Power Of Beta Oscillations Research Articles

Beta bursts in the parkinsonian cortico-basal ganglia network form spatially discrete ensembles

Defining spatial synchronisation of pathological beta oscillations is important, given that many theories linking them to parkinsonian symptoms propose a reduction in the dimensionality of the coding space within and/or across cortico-basal ganglia structures. Such spatial synchronisation could arise from a single process, with widespread entrainment of neurons to the same oscillation. Alternatively, the partially segregated structure of cortico-basal ganglia loops could provide a substrate for multiple ensembles that are independently synchronized at beta frequencies. Addressing this question requires an analytical approach that identifies groups of signals with a statistical tendency for beta synchronisation, which is unachievable using standard pairwise measures. Here, we utilized such an approach on multichannel recordings of background unit activity (BUA) in the external globus pallidus (GP) and subthalamic nucleus (STN) in parkinsonian rats. We employed an adapted version of a principle and independent component analysis-based method commonly used to define assemblies of single neurons (i.e., neurons that are synchronized over short timescales). This analysis enabled us to define whether changes in the power of beta oscillations in local ensembles of neurons (i.e., the BUA recorded from single contacts) consistently covaried over time, forming a “beta ensemble”. Multiple beta ensembles were often present in single recordings and could span brain structures. Membership of a beta ensemble predicted significantly higher levels of short latency (<5 ms) synchrony in the raw BUA signal and phase synchronisation with cortical beta oscillations, suggesting that they comprised clusters of neurons that are functionally connected at multiple levels, despite sometimes being non-contiguous in space. Overall, these findings suggest that beta oscillations do not comprise of a single synchronisation process, but rather multiple independent activities that can bind both spatially contiguous and non-contiguous pools of neurons within and across structures. As previously proposed, such ensembles provide a substrate for beta oscillations to constrain the coding space of cortico-basal ganglia circuits.

Hebbian plasticity induced by temporally coincident BCI enhances post-stroke motor recovery

Functional electrical stimulation (FES) can support functional restoration of a paretic limb post-stroke. Hebbian plasticity depends on temporally coinciding pre- and post-synaptic activity. A tight temporal relationship between motor cortical (MC) activity associated with attempted movement and FES-generated visuo-proprioceptive feedback is hypothesized to enhance motor recovery. Using a brain–computer interface (BCI) to classify MC spectral power in electroencephalographic (EEG) signals to trigger FES-delivery with detection of movement attempts improved motor outcomes in chronic stroke patients. We hypothesized that heightened neural plasticity earlier post-stroke would further enhance corticomuscular functional connectivity and motor recovery. We compared subcortical non-dominant hemisphere stroke patients in BCI-FES and Random-FES (FES temporally independent of MC movement attempt detection) groups. The primary outcome measure was the Fugl-Meyer Assessment, Upper Extremity (FMA-UE). We recorded high-density EEG and transcranial magnetic stimulation-induced motor evoked potentials before and after treatment. The BCI group showed greater: FMA-UE improvement; motor evoked potential amplitude; beta oscillatory power and long-range temporal correlation reduction over contralateral MC; and corticomuscular coherence with contralateral MC. These changes are consistent with enhanced post-stroke motor improvement when movement is synchronized with MC activity reflecting attempted movement.

Exploring the Feasibility of Bidirectional Control of Beta Oscillatory Power in Healthy Controls as a Potential Intervention for Parkinson's Disease Movement Impairment.

Neurofeedback (NF) is a promising intervention for improvements in motor performance in Parkinson's disease. This NF pilot study in healthy participants aimed to achieve the following: (1) determine participants' ability to bi-directionally modulate sensorimotor beta power and (2) determine the effect of NF on movement performance. A real-time EEG-NF protocol was used to train participants to increase and decrease their individual motor cortex beta power amplitude, using a within-subject double-blind sham-controlled approach. Movement was assessed using a Go/No-go task. Participants completed the NASA Task Load Index and provided verbal feedback of the NF task difficulty. All 17 participants (median age = 38 (19-65); 10 females) reliably reduced sensorimotor beta power. No participant could reliably increase their beta activity. Participants reported that the NF task was challenging, particularly increasing beta. A modest but significant increase in reaction time correlated with a reduction in beta power only in the real condition. Findings suggest that beta power control difficulty varies by modulation direction, affecting participant perceptions. A correlation between beta power reduction and reaction times only in the real condition suggests that intentional beta power reduction may shorten reaction times. Future research should examine the minimum beta threshold for meaningful motor improvements, and the relationship between EEG mechanisms and NF learning to optimise NF outcomes.

Visual perspective taking neural processing in forensic cases with high density EEG

This EEG study aims at dissecting the differences in the activation of neural generators between borderline personality disorder patients with court-ordered measures (BDL-COM) and healthy controls in visual perspective taking. We focused on the distinction between mentalizing (Avatar) and non-mentalizing (Arrow) stimuli as well as self versus other-perspective in the dot perspective task (dPT) in a sample of 15 BDL-COM cases and 54 controls, all of male gender. BDL-COM patients showed a late and diffuse right hemisphere involvement of neural generators contrasting with the occipitofrontal topography observed in controls. For Avatars only and compared to controls, the adoption of Self perspective involved a lower EEG activity in the left inferior frontal, right middle temporal cortex and insula in BDL-COM patients prior to 80 ms post-stimulus. When taking the Other-perspective, BDL-COM patients also showed a lower activation of superior frontal, right inferior temporal and fusiform cortex within the same time frame. The beta oscillation power was significantly lower in BDL-COM patients than controls between 400 and 1300 ms post stimulus in the Avatar-Other condition. These results indicate that BDL-COM patients display both altered topography of EEG activation patterns and reduced abilities to mobilize beta oscillations during the treatment of mentalistic stimuli in dPT.

Aging suppresses subthalamic neuronal activity in patients with Parkinson's disease.

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.

Potentiation of the depressant effect of alcohol by flunitrazepam in rats: an electrocorticographic, respiratory and electrocardiographic study.

Alcohol, a widely commercialized psychotropic drug, and the benzodiazepine Flunitrazepam, an anxiolytic widely prescribed for patients with anxiety and insomnia problems, are well known drugs and both act on the central nervous system. The misuse and the association of these two drugs are public health concerns in several countries and could cause momentary, long-lasting and even lethal neurophysiological problems due to the potentiation of their adverse effects in synergy. The present study observed the result of the association of these drugs on electrophysiological responses in the brain, heart, and respiratory rate in Wistar rats. 8 experimental groups were determined: control, one alcohol group (20% at a dose of 1ml/100g VO), three Flunitrazepam groups (doses 0.1; 0.2 and 0.3mg/kg) and three alcohol-Flunitrazepam groups (20% at a dose of 1ml/100g VO of alcohol, combined with 0.1; 0.2 and 0.3mg/kg of Flunitrazepam, respectively). The results showed that there was a more pronounced reduction in alpha and theta wave power in the alcohol-Flunitrazepam groups, a decrease in the power of beta oscillations and greater sedation. There was a progressive decrease in respiratory rate linked to the increase of Flunitrazepam dose in the alcohol-Flunitrazepam associated administration. It was observed alteration in heart rate and Q-T interval in high doses of Flunitrazepam. Therefore, we conclude that the association alcohol-Flunitrazepam presented deepening of depressant synergistic effects according to the increase in the dose of the benzodiazepine, and this could cause alterations in low frequency brain oscillations, breathing, and hemodynamics of the patient.

Changes in visually and auditory attended audiovisual speech processing in cochlear implant users: A longitudinal ERP study

Limited auditory input, whether caused by hearing loss or by electrical stimulation through a cochlear implant (CI), can be compensated by the remaining senses. Specifically for CI users, previous studies reported not only improved visual skills, but also altered cortical processing of unisensory visual and auditory stimuli. However, in multisensory scenarios, it is still unclear how auditory deprivation (before implantation) and electrical hearing experience (after implantation) affect cortical audiovisual speech processing.Here, we present a prospective longitudinal electroencephalography (EEG) study which systematically examined the deprivation- and CI-induced alterations of cortical processing of audiovisual words by comparing event-related potentials (ERPs) in postlingually deafened CI users before and after implantation (five weeks and six months of CI use). A group of matched normal-hearing (NH) listeners served as controls. The participants performed a word-identification task with congruent and incongruent audiovisual words, focusing their attention on either the visual (lip movement) or the auditory speech signal. This allowed us to study the (top-down) attention effect on the (bottom-up) sensory cortical processing of audiovisual speech.When compared to the NH listeners, the CI candidates (before implantation) and the CI users (after implantation) exhibited enhanced lipreading abilities and an altered cortical response at the N1 latency range (90–150 ms) that was characterized by a decreased theta oscillation power (4–8 Hz) and a smaller amplitude in the auditory cortex. After implantation, however, the auditory-cortex response gradually increased and developed a stronger intra-modal connectivity. Nevertheless, task efficiency and activation in the visual cortex was significantly modulated in both groups by focusing attention on the visual as compared to the auditory speech signal, with the NH listeners additionally showing an attention-dependent decrease in beta oscillation power (13–30 Hz).In sum, these results suggest remarkable deprivation effects on audiovisual speech processing in the auditory cortex, which partially reverse after implantation. Although even experienced CI users still show distinct audiovisual speech processing compared to NH listeners, pronounced effects of (top-down) direction of attention on (bottom-up) audiovisual processing can be observed in both groups. However, NH listeners but not CI users appear to show enhanced allocation of cognitive resources in visually as compared to auditory attended audiovisual speech conditions, which supports our behavioural observations of poorer lipreading abilities and reduced visual influence on audition in NH listeners as compared to CI users.

Modulation of DBS-induced cortical responses and movement by the directionality and magnitude of current administered

Subthalamic deep brain stimulation (STN-DBS) is an effective therapy for alleviating motor symptoms in people with Parkinson’s disease (PwP), although some may not receive optimal clinical benefits. One potential mechanism of STN-DBS involves antidromic activation of the hyperdirect pathway (HDP), thus suppressing cortical beta synchrony to improve motor function, albeit the precise mechanisms underlying optimal DBS parameters are not well understood. To address this, 18 PwP with STN-DBS completed a 2 Hz monopolar stimulation of the left STN during MEG. MEG data were imaged in the time-frequency domain using minimum norm estimation. Peak vertex time series data were extracted to interrogate the directional specificity and magnitude of DBS current on evoked and induced cortical responses and accelerometer metrics of finger tapping using linear mixed-effects models and mediation analyses. We observed increases in evoked responses (HDP ~ 3–10 ms) and synchronization of beta oscillatory power (14–30 Hz, 10–100 ms) following DBS pulse onset in the primary sensorimotor cortex (SM1), supplementary motor area (SMA) and middle frontal gyrus (MFG) ipsilateral to the site of stimulation. DBS parameters significantly modulated neural and behavioral outcomes, with clinically effective contacts eliciting significant increases in medium-latency evoked responses, reductions in induced SM1 beta power, and better movement profiles compared to suboptimal contacts, often regardless of the magnitude of current applied. Finally, HDP-related improvements in motor function were mediated by the degree of SM1 beta suppression in a setting-dependent manner. Together, these data suggest that DBS-evoked brain-behavior dynamics are influenced by the level of beta power in key hubs of the basal ganglia-cortical loop, and this effect is exacerbated by the clinical efficacy of DBS parameters. Such data provides novel mechanistic and clinical insight, which may prove useful for characterizing DBS programming strategies to optimize motor symptom improvement in the future.

Neurophysiological mechanisms of exploration and exploitation in high-functioning autism: Magnetoencephalographic study

Intolerance of uncertainty and high sensitivity to the threat of failure are believed to contribute to chronic anxiety in individuals with high-functioning autism. This study examines the influence of these personality traits on the brain processes involved in decision-making in a probabilistic setting among autism patients. Furthermore, we explore the causal relationship between these personality traits and chronic anxiety in individuals with high-functioning autism. Twenty-one high-functioning autistic individuals who are intolerant to uncertainty, aged 19 to 46, and 21 neurotypical volunteers of the same age, carried out a probabilistic choice experiment with two alternatives. One option yielded a monetary profit of 70% of the time, while the other brought only a 30% gain. Following each selection, the subjects received feedback on their decision and gradually learned, through trial and error, to prefer the more advantageous option. From this point forward, we consider frequent selections of a beneficial stimulus to align with the internal utility model, specifically the exploitation strategy. On the other hand, sporadic choices of a detrimental stimulus correspond to an exploration strategy, which may prove disadvantageous in a stable environment but enables adaptation to unforeseen changes in the surroundings. We hypothesized that there are characteristic differences in brain activity reflecting exploration and exploitation strategies between groups, which would emerge during the decision-making period and after internal feedback evaluation regarding advantageous and disadvantageous choices [1]. Beta oscillations (16–30 Hz) were analyzed in the magnetoencephalographic recordings. The decrease in beta oscillation power below baseline during the period between stimulus presentation and subjects’ response indicates activation in brain regions related to decision-making strategy. Conversely, an increase in beta oscillation power following feedback signaling a disadvantageous choice reflects a mechanism that reinforces internal value models in current task conditions [1]. The cortical sources of beta oscillations in 448 cortical areas were estimated using the sLoreta technique at the single-trial level. Mixed linear models (LMM) were used for statistical analysis with correction for multiple comparisons via the FDR method for the number of cortical areas analyzed. The study concentrated on the time interval for decision-making (–900 to –300 ms prior to the motor action of choice) and the post-feedback period (500 to 900 ms after the commencement of the feedback presentation) [1]. Based on questionnaire results, individuals with high-functioning autism exhibited a significantly lower tolerance for uncertainty and a greater intolerance for uncertainty when compared to neurotypical participants. The study generated two primary findings. Initially, the extent of brain activity during decision-making differed in control subjects and subjects with autism based on the type of choice, with exact opposition. Opting for an advantageous vs. disadvantageous choice was linked with reduced activation of the inferior temporal, parietal, and medial frontal cortex regions in control subjects and elevated activation in these regions for subjects with autism spectrum disorder. These findings suggest that neurotypical individuals utilize fewer neural resources and exhibit decreased emotional response while deciding in favor of a known profitable outcome compared to opting for an uncertain choice — one that is more likely to result in a negative outcome based on previous experiences. Individuals with autism allocate disproportionate amounts of attention and emotional resources towards planning actions that are deemed safe and offer only a probable (though not definite) advantage. Conversely, the prospect of failure due to risky behavior induces a comparatively muted response in their brains. Second, our internal evaluation of feedback focused on variations in functional activity within the orbitofrontal and lateral prefrontal cortical areas during exploratory (disadvantageous) choices between individuals with autism and control subjects. As previously reported, neurotypical subjects demonstrated significant beta synchronization following negative feedback after disadvantageous choices [1]. Contrary to control participants, individuals with autism spectrum disorder exhibited a lack of synchronization in frontal beta oscillations following losses incurred from unfavorable selections. This observation may indicate insufficient reinforcement of the internal utility model, which typically strengthens in response to negative outcomes that align with predicted results [1]. Overall, our study found that individuals on the autism spectrum with a high intolerance for uncertainty exhibit significantly increased activation of brain decision-making systems in situations that are perceived to be low-risk and with a high probability of a successful outcome. These findings clarify the reasons behind the puzzling rise in anxiety and autonomic reactivity among individuals in situations where they anticipate rewards, which are not inherently aversive unlike fear of punishment [2].

Corticostriatal beta oscillation changes associated with cognitive function in Parkinson's disease.

Cognitive impairment is the most frequent non-motor symptom in Parkinson's disease and is associated with deficits in a number of cognitive functions including working memory. However, the pathophysiology of Parkinson's disease cognitive impairment is poorly understood. Beta oscillations have previously been shown to play an important role in cognitive functions including working memory encoding. Decreased dopamine in motor cortico-striato-thalamo-cortical (CSTC) circuits increases the spectral power of beta oscillations and results in Parkinson's disease motor symptoms. Analogous changes in parallel cognitive CSTC circuits involving the caudate and dorsolateral prefrontal cortex (DLPFC) may contribute to Parkinson's disease cognitive impairment. The objective of our study is to evaluate whether changes in beta oscillations in the caudate and DLPFC contribute to cognitive impairment in Parkinson's disease patients. To investigate this, we used local field potential recordings during deep brain stimulation surgery in 15 patients with Parkinson's disease. Local field potentials were recorded from DLPFC and caudate at rest and during a working memory task. We examined changes in beta oscillatory power during the working memory task as well as the relationship of beta oscillatory activity to preoperative cognitive status, as determined from neuropsychological testing results. We additionally conducted exploratory analyses on the relationship between cognitive impairment and task-based changes in spectral power in additional frequency bands. Spectral power of beta oscillations decreased in both DLPFC and caudate during working memory encoding and increased in these structures during feedback. Subjects with cognitive impairment had smaller decreases in caudate and DLPFC beta oscillatory power during encoding. In our exploratory analysis, we found that similar differences occurred in alpha frequencies in caudate and theta and alpha in DLPFC. Our findings suggest that oscillatory power changes in cognitive CSTC circuits may contribute to cognitive symptoms in patients with Parkinson's disease. These findings may inform the future development of novel neuromodulatory treatments for cognitive impairment in Parkinson's disease.

Differential Effects of Chronic Methamphetamine Treatment on High-Frequency Oscillations and Responses to Acute Methamphetamine and NMDA Receptor Blockade in Conscious Mice.

Dysregulation of high-frequency neuronal oscillations has been implicated in the pathophysiology of schizophrenia. Chronic methamphetamine (METH) use can induce psychosis similar to paranoid schizophrenia. The current study in mice aimed to determine the effect of chronic METH treatment on ongoing and evoked neuronal oscillations. C57BL/6 mice were treated with METH or vehicle control for three weeks and implanted with extradural recording electrodes. Two weeks after the last METH injection, mice underwent three EEG recording sessions to measure ongoing and auditory-evoked gamma and beta oscillatory power in response to an acute challenge with METH (2 mg/kg), the NMDA receptor antagonist MK-801 (0.3 mg/kg), or saline control. A separate group of mice pretreated with METH showed significantly greater locomotor hyperactivity to an acute METH challenge, confirming long-term sensitisation. Chronic METH did not affect ongoing or evoked gamma or beta power. Acute MK-801 challenge reduced ongoing beta power whereas acute METH challenge significantly increased ongoing gamma power. Both MK-801 and METH challenge suppressed evoked gamma power. Chronic METH treatment did not modulate these acute drug effects. There were minor effects of chronic METH and acute METH and MK-801 on selected components of event-related potential (ERP) waves. In conclusion, chronic METH treatment did not exert neuroplastic effects on the regulation of cortical gamma oscillations in a manner consistent with schizophrenia, despite causing behavioural sensitisation.

Characterizing cortical responses to short-term multidisciplinary intensive rehabilitation treatment in patients with Parkinson's disease: A transcranial magnetic stimulation and electroencephalography study.

Combined transcranial magnetic stimulation and electroencephalography (TMS-EEG) is a powerful non-invasive tool for qualifying the neurophysiological effects of interventions by recording TMS-induced cortical activation with high temporal resolution and generates reproducible and reliable waves of activity without participant cooperation. Cortical dysfunction contributes to the pathogenesis of the clinical symptoms of Parkinson's disease (PD). Here, we examined changes in cortical activity in patients with PD following multidisciplinary intensive rehabilitation treatment (MIRT). Forty-eight patients with PD received 2 weeks of MIRT. The cortical response was examined following single-pulse TMS over the primary motor cortex by 64-channel EEG, and clinical symptoms were assessed before and after MIRT. TMS-evoked potentials were quantified by the global mean field power, as well as oscillatory power in theta, alpha, beta, and gamma bands, and their clinical correlations were calculated. After MIRT, motor and non-motor symptoms improved in 22 responders, and only non-motor function was enhanced in 26 non-responders. Primary motor cortex stimulation reduced global mean field power amplitudes in responders but not significantly in non-responders. Oscillations exhibited attenuated power in the theta, beta, and gamma bands in responders but only reduced gamma power in non-responders. Associations were observed between beta oscillations and motor function and between gamma oscillations and non-motor symptoms. Our results suggest that motor function enhancement by MIRT may be due to beta oscillatory power modulation and that alterations in cortical plasticity in the primary motor cortex contribute to PD recovery.

Diurnal modulation of subthalamic beta oscillatory power in Parkinson’s disease patients during deep brain stimulation

Beta-band activity in the subthalamic local field potential (LFP) is correlated with Parkinson’s disease (PD) symptom severity and is the therapeutic target of deep brain stimulation (DBS). While beta fluctuations in PD patients are well characterized on shorter timescales, it is not known how beta activity evolves around the diurnal cycle, outside a clinical setting. Here, we obtained chronic recordings (34 ± 13 days) of subthalamic beta power in PD patients implanted with the Percept DBS device during high-frequency DBS and analysed their diurnal properties as well as sensitivity to artifacts. Time of day explained 41 ± 9% of the variance in beta power (p < 0.001 in all patients), with increased beta during the day and reduced beta at night. Certain movements affected LFP quality, which may have contributed to diurnal patterns in some patients. Future DBS algorithms may benefit from taking such diurnal and artifactual fluctuations in beta power into account.

Closed-loop modulation of model parkinsonian beta oscillations based on CAR-fuzzy control algorithm.

Closed-loop deep brain stimulation (DBS) can apply on-demand stimulation based on the feedback signal (e.g. beta band oscillation), which is deemed to lower side effects of clinically used open-loop DBS. To facilitate the application of model-based closed-loop DBS in clinical, studies must consider state variations, e.g., variation of desired signal with different movement conditions and variation of model parameters with time. This paper proposes to use the controlled autoregressive (CAR)-fuzzy control algorithm to modulate the pathological beta band (13-35Hz) oscillation of a basal ganglia-cortex-thalamus model. The CAR model is used to identify the relationship between DBS frequency parameter and beta oscillation power. Then the error between the one-step-ahead predicted beta power of CAR model and the desired value is innovatively used as the input of fuzzy controller to calculate the next step stimulation frequency. Compared with 130Hz open-loop DBS, the proposed closed-loop DBS method could lower the mean stimulation frequency to 74.04Hz with similar beta oscillation suppression performance. The Mamdani fuzzy controller is selected because which could establish fuzzy controller rules according to human operation experience. Adding prediction module to closed-loop control improves the accuracy of fuzzy control, compared with proportional-integral control and fuzzy control, the proposed CAR-fuzzy control algorithm has higher tracking reliability, response speed and robustness.

Effects of beta-band and gamma-band rhythmic stimulation on motor inhibition

SummaryTo investigate whether beta oscillations are causally related to motor inhibition, thirty-six participants underwent two concurrent transcranial alternating current stimulation (tACS) and electroencephalography (EEG) sessions during which either beta (20 Hz) or gamma (70 Hz) stimulation was applied while participants performed a stop-signal task. In addition, we acquired magnetic resonance images to simulate the electric field during tACS. 20 Hz stimulation targeted at the pre-supplementary motor area enhanced inhibition and increased beta oscillatory power around the time of the stop-signal in trials directly following stimulation. The increase in inhibition on stop trials followed a dose-response relationship with the strength of the individually simulated electric field. Computational modeling revealed that 20 and 70 Hz stimulation had opposite effects on the braking process. These results highlight that the effects of tACS are state-dependent and demonstrate that fronto-central beta activity is causally related to successful motor inhibition, supporting its use as a functional biomarker.

Subthalamic Beta Activity in Parkinson's Disease May Be Linked to Dorsal Striatum Gray Matter Volume and Prefrontal Cortical Thickness: A Pilot Study.

BackgroundExcessive oscillations at beta frequencies (13–35 Hz) in the subthalamic nucleus (STN) represent a pathophysiological hallmark of Parkinson's disease (PD), which correlates well with parkinsonian symptoms and is reduced in response to standard disease treatments. However, the association of disease-specific regional gray matter (GM) atrophy or cortical thickness (CT) with the presence of STN beta oscillatory activity has been poorly investigated but is of relevance given the potential of these variables for extracting information about PD pathophysiology. This exploratory study investigated the involvement of regional GM volume and CT in the basal ganglia-cortical network and its potential association with the presence of STN beta oscillatory activity in PD.MethodsWe acquired preoperative GM densities on T1-weighted magnetic resonance imaging scans and we carried out regional estimation of GM volume and CT. LFP activities from the STN were recorded post-operatively in 7 cognitively preserved PD patients off dopaminergic medication undergoing deep-brain stimulation surgery. Oscillatory beta power was determined by power spectral density of 4-min resting state STN LFP activity. Spearman partial correlations and regression analysis were used to screen the presence of STN beta power for their relationship with GM volume and CT measurements.ResultsAfter controlling for the effects of age, educational level, and disease duration, and after correcting for multiple testing, enhanced STN beta power showed significant and negative correlations between, first, volume of the right putamen and left caudate nucleus, and second, smaller CT in frontal regions involving the left rostral middle frontal gyrus (MFG) and left medial orbitofrontal gyrus. A lower volume in the right putamen and a lower CT in the left MFG demonstrated the strongest associations with increased STN beta power.ConclusionsThese tentative results seem to suggest that STN LFP beta frequencies may be mainly linked to different but ongoing parallel neurodegenerative processes, on the one hand, to GM volume reduction in dorsal striatum, and on the other hand, to CT reduction of prefrontal-“associative” regions. These findings could further delineate the brain structural interactions underpinning the exaggerated STN beta activity commonly observed in PD patients.

Therapeutic Lower Extremity Power Training Alters the Sensorimotor Cortical Activity of Individuals With Cerebral Palsy

ObjectiveTo utilize magnetoencephalographic (MEG) brain imaging to examine potential changes in sensorimotor cortical oscillations after therapeutic power training in individuals with cerebral palsy (CP). DesignCohort. SettingAcademic medical center. ParticipantsIndividuals with CP (N=11; age=15.9±1.1 years; Gross Motor Function Classification System I- III) and neurotypical controls (NTs; N=16; age=14.6±0.8 years). InterventionsParticipants with CP underwent 24 (8 weeks; 3 days a week) sessions of high-velocity lower extremity power training on a leg press. The NTs underwent single baseline MEG assessments. Main Outcome MeasuresPre-post bilateral leg press 1-repetition maximum and peak power production were used to assess the muscular performance changes. The 10-m walk and 1-minute walk tests were used to assess mobility changes. During MEG recordings, participants used their right leg to complete a goal-directed isometric target-matching task. Advanced beamforming methods were subsequently used to image the strength of the sensorimotor beta oscillatory power. ResultsBefore the therapeutic power training, the participants with CP had stronger beta sensorimotor cortical oscillations compared with the NT controls. However, the beta sensorimotor cortical oscillations were weaker and approximated the controls after the participants with CP completed the therapeutic power training protocol. There also was a link between the amount of improvement in leg peak power production and the amount of reduction in sensorimotor cortical oscillations seen after therapy. ConclusionsTherapeutic power training appears to optimize the sensorimotor cortical oscillations of individuals with CP, and these neuroplastic changes partly contribute to improvements in the leg peak power production of individuals with CP. Therapeutic power training might provide the key ingredients for beneficial neuroplastic change.

Alpha oscillatory power decreases are associated with better memory for higher valued information

ABSTRACT Items associated with high value are often better remembered. Value may increase attention toward item in context associations. Alpha oscillations (8–13 Hz) are thought to underlie attention and their observation may reveal the role attention plays in value-based memory. In the current study, EEG is used to record brain activity while participants (n = 30) completed a source recognition memory task where items were associated with either high or low value backgrounds to determine whether greater attentional resources are deployed when encoding high value information. Participants demonstrated better memory for objects associated with high value backgrounds. Alpha oscillatory power in occipital/temporal brain regions exhibited greater desynchronization when encoding objects associated with high value that were later successfully recalled compared to those associated with low value. In addition, beta oscillatory power in midfrontal brain regions exhibited greater desynchronization during successful recall of high value objects compared to low value objects. Together these results suggest that more attentional resources are used to encode information that is associated with high value, which increases the likelihood of later successful memory recall.

Alpha and beta neural oscillations differentially reflect age-related differences in bilateral coordination

Bilateral in-phase (IP) and anti-phase (AP) movements represent two fundamental modes of bilateral coordination that are essential for daily living. Although previous studies have shown that aging is behaviorally associated with decline in bilateral coordination, especially in AP movements, the underlying neural mechanisms remain unclear. Here, we use kinematic measurements and electroencephalography to compare motor performance of young and older adults executing bilateral IP and AP hand movements. On the behavioral level, inter-limb synchronization was reduced during AP movements compared to IP and this reduction was stronger in the older adults. On the neural level, we found interactions between group and condition for task-related power change in different frequency bands. The interaction was driven by smaller alpha power decreases over the non-dominant cortical motor area in young adults during IP movements and larger beta power decreases over the midline region in older adults during AP movements. In addition, the decrease in inter-limb synchronization during AP movements was predicted by stronger directional connectivity in the beta-band: an effect more pronounced in older adults. Our results therefore show that age-related differences in the two bilateral coordination modes are reflected on the neural level by differences in alpha and beta oscillatory power as well as interhemispheric directional connectivity.

Eight cylindrical contact lead recordings in the subthalamic region localize beta oscillations source to the dorsal STN

BackgroundIn Parkinson's disease (PD) patients, the subthalamic nucleus (STN) has prominent oscillatory activity in the beta band, which may be related to the motor symptoms severity. Local field potential (LFP) studies using standard four-contact deep brain stimulation (DBS) leads indicate that the source of beta activity in the STN region is the dorsolateral segment of the nucleus. However, these leads have few contacts outside of the STN, making the source localization of beta activity around the STN region uncertain. ObjectiveThis study aimed to investigate the electrophysiological characteristics of the STN and the surrounding area in PD to better locate the source of these oscillations and their clinical relevance. MethodsEight PD patients were bilaterally implanted in the STN with the eight ring-contact DBS lead (Boston Scientific Corporation). LFPs were recorded intra-operatively from each DBS contact in the off medication state at rest. Each contact location was normalized relative to the STN borders based on microelectrode recordings. For each recording, power spectral density was computed, averaged over multiple frequency bands and phase reversal analysis was used to localize the source of oscillatory activity. Beta burst, high-frequency activity (HFA), and phase-amplitude coupling (PAC) were also computed. Neurophysiological signatures were correlated with hemibody symptoms severity and clinical outcomes. ResultsBeta band power and phase reversal localized the beta oscillator to the dorsal STN and correlated with pre-operative off medication hemibody bradykinesia and rigidity score.The contact along the electrode with the largest beta oscillatory power co-localized with the independently chosen optimized contact used for long-term chronic DBS. Lastly, beta bursting, HFA, and Beta-HFA PAC co-localized with the beta oscillator at the dorsal STN, and Beta-HFA PAC correlated with DBS effect. ConclusionsOur findings support the hypothesis that the primary source of beta oscillations is located in dorsal STN, and argue against the alternative hypothesis that beta activity in the STN region arises from volume conduction from other sources. We demonstrate intrinsic STN beta-HFA PAC as an independent marker of DBS effect.