The effect of Recent Trial History on Response Times and Beta-Burst rates in the Stop-Signal task

Det er ingen konsensus rundt en direkte nevral markør for inhibisjon i litteraturen om responsinhibering. Tidligere studier har undersøkt forholdet mellom inhibering og EEG-baserte mål, som P3 og N2 ERP-komponentene og aktivitet i beta (15-30 Hz) frekvensbåndet. Nylige studier har observert plutselige økninger i aktivitet i beta frekvensbåndet som kun er synlige på single-trial nivå. Beta-Burst rate, som er antallet slike plutselige økninger i aktivitet i hver enkelt trial, har blitt foreslått å reflektere inhibisjon. Formålet med denne studien er å undersøke forholdet mellom sensorimotor post-go Beta-Burst rater og atferdsmål på responsinhibering. Trettifire deltakere utførte Stop-Signal task mens hjerneaktiviteten deres ble målt med EEG. Lengden på trial-sekvenser var predeterminert med det formål å undersøke hvordan antallet foregående trials påvirket deltakernes atferd. Vi forventer kortere responstider og lavere Beta-Burst rater før mislykket sammenlignet med vellykket inhibering. Vi forventet også at både responstider og Beta-Burst rater var negativt korrelert med Sekvenslengde. Resultatene viste kortere responstider før mislykket sammenlignet med vellykket inhibering. Det var imidlertid ingen forskjell i Beta-Burst rater før mislykket sammenlignet med vellykket inhibering. Resultatene viste også at Sekvenslengde hadde ingen effekt på hverken responstider eller Beta-Burst rater. Totalt sett støttet ikke resultatene en sammenheng mellom Beta-Burst rater og responsinhibering.Masteroppgave i psykologiMAPSYK360INTL-MEDINTL-JUSINTL-PSYKINTL-HFMAPS-PSYKINTL-SVINTL-MNINTL-KM

The modulatory effect of self-paced and cued motor execution on subthalamic beta-bursts in Parkinson's disease: Evidence from deep brain recordings in humans

Deep brain stimulation (DBS) electrodes provide an unparalleled window to record and investigate neuronal activity right at the core of pathological brain circuits. In Parkinson's disease (PD), basal ganglia beta-oscillatory activity (13-35 Hz) seems to play an outstanding role. Conventional DBS, which globally suppresses beta-activity, does not meet the requirements of a targeted treatment approach given the intricate interplay of physiological and pathological effects of beta-frequencies. Here, we wanted to characterise the local field potential (LFP) in the subthalamic nucleus (STN) in terms of beta-burst prevalence, amplitude and length between movement and rest as well as during self-paced as compared to goal-directed motor control. Our electrophysiological recordings from externalised DBS-electrodes in nine patients with PD showed a marked decrease in beta-burst durations and prevalence during movement as compared to rest as well as shorter and less frequent beta-bursts during cued as compared to self-paced movements. These results underline the importance of beta-burst modulation in movement generation and are in line with the clinical observation that cued motor control is better preserved than self-paced movements. Furthermore, our findings motivate the use of adaptive DBS based on beta-bursts, which selectively trim longer beta-bursts, as it is more suitable and efficient over a range of motor behaviours than conventional DBS

Spatiotemporal organisation of human sensorimotor beta burst activity

Beta oscillations in human sensorimotor cortex are hallmark signatures of healthy and pathological movement. In single trials, beta oscillations include bursts of intermittent, transient periods of high-power activity. These burst events have been linked to a range of sensory and motor processes, but their precise spatial, spectral, and temporal structure remains unclear. Specifically, a role for beta burst activity in information coding and communication suggests spatiotemporal patterns, or travelling wave activity, along specific anatomical gradients. We here show in human magnetoencephalography recordings that burst activity in sensorimotor cortex occurs in planar spatiotemporal wave-like patterns that dominate along two axes either parallel or perpendicular to the central sulcus. Moreover, we find that the two propagation directions are characterised by distinct anatomical and physiological features. Finally, our results suggest that sensorimotor beta bursts occurring before and after a movement can be distinguished by their anatomical, spectral and spatiotemporal characteristics, indicating distinct functional roles

A global single beta burst prior to stopping an ongoing movement suggests a causal role of beta in movement cancellation

The general question of this research is how beta oscillations are implicated in stopping an ongoing movement. Previous studies regarding movement cancellation have found a significant increase in beta activity in sensorimotor areas, especially in the form of transient increases in beta oscillations, called beta bursts. However, the functional role of beta band activity in stopping is still unclear, mainly because the behavioural tasks used cannot measure the exact timing when the subjects start the stopping process and therefore it is only possible to infer the stopping time. To resolve this, we used head-fixed rats running on a treadmill while performing a Go/NoGo task. In some NoGo trials, the rat starts to run, realizes the mistake and stops before crossing a fixed distance threshold. These are the events being analyzed, called near-mistake events (N=39,366). We found a single beta burst occurring prior to stopping in all five brain regions analyzed (from 44.2±20.1 ms to 55.8±16.0 ms) and positive correlations of beta burst number and power increase with movement speed before stopping. We also found a single alpha burst prior to and during stopping in all brain regions (from 45.9±20.1 ms to 57.1±19.3 ms), supporting previous studies’ findings of alpha band involvement in inhibitory motor actions. Our findings on beta bursts suggest a causality role in stopping an ongoing movement while our results of alpha bursts need to be further analyzed to understand its functional role

The cross-frequency mediation mechanism of intracortical information transactions

In a seminal paper by von Stein and Sarnthein (2000), it was hypothesized that "bottom-up" information processing of "content" elicits local, high frequency (beta-gamma) oscillations, whereas "top-down" processing is "contextual", characterized by large scale integration spanning distant cortical regions, and implemented by slower frequency (theta-alpha) oscillations. This corresponds to a mechanism of cortical information transactions, where synchronization of beta-gamma oscillations between distant cortical regions is mediated by widespread theta-alpha oscillations. It is the aim of this paper to express this hypothesis quantitatively, in terms of a model that will allow testing this type of information transaction mechanism. The basic methodology used here corresponds to statistical mediation analysis, originally developed by (Baron and Kenny 1986). We generalize the classical mediator model to the case of multivariate complex-valued data, consisting of the discrete Fourier transform coefficients of signals of electric neuronal activity, at different frequencies, and at different cortical locations. The "mediation effect" is quantified here in a novel way, as the product of "dual frequency RV-coupling coefficients", that were introduced in (Pascual-Marqui et al 2016, http://arxiv.org/abs/1603.05343). Relevant statistical procedures are presented for testing the cross-frequency mediation mechanism in general, and in particular for testing the von Stein & Sarnthein hypothesis.Comment: https://doi.org/10.1101/119362 licensed as CC-BY-NC-ND 4.0 International license: http://creativecommons.org/licenses/by-nc-nd/4.0

Bursts of beta oscillations across the brain as a neurophysiological correlate of contextual novelty

The retrosplenial cortex and hippocampus are brain regions which have been shown to be highly involved in contextual memory. In order to discover neurophysiological correlates of contextual memory in these regions, we used in vivo electrophysiology in awake, behaving mice while they explored a series of novel and familiar environments. Additionally, in order to better understand the specific neurophysiological effects of Alzheimer’s disease-associated amyloid pathology on the retrosplenial cortex and hippocampus, we compared network activity between wild-type mice and J20 mice, a transgenic mouse model which develops widespread age-related amyloid pathology and memory impairments. We detected transient bursts of beta oscillations in both the retrosplenial cortex and hippocampus that were synchronous between these regions and upregulated during contextual novelty. Moreover, spiking of neurons in the retrosplenial cortex was significantly increased during beta bursts. In J20 mice, we noted numerous examples of altered network activity, including aberrant beta bursting which is not coupled to neuronal spiking. Through the use of EEG recordings in mice, we demonstrated that beta bursts can be detected across the cortex, and are highly synchronous between different brain regions. Finally, we demonstrated that it is possible to pharmacologically induce beta bursting in the retrosplenial cortex in vitro through the use of carbachol, a muscarinic acetylcholine receptor agonist, providing an assay for better understanding the mechanisms underlying beta bursting. These findings suggest that transient beta bursting across the brain provides brief windows of effective communication between brain regions, which may underlie the formation of cortical representation of contexts, and may be impaired in Alzheimer’s disease

Feeling ready: neural bases of prospective motor readiness judgements

The idea that human agents voluntarily control their actions, including their spontaneous movements, strongly implies an anticipatory awareness of action. That is, agents should be aware they are about to act before actually executing a movement. Previous research has identified neural signals that could underpin prospective conscious access to motor preparation, including the readiness potential and the beta-band event-related desynchronization. In this study, we ran two experiments to test whether these two neural precursors of action also tracka subjective feeling of readiness. In Experiment 1, we combined a self-paced action task with an intention-probing design where participants gave binary responses to indicate whether they felt they had been about to move when a probe was presented. In Experiment 2, participants reported their feeling of readiness on a graded scale. We found that the feeling of readiness reliably correlates with the beta-band amplitude, but not with the readiness potential

Neuronal biomarkers of Parkinson's disease are present in healthy aging

The prevalence of Parkinson's disease (PD) increases with aging and both processes share similar cellular mechanisms and alterations in the dopaminergic system. Yet it remains to be investigated whether aging can also demonstrate electrophysiological neuronal signatures typically associated with PD. Previous work has shown that phase-amplitude coupling (PAC) between the phase of beta oscillations and the amplitude of gamma oscillations as well as beta bursts features can serve as electrophysiological biomarkers for PD. Here we hypothesize that these metrics are also present in apparently healthy elderly subjects. Using resting state multichannel EEG measurements, we show that PAC between beta oscillation and broadband gamma activity (50–150 Hz) is elevated in a group of elderly (59–77 years) compared to young volunteers (20–35 years) without PD. Importantly, the increase of PAC is statistically significant even after ruling out confounds relating to changes in spectral power and non-sinusoidal shape of beta oscillation. Moreover, a trend for a higher percentage of longer beta bursts (> 0.2 s) along with the increase in their incidence rate is also observed for elderly subjects. Using inverse modeling, we further show that elevated PAC and longer beta bursts are most pronounced in the sensorimotor areas. Moreover, we show that PAC and longer beta bursts might reflect distinct mechanisms, since their spatial patterns only partially overlap and the correlation between them is weak. Taken together, our findings provide novel evidence that electrophysiological biomarkers of PD may already occur in apparently healthy elderly subjects. We hypothesize that PAC and beta bursts characteristics in aging might reflect a pre-clinical state of PD and suggest their predictive value to be tested in prospective longitudinal studies

Laminar dynamics of high amplitude beta bursts in human motor cortex

Motor cortical activity in the beta frequency range is one of the strongest and most studied movement-related neural signals. At the single trial level, beta band activity is often characterized by transient, high amplitude, bursting events rather than slowly modulating oscillations. The timing of these bursting events is tightly linked to behavior, suggesting a more dynamic functional role for beta activity than previously believed. However, the neural mechanisms underlying beta bursts in sensorimotor circuits are poorly understood. To address this, we here leverage and extend recent developments in high precision MEG for temporally resolved laminar analysis of burst activity, combined with a neocortical circuit model that simulates the biophysical generators of the electrical currents which drive beta bursts. This approach pinpoints the generation of beta bursts in human motor cortex to distinct excitatory synaptic inputs to deep and superficial cortical layers, which drive current flow in opposite directions. These laminar dynamics of beta bursts in motor cortex align with prior invasive animal recordings within the somatosensory cortex, and suggest a conserved mechanism for somatosensory and motor cortical beta bursts. More generally, we demonstrate the ability for uncovering the laminar dynamics of event-related neural signals in human non-invasive recordings. This provides important constraints to theories about the functional role of burst activity for movement control in health and disease, and crucial links between macro-scale phenomena measured in humans and micro-circuit activity recorded from animal models

Cortical beta burst dynamics are altered in Parkinson's disease but normalized by deep brain stimulation

Exaggerated subthalamic beta oscillatory activity and increased beta range cortico-subthalamic synchrony have crystallized as the electrophysiological hallmarks of Parkinson's disease. Beta oscillatory activity is not tonic but occurs in 'bursts' of transient amplitude increases. In Parkinson's disease, the characteristics of these bursts are altered especially in the basal ganglia. However, beta oscillatory dynamics at the cortical level and how they compare with healthy brain activity is less well studied. We used magnetoencephalography (MEG) to study sensorimotor cortical beta bursting and its modulation by subthalamic deep brain stimulation in Parkinson's disease patients and age-matched healthy controls. We show that the changes in beta bursting amplitude and duration typical of Parkinson's disease can also be observed in the sensorimotor cortex, and that they are modulated by chronic subthalamic deep brain stimulation, which, in turn, is reflected in improved motor function at the behavioural level. In addition to the changes in individual beta bursts, their timing relative to each other was altered in patients compared to controls: bursts were more clustered in untreated Parkinson's disease, occurring in 'bursts of bursts', and re-burst probability was higher for longer compared to shorter bursts. During active deep brain stimulation, the beta bursting in patients resembled healthy controls' data. In summary, both individual bursts' characteristics and burst patterning are affected in Parkinson's disease, and subthalamic deep brain stimulation normalizes some of these changes to resemble healthy controls' beta bursting activity, suggesting a non-invasive biomarker for patient and treatment follow-up.Peer reviewe