Thomas Foki1, Walter Pirker2, Alexander Geißler3, Dietrich Haubenberger4, Markus Hilbert5, Ilse Hoellinger6, Moritz Wurnig7, Jakob Rath8, Johann Lehrner9, Eva Matt10, Florian Fischmeister11, Siegfried Trattnig12, Eduard Auff13, Roland Beisteiner14. 1. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: thomas.foki@meduniwien.ac.at. 2. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: walter.pirker@meduniwien.ac.at. 3. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: alexander.geissler@meduniwien.ac.at. 4. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: dietrich.haubenberger@meduniwien.ac.at. 5. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: hilbert.fmri@gmail.com. 6. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: ilse.hoellinger@gmail.com. 7. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: mwurnig@gmail.com. 8. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: jakob.rath@meduniwien.ac.at. 9. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: johann.lehrner@meduniwien.ac.at. 10. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: eva.matt@meduniwien.ac.at. 11. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: florian.fischmeister@meduniwien.ac.at. 12. MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; Department of Radiology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: siegfried.trattnig@meduniwien.ac.at. 13. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: eduard.auff@meduniwien.ac.at. 14. Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria; MR Center of Excellence, Medical University of Vienna, Waehringer Guertel 18-20, A-1090, Vienna, Austria. Electronic address: roland.beisteiner@meduniwien.ac.at.
Abstract
INTRODUCTION: The patho-physiological basis for finger dexterity deficits in Parkinson's disease (PD) is controversial. Previously, bradykinesia was regarded as the major mechanism. However, recent research suggested limb-kinetic apraxia as an important component of impaired fine motor skills in PD. In contrast to bradykinesia, limb-kinetic apraxia only marginally responds to dopaminergic treatment. Here we investigate the novel hypothesis that the dexterity deficits are related to an intrinsic dysfunction of primary somatosensory cortex (S1), which is not reversible by dopaminergic medication. METHODS: Applying a standard and approved dexterity task (coin rotation), brain activation networks were investigated using functional magnetic resonance imaging in PD patients both ON and OFF medication and matched healthy controls. RESULTS: PD patients both ON and OFF medication showed impaired S1 activation relative to controls (p < 0.05; region of interest based analysis). The impaired S1 activation remained unchanged by dopaminergic medication. Despite the considerable clinical deficit, no other brain area showed impaired activation. In contrast, structures of the basal ganglia--motor cortex loop responded to dopaminergic medication. Behaviorally, dexterity performance both ON and OFF was significantly (p < 0.05) reduced relative to controls. CONCLUSIONS: Our results provide first evidence that dexterity deficits in PD are related to an S1 dysfunction which is insensitive to dopaminergic treatment.
INTRODUCTION: The patho-physiological basis for finger dexterity deficits in Parkinson's disease (PD) is controversial. Previously, bradykinesia was regarded as the major mechanism. However, recent research suggested limb-kinetic apraxia as an important component of impaired fine motor skills in PD. In contrast to bradykinesia, limb-kinetic apraxia only marginally responds to dopaminergic treatment. Here we investigate the novel hypothesis that the dexterity deficits are related to an intrinsic dysfunction of primary somatosensory cortex (S1), which is not reversible by dopaminergic medication. METHODS: Applying a standard and approved dexterity task (coin rotation), brain activation networks were investigated using functional magnetic resonance imaging in PDpatients both ON and OFF medication and matched healthy controls. RESULTS:PDpatients both ON and OFF medication showed impaired S1 activation relative to controls (p < 0.05; region of interest based analysis). The impaired S1 activation remained unchanged by dopaminergic medication. Despite the considerable clinical deficit, no other brain area showed impaired activation. In contrast, structures of the basal ganglia--motor cortex loop responded to dopaminergic medication. Behaviorally, dexterity performance both ON and OFF was significantly (p < 0.05) reduced relative to controls. CONCLUSIONS: Our results provide first evidence that dexterity deficits in PD are related to an S1 dysfunction which is insensitive to dopaminergic treatment.
Authors: T Foki; T Vanbellingen; C Lungu; W Pirker; S Bohlhalter; T Nyffeler; J Kraemmer; D Haubenberger; F Ph S Fischmeister; E Auff; M Hallett; R Beisteiner Journal: Eur J Neurol Date: 2016-05-01 Impact factor: 6.089
Authors: Tim Vanbellingen; Manuela Wapp; Katharina Stegmayer; Manuel Bertschi; Eugenio Abela; Stefanie Kübel; Thomas Nyffeler; René Müri; Sebastian Walther; Tobias Nef; Mark Hallett; Stephan Bohlhalter Journal: J Neural Transm (Vienna) Date: 2016-09-12 Impact factor: 3.575
Authors: Eva Matt; Thomas Foki; Florian Fischmeister; Walter Pirker; Dietrich Haubenberger; Jakob Rath; Johann Lehrner; Eduard Auff; Roland Beisteiner Journal: Brain Imaging Behav Date: 2017-04 Impact factor: 3.978