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1.
Parkinsonism Relat Disord ; 21(3): 259-65, 2015 Mar.
Article in English | MEDLINE | ID: mdl-25596880

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.


Subject(s)
Fingers/physiopathology , Parkinson Disease/complications , Parkinson Disease/pathology , Psychomotor Disorders/etiology , Somatosensory Cortex/physiopathology , Aged , Analysis of Variance , Female , Humans , Image Processing, Computer-Assisted , Magnetic Resonance Imaging , Male , Middle Aged , Oxygen/blood , Pain Measurement , Somatosensory Cortex/blood supply
2.
Arch Neurol ; 68(11): 1467-70, 2011 Nov.
Article in English | MEDLINE | ID: mdl-22084132

ABSTRACT

BACKGROUND: In brachial plexus avulsion, a recent technique connects the ending of the disrupted musculocutaneous nerve to the side of the intact phrenic nerve to regain elbow flexion. This requires the phrenic nerve to perform a new double function: independent control of breathing and elbow flexion. Neuroplastic changes associated with acquisition of double nerve functions have not yet been investigated. OBJECTIVE: To evaluate neuroplastic changes associated with acquisition of double nerve functions in a monofunctional nerve (phrenic nerve). DESIGN: Clinical and functional magnetic resonance imaging investigations during arm movements, forced inspiration, and motor control tasks. SETTING: Investigations at the Medical University of Vienna, Vienna, Austria. PARTICIPANTS: Three healthy control subjects, 2 patients with phrenic nerve end-to-side coaptation, and 1 control patient with C7 end-to-end coaptation (same clinical presentation but phrenic nerve unchanged). RESULTS: Clinical documentation showed that both patients with phrenic nerve end-to-side coaptation were able to control the diaphragm and the biceps independently via the same phrenic nerve. In contrast to all controls, both patients with phrenic nerve end-to-side coaptation activated the cortical diaphragm areas with flexion of the diseased arm. CONCLUSION: Our functional magnetic resonance imaging data indicate that the patient's cortical diaphragm areas reorganize in such a way that independent control of breathing and elbow flexion is possible with the same neuronal population.


Subject(s)
Brachial Plexus/injuries , Brachial Plexus/surgery , Motor Cortex/physiology , Neuronal Plasticity/physiology , Neurosurgical Procedures/methods , Adult , Child , Female , Humans , Male , Nerve Regeneration/physiology , Phrenic Nerve/physiology
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