Altered sensorimotor integration in Parkinson’s disease

Transcranial magnetic stimulation (TMS) was used to investigate sensorimotor integration in the upper limb of 10 patients with Parkinson’s disease and 10 age‐matched controls. Non‐conditioned and subthreshold conditioned (2 ms interstimulus interval) responses were recorded in the flexor and extenso...

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Published inBrain (London, England : 1878) Vol. 125; no. 9; pp. 2089 - 2099
Main Authors Lewis, Gwyn N., Byblow, Winston D.
Format Journal Article
LanguageEnglish
Published Oxford Oxford University Press 01.09.2002
Oxford Publishing Limited (England)
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ISSN0006-8950
1460-2156
1460-2156
DOI10.1093/brain/awf200

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Summary:Transcranial magnetic stimulation (TMS) was used to investigate sensorimotor integration in the upper limb of 10 patients with Parkinson’s disease and 10 age‐matched controls. Non‐conditioned and subthreshold conditioned (2 ms interstimulus interval) responses were recorded in the flexor and extensor carpi radialis muscles (FCR and ECR) of the more impaired (non‐dominant) limb. Stimuli were delivered while the wrist joint was positioned statically at various joint angles as well as during different phases of passive movement of the wrist joint (90° amplitude, 0.2 Hz). The FCR and ECR muscles remained relaxed during all stimulation. In both groups, responses in the static condition were larger when the target muscle was in a shortened position. Responses were also facilitated in the muscle shortening phases of passive movement. In both static and dynamic conditions, the extent of modulations in response amplitude was significantly reduced in the patient group. The level of intracortical inhibition (ICI) was also significantly less in the Parkinson’s disease patients in static conditions. During passive movement, control subjects demonstrated a clear reduction in ICI compared with the static trials; however, the level of ICI was unchanged in the Parkinson’s disease group in the dynamic condition. The results suggest an abnormal influence of afference on corticomotor excitability in Parkinson’s disease. This may be related to abnormal sensory input, a defective integrative unit or an inappropriate motor response.
Bibliography:local:awf200
istex:653462B6F5B131E7C3F2DE8DAF82896D52DE6945
Correspondence to: Gwyn N. Lewis, Department of Sport and Exercise Science, University of Auckland, Private Bag 92019, Auckland, New Zealand E‐mail: gn.lewis@auckland.ac.nz
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ISSN:0006-8950
1460-2156
1460-2156
DOI:10.1093/brain/awf200