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Impact of deep brain stimulation on upper limb akinesia in Parkinson's disease

Recent pathophysiological models of Parkinson's disease have led to new surgical approaches to treatment including deep brain stimulation (DBS) and lesioning of basal ganglia structures. Various measures of upper limb akinesia were assessed in 6 patients with bilateral DBS of the internal palli...

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Bibliographic Details
Published in:Annals of neurology 1999-04, Vol.45 (4), p.473-488
Main Authors: Brown, R. G., Limousin Dowsey, P., Brown, P., Jahanshahi, M., Pollak, P., Benabid, A. L., Rodriguez-Oroz, M. C., Obeso, J., Rothwell, J. C.
Format: Article
Language:English
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Summary:Recent pathophysiological models of Parkinson's disease have led to new surgical approaches to treatment including deep brain stimulation (DBS) and lesioning of basal ganglia structures. Various measures of upper limb akinesia were assessed in 6 patients with bilateral DBS of the internal pallidum and 6 with DBS of the subthalamic nucleus. Stimulation improved a number of aspects of motor function, and particularly movement time, and force production. Time to initiate movements, and to perform repetitive movements also improved but less dramatically. Processes indicating preparatory motor processes showed no significant change. Few significant differences were found between the internal pallidum and subthalamic nucleus groups. In general, the effects of DBS closely parallel previous reports of the effects of dopaminergic medication. It is suggested that disrupted pallidal output in Parkinson's disease interferes with the rate, level, and coordination of force production but has little effect on preparatory processes. The similarity of the effects of subthalamic nucleus and internal pallidum stimulation suggests this disrupted outflow is the most important determinant of upper limb akinesia in Parkinson's disease. The effects of DBS were similar to the effects of unilateral pallidal lesions reported elsewhere. Ann Neurol 1999;45:473–488
ISSN:0364-5134
1531-8249
DOI:10.1002/1531-8249(199904)45:4<473::AID-ANA9>3.0.CO;2-V