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Eur J Neurol. 2010 Mar;17(3):513-7. doi: 10.1111/j.1468-1331.2009.02797.x. Epub 2009 Oct 23.

Somatosensory function in asymptomatic Parkin-mutation carriers.

Author information

1
Division of Neurological Pain Research and Therapy, Department of Neurology, University of Kiel, Kiel, Germany. j.gierthmuehlen@neurologie.uni-kiel.de

Abstract

BACKGROUND AND PURPOSE:

It is a matter of debate whether somatosensory abnormalities in Parkinson's disease (PD) precede or follow PD motor signs and whether they are of central or peripheral origin. The sensory sural nerve action potential amplitude (SNAP) was previously reported to be reduced in symptomatic Parkin-associated PD. The aim of our study was to investigate asymptomatic Parkin-mutation carriers to elucidate whether putative somatosensory abnormalities precede motor symptoms therewith helping to determine the origin of somatosensory signs.

METHODS:

Nine subjects with Parkin-mutations and nine healthy controls were examined clinically, with quantitative sensory testing (QST) and neurography.

RESULTS:

There was a higher frequency of cold pain threshold abnormalities and hypofunction of Abeta-fibres/central afferent pathways in Parkin-mutation carriers compared to controls. Neurography of Parkin-mutation carriers did not indicate peripheral neuropathy.

CONCLUSIONS:

Sensory abnormalities of asymptomatic Parkin-mutation carriers as obtained by QST suggest impairment of either small and large peripheral pathways or central somatosensory processing. In contrast to Parkin-associated PD, asymptomatic Parkin-mutation carriers do not show a reduced SNAP.

[Indexed for MEDLINE]

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