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Brain Advance Access published online on December 8, 2003
Brain, doi:10.1093/brain/awh057
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© 2003 The Guarantors of Brain

Article

Effects of deep brain stimulation and medication on bradykinesia and muscle activation in Parkinson’s disease

David E. Vaillancourt 1*, Janey Prodoehl 1, Leo Verhagen Metman 2, Roy A. Bakay 3, and Daniel M. Corcos 4

1 Department of Movement Science, University of Illinois at Chicago, USA
2 Neurological Sciences, Rush Presbyterian-St Luke’s Medical Center, Chicago, Illinois, USA
3 Neurosurgery, Rush Presbyterian-St Luke’s Medical Center, Chicago, Illinois, USA
4 Department of Movement Science, University of Illinois at Chicago, USA; Departments of Neurology, Bioengineering, and Physical Therapy, University of Illinois at Chicago, USA

* Corresponding author. E-mail: court1{at}uic.edu.

Received 29 May 2003 ; revised 13 October 2003 ; accepted 14 October 2003

Abstract

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.

Keywords: deep brain stimulation; subthalamic nucleus; bradykinesia; EMG; Parkinson’s disease
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