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Sensory attenuation in Parkinson’s disease is related to disease severity and dopamine dose

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 integrati...

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Autores principales: Wolpe, Noham, Zhang, Jiaxiang, Nombela, Cristina, Ingram, James N., Wolpert, Daniel M., Rowe, James B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6199336/
https://www.ncbi.nlm.nih.gov/pubmed/30353104
http://dx.doi.org/10.1038/s41598-018-33678-3
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author Wolpe, Noham
Zhang, Jiaxiang
Nombela, Cristina
Ingram, James N.
Wolpert, Daniel M.
Rowe, James B.
author_facet Wolpe, Noham
Zhang, Jiaxiang
Nombela, Cristina
Ingram, James N.
Wolpert, Daniel M.
Rowe, James B.
author_sort Wolpe, Noham
collection PubMed
description 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.
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spelling pubmed-61993362018-10-25 Sensory attenuation in Parkinson’s disease is related to disease severity and dopamine dose Wolpe, Noham Zhang, Jiaxiang Nombela, Cristina Ingram, James N. Wolpert, Daniel M. Rowe, James B. Sci Rep Article 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. Nature Publishing Group UK 2018-10-23 /pmc/articles/PMC6199336/ /pubmed/30353104 http://dx.doi.org/10.1038/s41598-018-33678-3 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Wolpe, Noham
Zhang, Jiaxiang
Nombela, Cristina
Ingram, James N.
Wolpert, Daniel M.
Rowe, James B.
Sensory attenuation in Parkinson’s disease is related to disease severity and dopamine dose
title Sensory attenuation in Parkinson’s disease is related to disease severity and dopamine dose
title_full Sensory attenuation in Parkinson’s disease is related to disease severity and dopamine dose
title_fullStr Sensory attenuation in Parkinson’s disease is related to disease severity and dopamine dose
title_full_unstemmed Sensory attenuation in Parkinson’s disease is related to disease severity and dopamine dose
title_short Sensory attenuation in Parkinson’s disease is related to disease severity and dopamine dose
title_sort sensory attenuation in parkinson’s disease is related to disease severity and dopamine dose
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6199336/
https://www.ncbi.nlm.nih.gov/pubmed/30353104
http://dx.doi.org/10.1038/s41598-018-33678-3
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