Background: The primary motor sign of Parkinson's disease is bradykinesia. It has been surprisingly difficult to provide a clear neurobiological mechanism for this fundamental movement deficit in Parkinson's disease. It has been proposed that in healthy individuals the gating of sensory afferents prior to and during movement is an essential step in initiating movement. This down-weighting has been proposed to account for the attenuation of the somatosensory evoked potential following median nerve stimulation at the onset of and during hand movements. The objective of this study was to test whether this sensory attenuation present at movement onset in healthy controls is present in patients with Parkinson's disease.

Methods: Eighteen right-handed patients with idiopathic Parkinson's disease and 16 right-handed age-matched healthy participants were studied. Somatosensory evoked potentials were elicited after electrical stimulation of the median nerve at the wrist. Electroencephalograms were recorded over the scalp at 3 sites on according to the International 10-20 System (F3, C3, and P3). Somatosensory evoked potentials were recorded in 2 conditions: at rest and at the onset of movement (a self-paced abduction movement of the right thumb).

Results: Off medication, Parkinson's disease patients had no sensory attenuation at movement onset. On medication, sensory attenuation at movement onset was present.

Conclusions: We suggest that this preliminary result is consistent with the hypothesis that, a failure in sensory attenuation contributes to the difficulties in movement initiation in Parkinson's disease.

Download full-text PDF

Source
http://dx.doi.org/10.1002/mds.26493DOI Listing

Publication Analysis

Top Keywords

parkinson's disease
24
sensory attenuation
20
somatosensory evoked
12
attenuation movement
12
movement onset
12
movement
10
onset movement
8
median nerve
8
evoked potentials
8
parkinson's
7

Similar Publications

Global Perspectives on Returning Genetic Research Results in Parkinson Disease.

Neurol Genet

December 2024

From the Division of Neurology (A.H.T., S.-Y.L.), Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; Programa de Pós-Graduação em Ciências Médicas da Universidade Federal do Rio Grande do Sul (P.S.-A.), Clínica Santa María, Santiago, Chile; Departamento de Farmacologia (A.F.S.S.), Universidade Federal do Rio Grande do Sul; Serviço de Neurologia (A.F.S.S.), Hospital de Clínicas de Porto Alegre, Brazil; Institute of Neurogenetics (H.M., M.L.D., C.K.), University of Lübeck, Germany; Department of Biomedical Science (A.A.-A.), Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; The Michael J. Fox Foundation for Parkinson's Research (J.S., B.F.), New York; Department of Medical and Molecular Genetics (C.E.W.), Indiana University, Indianapolis; Department of Neuroscience and Brain Health (M.L.D.), Metropolitan Medical Center, Manila, Philippines; Centre for Preventive Neurology (S.D., M.T.P., A.J.N.), Wolfson Institute of Population Health, Queen Mary University of London, United Kingdom; Unidad de Trastornos del Movimiento (M.T.P.), Servicio de Neurología y Neurofisiología Clínica, Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Spain; Laboratory of Neurogenetics (M.B.M.), National Institute on Aging, National Institutes of Health, Bethesda, MD; Department of Clinical and Movement Neurosciences (M.B.M., H.R.M.), UCL Queen Square Institute of Neurology, University College London, United Kingdom; Department of Neurology (R.N.A.), Columbia University Irving Medical Center, New York; Movement Disorders Division (R.N.A.), Neurological Institute, Tel Aviv Sourasky Medical Center and Tel Aviv School of Medicine, Tel Aviv University, Israel; Molecular Medicine Laboratory and Neurology Department (K.R.K.), Concord Clinical School, Concord Repatriation General Hospital, The University of Sydney; Translational Neurogenomics Group (K.R.K.), Genomic and Inherited Disease Program, Garvan Institute of Medical Research; and St Vincent's Healthcare Campus (K.R.K.), Faculty of Medicine, UNSW Sydney, Darlinghurst, New South Wales, Australia.

Background And Objectives: In the era of precision medicine, genetic test results have become increasingly relevant in the care of patients with Parkinson disease (PD). While large research consortia are performing widespread research genetic testing to accelerate discoveries, debate continues about whether, and to what extent, the results should be returned to patients. Ethically, it is imperative to keep participants informed, especially when findings are potentially actionable.

View Article and Find Full Text PDF

Application trends of hydrogen-generating nanomaterials for the treatment of ROS-related diseases.

Biomater Sci

January 2025

Center for Molecular Recognition and Biosensing, School of Life Sciences, Shanghai University, Shanghai 200444, China.

Reactive oxygen species (ROS) play essential roles in both physiological and pathological processes. Under physiological conditions, appropriate amounts of ROS play an important role in signaling and regulation in cells. However, too much ROS can lead to many health problems, including inflammation, cancer, delayed wound healing, neurodegenerative diseases (such as Parkinson's disease and Alzheimer's disease), and autoimmune diseases, and oxidative stress from excess ROS is also one of the most critical factors in the pathogenesis of cardiovascular and metabolic diseases such as atherosclerosis.

View Article and Find Full Text PDF

Introduction: Parkinson's disease is a neurodegenerative disorder that presents with motor symptoms such as tremors, slowness and gait difficulties, in addition to various non-motor symptoms such as anxiety, depression and autonomic and sleep disturbances. Pranayama (yogic breathing practices) has been studied as a part of yoga interventions in Parkinson's disease. Previous systematic reviews and meta-analyses have not detailed the pranayama practices used in clinical studies, and there is no clarity on the pranayama practices that would be most beneficial for Parkinson's disease.

View Article and Find Full Text PDF

Oxidation of dopamine can cause various side effects, which ultimately leads to cell death and contributes to Parkinson's disease (PD). To counteract dopamine oxidation, newly synthesized dopamine is quickly transported into vesicles via vesicular monoamine transporter 2 (VMAT2) for storage. VMAT2 expression is reduced in patients with PD, and studies have shown increased accumulation of dopamine oxidation byproducts and α-synuclein in animals with low VMAT2 expression.

View Article and Find Full Text PDF

Nutritional epidemiology aims to link dietary exposures to chronic disease, but the instruments for evaluating dietary intake are inaccurate. One way to identify unreliable data and the sources of errors is to compare estimated intakes with the total energy expenditure (TEE). In this study, we used the International Atomic Energy Agency Doubly Labeled Water Database to derive a predictive equation for TEE using 6,497 measures of TEE in individuals aged 4 to 96 years.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!