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

This data was imported from PubMed:

Authors: Seiss, E., Praamstra, P., Hesse, C.W. and Rickards, H.

Journal: Exp Brain Res

Volume: 148

Issue: 3

Pages: 308-319

ISSN: 0014-4819

DOI: 10.1007/s00221-002-1291-6

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.

This data was imported from Scopus:

Authors: Seiss, E., Praamstra, P., Hesse, C.W. and Rickards, H.

Journal: Experimental Brain Research

Volume: 148

Issue: 3

Pages: 308-319

ISSN: 0014-4819

DOI: 10.1007/s00221-002-1291-6

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.

This data was imported from Web of Science (Lite):

Authors: Seiss, E., Praamstra, P., Hesse, C.W. and Rickards, H.

Journal: EXPERIMENTAL BRAIN RESEARCH

Volume: 148

Issue: 3

Pages: 308-319

eISSN: 1432-1106

ISSN: 0014-4819

DOI: 10.1007/s00221-002-1291-6

This data was imported from Europe PubMed Central:

Authors: Seiss, E., Praamstra, P., Hesse, C.W. and Rickards, H.

Journal: Experimental brain research

Volume: 148

Issue: 3

Pages: 308-319

eISSN: 1432-1106

ISSN: 0014-4819

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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