Effects of deep brain stimulation and medication on bradykinesia and muscle activation in Parkinson’s disease
Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and antiparkinsonian medication (Meds) have proved to be effective therapies for treating bradykinesia in Parkinson’s disease. However, it is not currently known how or to what extent STN stimulation alters the control signals to agonist...
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Published in | Brain (London, England : 1878) Vol. 127; no. 3; pp. 491 - 504 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Oxford University Press
01.03.2004
Oxford Publishing Limited (England) |
Subjects | |
Online Access | Get full text |
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Summary: | Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and antiparkinsonian medication (Meds) have proved to be effective therapies for treating bradykinesia in Parkinson’s disease. However, it is not currently known how or to what extent STN stimulation alters the control signals to agonist and antagonist muscles to change movement speed. Our objective was to investigate movement speed along with the amplitude and temporal features of EMG activity to determine how and to what extent these parameters are changed by DBS and medication. Nine patients with Parkinson’s disease were studied following neurosurgery that implanted high‐frequency stimulating electrodes in the STN. The experiments for the patients were performed in each of four treatment conditions: (i) OFF treatment; (ii) STN DBS; (iii) Meds; and (iv) Meds plus STN DBS. Also, a group of age‐ and gender‐matched control subjects were examined. Medication and DBS had similar effects in that both treatments increased movement speed, increased the amplitude of the first agonist burst, increased burst duration, reduced the number of agonist bursts, reduced cocontraction, increased the size of the antagonist EMG, and reduced the centroid time of the antagonist EMG. When DBS and medication were combined, only temporal measures of burst duration and the number of agonist bursts were different from the medication alone condition. There was a positive association between the level of bradykinesia OFF treatment and the level of bradykinesia following DBS and medication. The movement speed of neurologically normal control subjects’ was over 40% higher during both flexion and extension movements when compared with the patients during Meds plus STN DBS. The changes in the muscle activation patterns provide a mechanism of action for the pharmacological and surgical interventions used to treat bradykinesia in Parkinson’s disease. However, despite the success of medication and DBS at improving bradykinesia in patients with Parkinson’s disease, patients’ movement speed was not restored to normal due to limitations in the amplitude and temporal scaling of the agonist and antagonist bursting pattern. These findings suggest a link between basal ganglia function in scaling both the amplitude and temporal parameters of the input to the motor neuron pool. |
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Bibliography: | Correspondence to: David E. Vaillancourt, Department of Movement Science (M/C 194) University of Illinois at Chicago, 901 West Roosevelt Road, Chicago, IL 60608, USAE‐mail: court1@uic.edu local:awh057 Received May 29, 2003. Revision September 12, 2003. Second revision October 13, 2003. Accepted October 14, 2003. istex:1328FFD167EF0DCF49944E16A2696B75E37E1A53 ark:/67375/HXZ-Z2HXKC51-L ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23 |
ISSN: | 0006-8950 1460-2156 1460-2156 |
DOI: | 10.1093/brain/awh057 |