Forced synchronisation of neurones to 20 Hz slows voluntary movement in both healthy subjects and patients with parkinson?s disease

Abstract

Event Abstract Back to Event Forced synchronisation of neurones to 20 Hz slows voluntary movement in both healthy subjects and patients with parkinson’s disease Ned Jenkinson1* and Peter Brown1 1 Oxford University, United Kingdom Motor processing is accompanied by changes in the degree of oscillatory synchronisation of neurones within motor loops. One of the most prominent changes is a suppression of activity in the beta (~20 Hz) frequency band. Interest in beta activity is heightened by its pathological exaggeration in Parkinson’s Disease (PD), where movements are dramatically slowed. However, whether attenuation of beta activity is a prerequisite for successful voluntary movement or just an epiphenomenon remains unclear. We investigated the question of causality by stimulating the motor cortex of healthy subjects using transcranial alternating current as they performed reaction time finger movements. Stimulation at 20 Hz did not affect response time but did reduce finger peak acceleration finger by ~20 %. This was not true of cortical stimulation at the control frequency of 5 Hz. Thus, artificially elevating neuronal synchronisation at 20 Hz impairs movement speed in healthy subjects. Does this mean that the elevated beta synchrony in PD compromises movement? Proving this is more difficult as spontaneous synchronisation may be at ceiling levels. Accordingly, we stimulated a subset of PD with relatively preserved finger tapping performance through existing therapeutic deep brain stimulation electrodes. Stimulating the subthalamic nucleus of such patients at 20 Hz again slowed movement. The results indicate that beta band synchronisation actively slows voluntary movement in both healthy subjects and PD patients, and that this is a property of beta activity at both cortical and subcortical levels. The findings also help explain why beta synchrony is increased in paradigms requiring response suppression and why therapeutic manoeuvres that reduce beta synchrony improve motor performance in PD. Keywords: cortical oscillations, Parkinson’s disease Conference: XI International Conference on Cognitive Neuroscience (ICON XI), Palma, Mallorca, Spain, 25 Sep - 29 Sep, 2011. Presentation Type: Symposium: Oral Presentation Topic: Symposium 14: Probing Cortical Oscillations with Transcranial Stimulation Citation: Jenkinson N and Brown P (2011). Forced synchronisation of neurones to 20 Hz slows voluntary movement in both healthy subjects and patients with parkinson’s disease. Conference Abstract: XI International Conference on Cognitive Neuroscience (ICON XI). doi: 10.3389/conf.fnhum.2011.207.00553 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 14 Nov 2011; Published Online: 28 Nov 2011. * Correspondence: Dr. Ned Jenkinson, Oxford University, Oxford, United Kingdom, ned.jenkinson@dpag.ox.ac.uk Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ned Jenkinson Peter Brown Google Ned Jenkinson Peter Brown Google Scholar Ned Jenkinson Peter Brown PubMed Ned Jenkinson Peter Brown Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.