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Proprioceptive sensory function in Parkinson's disease and Huntington's disease: evidence from proprioception-related EEG potentials

Proprioceptive sensory function in Parkinson's disease and Huntington's disease: evidence from proprioception-related EEG potentials
Proprioceptive sensory function in Parkinson's disease and Huntington's disease: evidence from proprioception-related EEG potentials
In both Parkinson's disease and Huntington's disease, proprioceptive sensory deficits have been suggested to contribute to the motor manifestations of the disease. Here, proprioceptive sensory function was investigated in Parkinson's disease patients, Huntington's disease patients, and healthy control subjects (each group n=8), using proprioception-related evoked potentials. Proprioception-related potentials were elicited by passive index finger movements and measured with high-density EEG. Conventional median nerve somatosensory evoked potentials (mnSEPs) were recorded in the same session. Analysis included amplitude and latency measures from selected scalp electrodes and dipole source reconstruction. We found a proprioception-related N90 component of normal latency in both Parkinson's disease and Huntington's disease. The source strength of the underlying cortical generator was normal in Parkinson's disease, but marginally reduced in Huntington's disease. Using the source location of the N20-P20 component of the mnSEP as a landmark for postcentral area 3b, the N90 was localized to the precentral motor cortex. At a latency around 170-180 ms proprioception-related potentials were explained by bilateral sensory cortex activation with an altered distribution in Parkinson's disease and a reduction of ipsilateral activation in Huntington's disease. Together, the results show largely normal early proprioception-related potentials, but changes in the cortical processing of kinaesthetic signals at longer latencies in both diseases.
parkinson's disease, huntington's disease, propriocepsis, evoked potentials
0014-4819
308-319
Seiss, E.
6d13313a-221c-47c8-b550-76ae4e758259
Praamstra, P.
5e90386c-1700-4216-bae8-90e9dc4a2189
Hesse, C.W.
53fee7f7-a12e-4783-a426-0d59afbf475d
Rickards, H.
4235a759-ce68-4414-97c3-1f54401eaaac
Seiss, E.
6d13313a-221c-47c8-b550-76ae4e758259
Praamstra, P.
5e90386c-1700-4216-bae8-90e9dc4a2189
Hesse, C.W.
53fee7f7-a12e-4783-a426-0d59afbf475d
Rickards, H.
4235a759-ce68-4414-97c3-1f54401eaaac

Seiss, E., Praamstra, P., Hesse, C.W. and Rickards, H. (2003) Proprioceptive sensory function in Parkinson's disease and Huntington's disease: evidence from proprioception-related EEG potentials. Experimental Brain Research, 148 (3), 308-319.

Record type: Article

Abstract

In both Parkinson's disease and Huntington's disease, proprioceptive sensory deficits have been suggested to contribute to the motor manifestations of the disease. Here, proprioceptive sensory function was investigated in Parkinson's disease patients, Huntington's disease patients, and healthy control subjects (each group n=8), using proprioception-related evoked potentials. Proprioception-related potentials were elicited by passive index finger movements and measured with high-density EEG. Conventional median nerve somatosensory evoked potentials (mnSEPs) were recorded in the same session. Analysis included amplitude and latency measures from selected scalp electrodes and dipole source reconstruction. We found a proprioception-related N90 component of normal latency in both Parkinson's disease and Huntington's disease. The source strength of the underlying cortical generator was normal in Parkinson's disease, but marginally reduced in Huntington's disease. Using the source location of the N20-P20 component of the mnSEP as a landmark for postcentral area 3b, the N90 was localized to the precentral motor cortex. At a latency around 170-180 ms proprioception-related potentials were explained by bilateral sensory cortex activation with an altered distribution in Parkinson's disease and a reduction of ipsilateral activation in Huntington's disease. Together, the results show largely normal early proprioception-related potentials, but changes in the cortical processing of kinaesthetic signals at longer latencies in both diseases.

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More information

Published date: 2003
Keywords: parkinson's disease, huntington's disease, propriocepsis, evoked potentials

Identifiers

Local EPrints ID: 10974
URI: https://eprints.soton.ac.uk/id/eprint/10974
ISSN: 0014-4819
PURE UUID: f993e84e-47b6-44a7-bf50-2a4855e78d40

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Date deposited: 28 Apr 2005
Last modified: 17 Jul 2017 17:05

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