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Adaptive grip force is modulated by subthalamic beta activity in Parkinson's disease patients


Imbach, Lukas L; Baumann-Vogel, Heide; Baumann, Christian R; Sürücü, Oguzkan; Hermsdörfer, Joachim; Sarnthein, Johannes (2015). Adaptive grip force is modulated by subthalamic beta activity in Parkinson's disease patients. NeuroImage: Clinical, 9:450-457.

Abstract

INTRODUCTION Healthy subjects scale grip force to match the load defined by physical object properties such as weight, or dynamic properties such as inertia. Patients with Parkinson's disease (PD) show an elevated grip force in dynamic object handling, but temporal aspects of anticipatory grip force control are relatively preserved. In PD patients, beta frequency oscillatory activity in the basal ganglia is suppressed prior to externally paced movements. However, the role of the subthalamic nucleus (STN) in anticipatory grip force control is not known. METHODS After implantation of deep brain stimulation (DBS) electrodes in the STN, PD patients performed adaptive and voluntary grip force tasks, while we recorded subthalamic local field potentials (LFP) and scalp EEG. RESULTS During adaptive grip force control (Shake), we found event related desynchronization (ERD) in the beta frequency band, which was time-locked to the grip force. In contrast, during voluntary grip force control (Press) we recorded a biphasic ERD, corresponding to peak grip force and grip force release. Beta synchronization between STN and cortical EEG was reduced during adaptive grip force control. CONCLUSION The time-locked suppression of beta oscillatory activity in the STN is in line with previous reports of beta ERD prior to voluntary movements. Our results show that the STN is involved in anticipatory grip force control in PD patients. The difference in the phasic beta ERD between the two tasks and the reduction of cortico-subthalamic synchronization suggests that qualitatively different neuronal network states are involved in different grip force control tasks.

Abstract

INTRODUCTION Healthy subjects scale grip force to match the load defined by physical object properties such as weight, or dynamic properties such as inertia. Patients with Parkinson's disease (PD) show an elevated grip force in dynamic object handling, but temporal aspects of anticipatory grip force control are relatively preserved. In PD patients, beta frequency oscillatory activity in the basal ganglia is suppressed prior to externally paced movements. However, the role of the subthalamic nucleus (STN) in anticipatory grip force control is not known. METHODS After implantation of deep brain stimulation (DBS) electrodes in the STN, PD patients performed adaptive and voluntary grip force tasks, while we recorded subthalamic local field potentials (LFP) and scalp EEG. RESULTS During adaptive grip force control (Shake), we found event related desynchronization (ERD) in the beta frequency band, which was time-locked to the grip force. In contrast, during voluntary grip force control (Press) we recorded a biphasic ERD, corresponding to peak grip force and grip force release. Beta synchronization between STN and cortical EEG was reduced during adaptive grip force control. CONCLUSION The time-locked suppression of beta oscillatory activity in the STN is in line with previous reports of beta ERD prior to voluntary movements. Our results show that the STN is involved in anticipatory grip force control in PD patients. The difference in the phasic beta ERD between the two tasks and the reduction of cortico-subthalamic synchronization suggests that qualitatively different neuronal network states are involved in different grip force control tasks.

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Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Neurology
04 Faculty of Medicine > University Hospital Zurich > Clinic for Neurosurgery
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2015
Deposited On:03 Dec 2015 15:54
Last Modified:08 Aug 2017 09:34
Publisher:Elsevier
ISSN:2213-1582
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.nicl.2015.09.010
PubMed ID:26594627

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