Abstract

Abnormal initiation and control of voluntary movements are among the principal manifestations of Parkinson’s disease (PD). However, the processes underlying these abnormalities and their potential remediation by dopamine treatment remain poorly understood. Normally, movements depend on the integration of sensory information with the predicted consequences of action. This integration leads to a suppression in the intensity of predicted sensations, reflected in a ‘sensory attenuation’. We examined this integration process and its relation to dopamine in PD, by measuring sensory attenuation. Patients with idiopathic PD (n = 18) and population-derived controls (n = 175) matched a set of target forces applied to their left index finger by a torque motor. To match the force, participants either pressed with their right index finger (‘Direct’ condition) or moved a knob that controlled a motor through a linear potentiometer (‘Slider’ condition). We found that despite changes in sensitivity to different forces, overall sensory attenuation did not differ between medicated PD patients and controls. Importantly, the degree of attenuation was negatively related to PD motor severity but positively related to individual patient dopamine dose, as measured by levodopa dose equivalent. The results suggest that dopamine could regulate the integration of sensorimotor prediction with sensory information to facilitate the control of voluntary movements.

Highlights

  • Abnormal initiation and control of voluntary movements are among the principal manifestations of Parkinson’s disease (PD)

  • We examined this integration process and its relation to dopamine in PD, by measuring sensory attenuation

  • We found that despite changes in sensitivity to different forces, overall sensory attenuation did not differ between medicated PD patients and controls

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Summary

Introduction

Abnormal initiation and control of voluntary movements are among the principal manifestations of Parkinson’s disease (PD). A key manifestation of Parkinson’s disease (PD) is bradykinesia – that is, patients have slowness associated with marked difficulties in planning, initiating and executing voluntary movements[1] This principal abnormality in motor control has been shown to correlate well with dopamine disruption in patients[2], the exact mechanism remains poorly understood. In order to better understand the mechanisms underlying movement disorders, previous studies have used the framework of optimal control theory[3,4,5] According to this theory, normal motor control depends on the integration of peripheral sensory information with predictions arising from internal models of action. Sensorimotor attenuation is the reduction in the perceived intensity of stimuli generated by one’s actions, compared to externally generated stimuli It reflects the suppression of predicted sensory consequences from. University, New York, United States. *A comprehensive list of consortium members appears at the end of the paper

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