Background And Purpose: This study aimed to assess the indices of corticomotor excitability (CE) in drug-naive Parkinson disease (PD) patients and to investigate its relationship with asymmetry and severity of clinical symptoms.
Material And Methods: Eleven (4 men) drug-naive PD patients (mean age: 53.1 ± 9.8 years) and 13 (7 men) healthy controls (mean age: 51.7 ± 4.2 years) were included. All PD patients were rated on the motor section of the Unified Parkinson's Disease Rating Scale (UPDRS) with measurement of the side-specific score separately for arms and legs. Resting motor threshold (RMT), central silent period (CSP), amplitude of motor evoked potential (MEP) and central motor conduction time (CMCT) evoked by a single pulse of the transcranial magnetic stimulation were recorded in all subjects from the left and right abductor digiti minimi (ADM) and extensor digitorum brevis (EDB).
Results: Parkinson disease patients showed higher MEP (1.8 ± 0.9 vs. 1.1 ± 0.8 mV, p < 0.05) and shorter CMCT (6.1 ± 0.9 vs. 7.4 ± 1.0 ms, p < 0.05) recorded from the ADM on the more affected side. CSP recorded from the more affected ADM was under the normal range in five and from the less affected ADM in four PD patients. For CSP recorded from the EDB, respective values are four for the more affected side and three for the less affected side. The rigidity from the more affected arm and leg correlated negatively with the respective CSP recorded from the ADM (r = -0.74, p < 0.01) and EDB (r = -0.68, p < 0.04).
Conclusions: In the early stage of untreated PD the CE parameters are altered only on the more affected side. The shortening of CSP reflects the severity of rigidity on the more affected side.
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http://dx.doi.org/10.5114/ninp.2013.34699 | DOI Listing |
J Neuroeng Rehabil
January 2025
Department of Mechanical and Aerospace Engineering, University of Florida, PO Box 116250, Gainesville, FL, 32611, USA.
Background: Motor module (a.k.a.
View Article and Find Full Text PDFMol Neurodegener
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Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, 20815, USA.
Gastrointestinal (GI) involvement in Lewy body diseases (LBDs) has been observed since the initial descriptions of patients by James Parkinson. Recent experimental and human observational studies raise the possibility that pathogenic alpha-synuclein (⍺-syn) might develop in the GI tract and subsequently spread to susceptible brain regions. The cellular and mechanistic origins of ⍺-syn propagation in disease are under intense investigation.
View Article and Find Full Text PDFNat Med
January 2025
Department of Neurology & Neurological Sciences, Stanford Movement Disorders Center, Stanford University, Stanford, CA, USA.
Cerebral accumulation of alpha-synuclein (αSyn) aggregates is the hallmark event in a group of neurodegenerative diseases-collectively called synucleinopathies-which include Parkinson's disease, dementia with Lewy bodies and multiple system atrophy. Currently, these are diagnosed by their clinical symptoms and definitively confirmed postmortem by the presence of αSyn deposits in the brain. Here, we summarize the drawbacks of the current clinical definition of synucleinopathies and outline the rationale for moving toward an earlier, biology-anchored definition of these disorders, with or without the presence of clinical symptoms.
View Article and Find Full Text PDFNPJ Parkinsons Dis
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Movement Disorders Unit, Department of Neurology, Hospital La Fe, Valencia, Spain.
Trends Neurosci
January 2025
Department of Neurosurgery, Department of Surgery, University of Toronto, Toronto, Ontario, Canada; Krembil Brain Institute, Toronto Western Hospital, Toronto, Ontario, Canada; Center for Advancing Neurotechnological Innovation to Application (CRANIA), Toronto, Ontario, Canada.
Parkinson's disease (PD) is a significant source of morbidity, especially with an aging population. Gait problems, particularly freezing of gait (FOG), remain a persistent issue, causing falls and reduced quality of life without consistent responses to therapies. PD and related symptoms have classically been attributed to dopamine deficiency secondary to substantia nigra degeneration from Lewy body (LB) and Lewy neurite (LN) infiltration.
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