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Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease
Published on: June 17, 2013
Somatosensory function in asymptomatic Parkin-mutation carriers
J Gierthmühlen1, S Schumacher, G Deuschl
1Division of Neurological Pain Research and Therapy, Department of Neurology, University of Kiel, Kiel, Germany. j.gierthmuehlen@neurologie.uni-kiel.de
European Journal of Neurology
|October 30, 2009
Summary
Somatosensory abnormalities, potentially affecting central pathways, may precede motor symptoms in Parkinson's disease (PD) linked to Parkin mutations. Asymptomatic carriers show sensory deficits but not reduced sural nerve action potentials (SNAP).
Area of Science:
- Neuroscience
- Genetics
- Neurology
Background:
- The origin and timing of somatosensory abnormalities in Parkinson's disease (PD) are debated.
- Reduced sensory sural nerve action potential amplitude (SNAP) is noted in symptomatic Parkin-associated PD.
Purpose of the Study:
- To investigate asymptomatic Parkin-mutation carriers for early somatosensory changes.
- To determine if these sensory abnormalities precede motor symptoms and their origin (central vs. peripheral).
Main Methods:
- Clinical examination, quantitative sensory testing (QST), and neurography were performed on nine Parkin-mutation carriers and nine healthy controls.
- Focus on identifying abnormalities in sensory pathways.
Main Results:
- Parkin-mutation carriers showed increased cold pain threshold abnormalities and Abeta-fibre/central afferent pathway hypofunction compared to controls.
- Neurography did not reveal peripheral neuropathy in carriers.
- Asymptomatic carriers did not exhibit reduced SNAP, unlike symptomatic PD patients.
Conclusions:
- QST findings suggest sensory pathway impairment (peripheral or central) in asymptomatic Parkin-mutation carriers.
- These early sensory changes may precede motor symptoms in Parkin-associated PD.
- The absence of reduced SNAP differentiates asymptomatic carriers from symptomatic PD.
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