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  • Differences in Cortical Oscillations During Self-initiated Movement Between Parkinson’s Disease and Essential Tremor

    Final Number:

    Jeong Woo Choi PhD; Mahsa Malekmohammadi PhD; Zhang Xu; Justin Sharim BS; William Speier; Nicholas Au Yong MD, PhD; Nader Pouratian MD PhD

    Study Design:
    Clinical Trial

    Subject Category:
    Movement Disorders

    Meeting: 2018 ASSFN Biennial Meeting

    Introduction: Patients with Parkinson disease (PD) express difficulty in initiating movements, particularly for those movements that are self-initiated (SI). These deficits are primarily associated with the rigidity and bradykinesia and have been linked to the beta (13-35 Hz) hypersynchrony within the basal ganglia thalamocortical network. While previous studies provided important insight, dynamics of cortical activity during the SI movement and how they relate to the disease symptoms remain relatively underexplored. Here, we explore the dynamics of movement-related cortical oscillatory activity in subjects with PD or essential tremor (ET).

    Methods: Sensorimotor cortical electrocorticogphy signals were recorded from 13 PD and 10 ET patients during awake intraoperative implantation of deep brain stimulation lead. Each subject performed two blocks of externally cued (EC) or SI finger tapping task of the contralateral hand. We assessed movement-related changes in local spectral power of the cortical signals during the period of movement initiation, and statistically compared those between two disease groups for each movement type.

    Results: For SI trials, movement related suppression of beta power and broadband gamma (70-200 Hz) increase, started earlier in PD compared to ET patients at motor/pre-motor cortices (p=0.007 for beta power, p=0.01 for gamma power, Wilcoxon rank-sum test). On the contrary, there was no significant difference in this timing between two disease groups during the EC trials. During SI movements, the magnitude of beta power suppression and gamma power increase at the sensory cortex was positively correlated with the severity of rigidity and bradykinesia in PD cohort (p=0.004 for beta power, p=0.007 for gamma power, Spearman correlation).

    Conclusions: Our findings show disease specific patterns of movement related power change at the motor cortex and provide new evidence that rigidity and bradykinesia in PD are associated with an earlier and stronger movement related power change at the motor cortex when subjects are performing a SI movement.

    Patient Care: Our study will provide the new insight to understand the pathophysiology of Parkinson’s disease in depth.

    Learning Objectives: Not applicable


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