afferent volley reaches the somatosensory cortex after about 20 ms, TMS on the motor cortex was either anticipating or following the cortical arrival of the peripheral stimulus. We show modulations in different beta sub-bands and in both hemispheres, following a pattern of greater resynchronization when motor signals are paired with a peripheral one. The beta rebound in the left hemisphere (stimulated) is modulated in its lower frequency range when TMS precedes the cortical arrival of the afferent volley. In the right hemisphere (unstimulated), instead, the increase is limited to higher beta frequencies when TMS is delivered after the arrival of the afferent signal. In general, we demonstrate that the temporal integration of afferent and efferent signals plays a key role in the genesis of the beta rebound and that these signals may be carried in parallel by different beta sub-bands.

Early Consciousness Disorder in Acute Large Hemispheric Infarction: An Analysis Based on Quantitative EEG and Brain Network Characteristics.

Large hemispheric infarction (LHI) is an ischemic stroke affecting at least two-thirds of the middle cerebral artery territory, with or without involvement of the anterior cerebral artery or posterior cerebral artery, and approximately 77% of LHI patients have early consciousness disorder (ECD). We constructed a functional brain network for LHI patients with an acute consciousness disorder to identify new diagnostic markers related to ECDs by analyzing brain network characteristics and mechanisms. Between August 1, 2017, and September 30, 2018, patients with acute (< 1month) LHI were admitted to the neurocritical care unit at Xuanwu Hospital of Capital Medical University. Electroencephalography (EEG) data were recorded, and the MATLAB platform (2017b) was used to calculate spectral power, entropy, coherence and phase synchronization. The quantitative EEG and brain network characteristics of different consciousness states and different frequency bands were analyzed (α = 0.05). EEG data were recorded 38 times in 30 patients, 25 of whom were in the ECD group, while 13 patients were in the conscious group. (1) Spectral power analysis: The conscious group had higher beta relative spectral power across the whole brain, higher alpha spectral power in the frontal-parietal lobe on the infarction contralateral side, and lower theta and delta spectral power in the central-occipital lobe on the infarction contralateral side than the ECD group. (2) Entropy analysis: The conscious group had higher approximate entropy (ApEn) and permutation entropy (PeEn) across the whole brain than the ECD group. (3) Coherence: The conscious group had higher alpha coherence in nearly the whole brain and higher beta coherence in the bilateral frontal-parietal and parietal-occipital lobes than the ECD group. (4) Phase synchronization: The conscious group had higher alpha and beta synchronization in nearly the whole brain, particularly in the frontal-parietal and parietal-occipital lobes, than the ECD group. (5) Graph theory: The conscious group had higher small-worldness in each frequency band than the ECD group. In patients with LHI, higher levels of consciousness were associated with more alpha and beta oscillations and fewer delta and theta oscillations. Higher ApEn, PeEn, total brain connectivity, and small-worldness and a wider signal distribution range corresponded to a higher consciousness level.

Supplementary Material for ``Long-lasting event-related beta synchronizations of electroencephalographic activity in response to support-surface perturbations during upright stance"

Supplementary Material for ``Long-lasting event-related beta synchronizations of electroencephalographic activity in response to support-surface perturbations during upright stance"

Supplementary Material for ``Long-lasting event-related beta synchronizations of electroencephalographic activity in response to support-surface perturbations during upright stance"

Supplementary Material for ``Long-lasting event-related beta synchronizations of electroencephalographic activity in response to support-surface perturbations during upright stance"

Movement speed effects on beta-band oscillations in sensorimotor cortex during voluntary activity.

Beta-band oscillations are a dominant feature in the sensorimotor system, which includes movement-related beta desynchronization (MRBD) during the preparation and execution phases of movement and postmovement beta synchronization (PMBS) on movement cessation. Many studies have linked this rhythm to motor functions. However, its associations to the movement speed are still unclear. We make a hypothesis that PMBS will be modulated with increasing of movement speeds. We assessed the MRBD and PMBS during isotonic slower self-paced and ballistic movements with 15 healthy subjects. Furthermore, we conduct an additional control experiment with the isometric contraction with two levels of forces to match those in the isotonic slower self-paced and ballistic movements separately. We found that the amplitude of PMBS but not MRBD in motor cortex is modulated by the speed during voluntary movement. PMBS was positively correlated with movement speed and acceleration through the partial correlation analysis. However, there were no changes in the PMBS and MRBD during the isometric contraction with two levels of forces. These results demonstrate a different function of PMBS and MRBD to the movement speed during voluntary activity and suggest that the movement speed would affect the amplitude of PMBS.NEW & NOTEWORTHY Beta-band oscillations are a dominant feature in the sensorimotor system that associate to the motor function. We found that the movement-related postmovement beta synchronization (PMBS) over the contralateral sensorimotor cortex was positively correlated with the speed of a voluntary movement, but the movement-related beta desynchronization (MRBD) was not. Our results show a differential response of the PMBS and MRBD to the movement speed during voluntary movement.

Synchrony Drives Motor Cortex Beta Bursting, Waveform Dynamics, and Phase-Amplitude Coupling in Parkinson's Disease.

Several lines of inquiry have separately identified beta oscillations, synchrony, waveform shape, and phase-amplitude coupling as important but sometimes inconsistent factors in the pathophysiology of Parkinson's disease. What has so far been lacking is a means by which these neurophysiological parameters are interrelated and how they relate to clinical symptomatology. To clarify the relationship among oscillatory power, bursting, synchrony, and phase-amplitude coupling, we recorded local field potentials/electrocorticography from hand motor and premotor cortical area in human subjects with c (N = 10) and Parkinson's disease (N = 22) during deep brain stimulator implantation surgery (14 females, 18 males). We show that motor cortical high beta oscillations in Parkinson's disease demonstrate increased burst durations relative to essential tremor patients. Notably, increased corticocortical synchrony between primary motor and premotor cortices precedes motor high beta bursts, suggesting a possible causal relationship between corticocortical synchrony and localized increases in beta power. We further show that high beta bursts are associated with significant changes in waveform shape and that beta-encoded phase-amplitude coupling is more evident during periods of high beta bursting. These findings reveal a deeper structure to the pathologic changes identified in the neurophysiology of Parkinson's disease, suggesting mechanisms by which the treatment may be enhanced using targeted network synchrony disruption approaches.SIGNIFICANCE STATEMENT Understanding Parkinson's disease pathophysiology is crucial for optimizing symptom management. Present inconsistencies in the literature may be explained by temporal transients in neural signals driven by transient fluctuations in network synchrony. Synchrony may also act as a unifying phenomenon for the pathophysiological observations reported in Parkinson's disease. Here, simultaneous recordings from motor cortices show that increases in network beta synchrony anticipate episodes of beta bursting. We furthermore identify beta bursting as being associated with changes in waveform shape and increases in phase-amplitude coupling. Our results identify network synchrony as a driver of various pathophysiological observations reported in the literature and account for inconsistencies in the literature by virtue of the temporally variable nature of the phenomenon.

2063-P: Quantitative Analysis of Human and Mouse Islet Tissue Structure

The pancreatic islet is a complex tissue consisting of multiple endocrine cell types, capillaries, and a peri-islet basement membrane. The 3D organization of cells, blood vessels, and basement membrane (BM), enhances islet function by (1) supporting beta cell electrochemical coupling and synchronization through gap junctions between adjacent cells and (2) providing access to nutrients and signals for beta cell survival and function through contact with capillaries and BM. Though a quantitative understanding of islet structure is lacking, there is strong evidence linking islet structural changes to diabetes progression. Studies of these changes in islet structure will enhance understanding of diabetes-related losses in islet function and lead to the development of new therapeutics for diabetic and prediabetic patients. Here, we have quantified healthy adult islet tissue structure through a single-cell analysis of the cell-cell and cell-BM interactions at individual endocrine cell plasma membranes. We have used this single-cell data to identify endocrine cell subtypes, as defined by cell morphology and structural niche. We have also identified spatially-defined clusters of beta cells through a graph analysis of cell-cell connectivity. We report a baseline quantification of structure for healthy adult human and mouse islets. These data both provide an answer to the ongoing debate regarding the differences in structure between human and mouse islets and set the stage for future quantification of islet structure in diabetes. Disclosure O.A. Creasey: None. J.B. Sneddon: Advisory Panel; Self; Encellin. Advisory Panel; Spouse/Partner; Encellin. Z.J. Gartner: None. Funding National Science Foundation (1650113, DBI-1548297); National Institutes of Health (P30DK063720); Chan-Zuckerberg Biohub; Bakar Foundation

Sensorimotor beta power reflects the precision-weighting afforded to sensory prediction errors

It has been proposed that accurate motor control relies on Bayesian inference that integrates sensory input with prior contextual knowledge (Bays and Wolpert, 2007; Körding and Wolpert, 2004; Wolpert et al., 1995). Recent evidence has suggested that modulations in beta power (∼12–30 Hz) measured over sensorimotor cortices using electroencephalography (EEG) may represent parameters of Bayesian inference. While the well characterised post-movement beta synchronisation has been shown to correlate with prediction error (H. Tan, Jenkinson, & Brown, 2014; Huiling Tan, Wade, & Brown, 2016), recent evidence suggests that beta power may also represent uncertainty measures (Tan et al., 2016; Tzagarakis et al., 2015). The current study aimed to measure the neurophysiological correlates of uncertainty mediating Bayesian updating during a visuomotor adaptation paradigm in healthy human participants. In particular, sensory uncertainty was directly modulated to measure its effect on sensorimotor beta power. Participant's behaviour was modelled using the Hierarchical Gaussian Filter (HGF) in order to extract the latent variables involved in learning actions required by the task and correlate these with the measured EEG. We found that sensorimotor beta power correlated with inverse uncertainty afforded to sensory prediction errors both prior to and following a movement. This suggests that sensorimotor beta oscillations may more readily represent relative uncertainty within the sensorimotor system rather than error. Neurophysiological models describing the generation of beta oscillations offer a potential mechanism by which this neural signature may encode latent uncertainty parameters. This is essential for understanding how the brain controls behaviour.

2151-P: Quantification of Tissue Structure in Human and Mouse Islets

The pancreatic islet is a complex tissue consisting of multiple endocrine cell types, capillaries, and a peri-islet basement membrane. The 3D organization of cells, blood vessels, and basement membrane (BM), enhances islet function by (1) supporting beta cell electrochemical coupling and synchronization through gap junctions between adjacent cells and (2) providing access to nutrients and integrin-mediated signals for beta cell survival and function through contact with capillaries and BM. Though a quantitative understanding of islet structure is lacking, there is strong evidence linking islet structural changes to diabetes progression. Studies of these changes in islet structure will enhance understanding of diabetes-related losses in islet function and lead to the development of new therapeutics for diabetic and prediabetic patients. Here, we present a novel method for quantitative analysis of islet structure in terms of local cell-cell and cell-BM interactions at endocrine cell plasma membrane surfaces. The number and surface area of individual cell-cell and cell-BM interfaces are measured from high-resolution 3D confocal images of human and mouse islets immunolabeled for endocrine cell markers, epithelial cell plasma membranes, and BM. These measurements quantify both cellular interconnectivity and access to signals supporting beta cell survival and function. We report a baseline quantification of structure for healthy adult human and mouse islets. These data both provide a definitive answer to the ongoing debate regarding the differences in structure between human and mouse islets and set the stage for future quantification of islet structure in diabetes. Disclosure O.A. Creasey: None. D. Elnatan: None. J.B. Sneddon: Advisory Panel; Spouse/Partner; Akouos. Advisory Panel; Self; Encellin. Advisory Panel; Spouse/Partner; Encellin. Consultant; Self; Semma Therapeutics, Inc. Z.J. Gartner: Stock/Shareholder; Self; Provenance, Scribe Biosciences. Funding National Institutes of Health; National Science Foundation Graduate Research Fellowship Program; National Science Foundation; University of California, San Francisco Center for Cellular Construction; University of California, San Francisco Diabetes Research Center

Low-intensity pulsed ultrasound modulates multi-frequency band phase synchronization between LFPs and EMG in mice

Objective. Low-intensity pulsed ultrasound stimulation (LIPUS) targeted to the mouse motor cortex can simultaneously induce local field potentials (LFPs) and electromyogram (EMG) responses. However, the functional coupling relationship between LFP and EMG signals has not been elucidated to date. This study aimed to investigate the phase synchronization between LFP and EMG signals induced by LIPUS over the mouse motor cortex. Approach. LIPUS at 500 kHz with varied sonication intensities and duty cycles (DCs), was delivered to the mouse motor cortex. LFPs of the motor cortex and EMG responses of the tail were simultaneously recorded during LIPUS. We then evaluated two control groups using the same experimental parameters, but changed the position of EMG recording to the hind leg and the ultrasound stimulus target to the primary visual cortex. The phase synchronization between LFPs and EMG signals was evaluated by performing a phase locking value (PLV) analysis in the time-frequency domain and was compared across specific frequency bands. Main results. The results showed that LIPUS increased the phase synchronization in a broad frequency band (5–150 Hz), and the maximum duration of the increased PLV was stable at approximately 200 ms. It is worth noting that the sonication parameters directly affected the time-frequency domain distribution of cortico-muscular synchronization. Specifically, significant alpha and beta synchronization appeared at 0.2 and 0.4 W cm−2 Isppa stimulation, while gamma synchronization occurred at 0.8 and 1.1 W cm−2 Isppa stimulation. The synchronization in all frequency bands apparently increased at 30% DC. Beta synchronization weakened when the DC was less than 30%. Furthermore, no significant phase synchronization was observed in the two control groups. Significance. Considering the close association between specific motor function and cortical-muscular synchronization in different frequency bands, we suggest that LIPUS over the motor cortex could selectively modulate motor function via different sonication parameters. Additionally, the phase synchronization between LFPs and EMG might be an invaluable index for assessing the ultrasonic effect on the motor system, which could be used in future clinical research to optimize ultrasound parameters. Thus, this study provides new insight into evaluating the neuromodulatory effects of ultrasound on motor function, thereby supporting the therapeutic application of ultrasound in neurological disorders characterized by motor deficits.

Thalamocortical dynamics underlying spontaneous transitions in beta power in Parkinsonism

Parkinson's disease (PD) is a neurodegenerative condition in which aberrant oscillatory synchronization of neuronal activity at beta frequencies (15–35 Hz) across the cortico-basal ganglia-thalamocortical circuit is associated with debilitating motor symptoms, such as bradykinesia and rigidity. Mounting evidence suggests that the magnitude of beta synchrony in the parkinsonian state fluctuates over time, but the mechanisms by which thalamocortical circuitry regulates the dynamic properties of cortical beta in PD are poorly understood. Using the recently developed generic Dynamic Causal Modelling (DCM) framework, we recursively optimized a set of plausible models of the thalamocortical circuit (n = 144) to infer the neural mechanisms that best explain the transitions between low and high beta power states observed in recordings of field potentials made in the motor cortex of anesthetized Parkinsonian rats. Bayesian model comparison suggests that upregulation of cortical rhythmic activity in the beta-frequency band results from changes in the coupling strength both between and within the thalamus and motor cortex. Specifically, our model indicates that high levels of cortical beta synchrony are mainly achieved by a delayed (extrinsic) input from thalamic relay cells to deep pyramidal cells and a fast (intrinsic) input from middle pyramidal cells to superficial pyramidal cells. From a clinical perspective, our study provides insights into potential therapeutic strategies that could be utilized to modulate the network mechanisms responsible for the enhancement of cortical beta in PD. Specifically, we speculate that cortical stimulation aimed to reduce the enhanced excitatory inputs to either the superficial or deep pyramidal cells could be a potential non-invasive therapeutic strategy for PD.

Beta synchrony in the cortico-basal ganglia network during regulation of force control on and off dopamine.

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 dopaminerelated suppression of cortico-basal ganglia beta coupling is linked to faster force adjustments.

Electroconvulsive Therapy Modulates Resting-State EEG Oscillatory Pattern and Phase Synchronization in Nodes of the Default Mode Network in Patients With Depressive Disorder.

Introduction: Electroconvulsive therapy (ECT) has antidepressant effects, but it also has possible cognitive side effects. The effects of ECT on neuronal oscillatory pattern and phase synchronization, and the relationship between clinical response or cognitive change and electroencephalogram (EEG) measurements remain elusive.Methods: Individuals with unipolar depressive disorder receiving bilateral ECT were recruited. Five minutes of resting, eyes-closed, 19-lead EEG recordings were obtained before and after a course of ECT. Non-overlapping 60 artifact-free epocs of 2-s duration were used for the analyses. We used exact low resolution electromagnetic tomography (eLORETA) to compute the whole-brain three-dimensional intracortical distribution of current source density (CSD) and phase synchronization among 28 regions-of-interest (ROIs). Paired t-tests were used to identify cortical voxels and connectivities showing changes after ECT. Montgomery Asberg Depression Rating Scale (MADRS) and Mini-Mental State Examination (MMSE) were used to evaluate the severity of depression and the global cognitive function. Correlation analyses were conducted to identify the relationship between changes in the EEG measurements and changes in MADRS or MMSE.Results: Thirteen depressed patients (five females, mean age: 58.4 years old) were included. ECT increased theta CSD in the anterior cingulate cortex (ACC), and decreased beta CSD in the frontal pole (FP), and gamma CSD in the inferior parietal lobule (IPL). ECT increased theta phase synchronization between the posterior cingulate cortex (PCC) and the anterior frontal cortex, and decreased beta phase synchronization between the PCC and temporal regions. A decline in beta synchronization in the left hemisphere was associated with cognitive changes after ECT.Conclusion: ECT modulated resting-state EEG oscillatory patterns and phase synchronization in central nodes of the default mode network (DMN). Changes in beta synchronization in the left hemisphere might explain the ECT-related cognitive side effects.

Cortical changes detected with MEG in Tourette syndrome following [formula omitted]9-tetrahydrocannabinol challenge test

Cannabinoids have surged as potential therapeutic drugs in neurological disorders, especially in movement disorders. We investigated the responsivity to Δ9-tetrahydrocannabinol (THC) of a 43-years-old woman affected by Tourette Syndrome (TS). To reveal cortical changes induced by THC and correlating with the decrease of tics, we acquired magnetoencephalography (MEG) during a Go/No Go (GNG) task, before and after THC administration. To characterize the modulation of cortical activity, the event-related desynchronization/synchronization (ERD/ERS) analysis was applied. To localize the source related to frequency of interest, the Dynamical Imaging of Coherent Sources method was applied4 contrasting two periods of interest (‘Go’ and ‘no Go’ conditions). In ‘Go’ condition, no differences between pre and post THC was noticed. In ‘No go’ condition, after the THC intake, a decrease in beta band activity of cortical motor areas was followed by a noteworthy increase of beta activity within 1s after the presentation of the cue, correlated with an amelioration of tics control. Our findings showed that the increased tics control after THC intake was associated to a restoration of the ERD/ERS (namely beta synchronization) involving precentral and postcentral gyri, thus highlighting that THC-induced modifications impacted on cortical motor circuitries.

Phase-Dependent Suppression of Beta Oscillations in Parkinson's Disease Patients.

Synchronized oscillations within and between brain areas facilitate normal processing, but are often amplified in disease. A prominent example is the abnormally sustained beta-frequency (∼20 Hz) oscillations recorded from the cortex and subthalamic nucleus of Parkinson's disease patients. Computational modeling suggests that the amplitude of such oscillations could be modulated by applying stimulation at a specific phase. Such a strategy would allow selective targeting of the oscillation, with relatively little effect on other activity parameters. Here, activity was recorded from 10 awake, parkinsonian patients (6 male, 4 female human subjects) undergoing functional neurosurgery. We demonstrate that stimulation arriving on a particular patient-specific phase of the beta oscillation over consecutive cycles could suppress the amplitude of this pathophysiological activity by up to 40%, while amplification effects were relatively weak. Suppressive effects were accompanied by a reduction in the rhythmic output of subthalamic nucleus (STN) neurons and synchronization with the mesial cortex. While stimulation could alter the spiking pattern of STN neurons, there was no net effect on firing rate, suggesting that reduced beta synchrony was a result of alterations to the relative timing of spiking activity, rather than an overall change in excitability. Together, these results identify a novel intrinsic property of cortico-basal ganglia synchrony that suggests the phase of ongoing neural oscillations could be a viable and effective control signal for the treatment of Parkinson's disease. This work has potential implications for other brain diseases with exaggerated neuronal synchronization and for probing the function of rhythmic activity in the healthy brain.SIGNIFICANCE STATEMENT In Parkinson's disease (PD), movement impairment is correlated with exaggerated beta frequency oscillations in the cerebral cortex and subthalamic nucleus (STN). Using a novel method of stimulation in PD patients undergoing neurosurgery, we demonstrate that STN beta oscillations can be suppressed when consecutive electrical pulses arrive at a specific phase of the oscillation. This effect is likely because of interrupting the timing of neuronal activity rather than excitability, as stimulation altered the firing pattern of STN spiking without changing overall rate. These findings show the potential of oscillation phase as an input for “closed-loop” stimulation, which could provide a valuable neuromodulation strategy for the treatment of brain disorders and for elucidating the role of neuronal oscillations in the healthy brain.

Magnitude of the post-movement beta synchronization correlates with the variability of the ankle torque production

Objectives During and after the completion of a motor task, an event-related desynchronization (ERD) and synchronization (ERS) – i.e., a decrease and increase of the 13–31 Hz spectral magnitude–are respectively recorded over the motor cortex (M1). The ERD is supposed to reflect M1 involvement to perform the motor task [1] , [2] while the ERS is supposed to reflect an active “top-down” cortical inhibition of the motor command [1] , [3] . Studies revealed that ERD/S are modulated with the force level [1] . However, it remains to know whether ERD/S are related to the task performance, reflecting force control. We investigated the relationship between the ERD/S and the accuracy and variability of the force production. Methods Eleven healthy participants performed 50 × 10-s isometric right plantar flexion contractions at 20% of their maximal torque. The ankle torque and the M1 EEG activity were recorded. After appropriate preprocessing, the absolute and variable errors (AE/VE) of the ankle torque, respectively reflecting accuracy and variability of the motor task and the ERD were computed during the holding force phase. The ERS was computed 1-s after the end of the contraction. All data were normally distributed. Pearson correlations between ERD/S and AE/VE were computed. Results No significant correlation was found between the ERD and VE (r2 = 0.11; P = 0.75) nor between the ERD and AE (r2 = 0.56; P = 0.07). The ERS significantly increased as the VE increased (r2 = 0.8; P Conclusion These results suggest that the ERD is not linked with fine motor control modulating accuracy and variability of force. However, the significant ERS-VE relationship suggests that the more variable is the force produced, the more M1 is deactivated, probably reflecting an increased inhibition of the motor command.