Motor cortical physiology in patients and asymptomatic carriers of parkin gene mutations
Identifieur interne : 002758 ( Main/Exploration ); précédent : 002757; suivant : 002759Motor cortical physiology in patients and asymptomatic carriers of parkin gene mutations
Auteurs : Susanne A. Schneider [Royaume-Uni] ; Penelope Talelli [Royaume-Uni] ; Binith J. Cheeran [Royaume-Uni] ; Naheed L. Khan [Royaume-Uni] ; Nicholas W. Wood [Royaume-Uni] ; John C. Rothwell [Royaume-Uni] ; Kailash P. Bhatia [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-10-15.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Adult, Aged, Analysis of Variance, Asymptomatic, Carrier, Case-Control Studies, Electric Stimulation, Electromyography, Evoked Potentials, Motor (physiology), Female, Human, Humans, Male, Middle Aged, Motor Cortex (physiopathology), Mutation, Mutation (genetics), Nervous system diseases, Neural Conduction (physiology), Neurophysiology, Parkin, Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease/Parkinsonism, Parkinsonism, Physiology, Pyramidal Tracts (physiopathology), Reaction Time (physiology), Recruitment, Neurophysiological (physiology), Sensory Thresholds, TMS, Transcranial Magnetic Stimulation (methods), Ubiquitin-Protein Ligases (genetics), carrier/asymptomatic, neurophysiology.
- MESH :
- chemical , genetics : Ubiquitin-Protein Ligases.
- genetics : Mutation, Parkinson Disease.
- methods : Transcranial Magnetic Stimulation.
- pathology : Parkinson Disease.
- physiology : Evoked Potentials, Motor, Neural Conduction, Reaction Time, Recruitment, Neurophysiological.
- physiopathology : Motor Cortex, Parkinson Disease, Pyramidal Tracts.
- Adult, Aged, Analysis of Variance, Case-Control Studies, Electric Stimulation, Electromyography, Female, Humans, Male, Middle Aged, Sensory Thresholds.
Abstract
Autosomal recessive parkin (PARK2) gene‐related parkinsonism may be phenotypically and pathophysiologically distinct from idiopathic Parkinson's disease (PD). Furthermore, asymptomatic subjects carrying a single parkin mutation (“parkin carriers”) may show striatal dopaminergic dysfunction and increased cortical movement‐related activation. Here, we used transcranial magnetic stimulation (TMS) to study corticospinal and intracortical excitability in manifesting parkin patients and asymptomatic carriers. We studied resting and active motor thresholds (RMT/AMT), central motor conduction time (CMCT), active recruitment curves, short‐interval intracortical inhibition (SICI) and facilitation (ICF), SICI recruitment curve, and cortical silent period (CSP) in 8 patients “off” medication, 7 carriers, and two groups of age‐matched controls (n = 21). Patients had longer CMCTs compared to controls with a significant negative correlation between CMCT duration and onset age (r = −0.83, P = 0.04). Carriers had increased RMT/AMT; the time course of SICI/ICF and the duration of CSP were normal in both patients and carriers; however slight abnormalities in the recruitment of SICI were found in the carriers. Prolonged CMCT and normal cortical inhibitory mechanisms in parkin patients may be of value in the differentiation from idiopathic PD. The subclinical electrophysiological abnormalities found in carriers may represent underlying compensatory mechanisms. © 2008 Movement Disorder Society
Url:
DOI: 10.1002/mds.22025
Affiliations:
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Schneider</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square London</wicri:regionArea><wicri:noRegion>Queen Square London</wicri:noRegion></affiliation></author><author><name sortKey="Talelli, Penelope" sort="Talelli, Penelope" uniqKey="Talelli P" first="Penelope" last="Talelli">Penelope Talelli</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, Queen Square London</wicri:regionArea><wicri:noRegion>Queen Square London</wicri:noRegion></affiliation></author><author><name sortKey="Cheeran, Binith J" sort="Cheeran, Binith J" uniqKey="Cheeran B" first="Binith J." last="Cheeran">Binith J. 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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008-10-15">2008-10-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">13</biblScope><biblScope unit="page" from="1812">1812</biblScope><biblScope unit="page" to="1819">1819</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">8DBA789A49FF28CEAAD756D3D45E723D8587E55E</idno><idno type="DOI">10.1002/mds.22025</idno><idno type="ArticleID">MDS22025</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Analysis of Variance</term><term>Asymptomatic</term><term>Carrier</term><term>Case-Control Studies</term><term>Electric Stimulation</term><term>Electromyography</term><term>Evoked Potentials, Motor (physiology)</term><term>Female</term><term>Human</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Motor Cortex (physiopathology)</term><term>Mutation</term><term>Mutation (genetics)</term><term>Nervous system diseases</term><term>Neural Conduction (physiology)</term><term>Neurophysiology</term><term>Parkin</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Parkinson's disease/Parkinsonism</term><term>Parkinsonism</term><term>Physiology</term><term>Pyramidal Tracts (physiopathology)</term><term>Reaction Time (physiology)</term><term>Recruitment, Neurophysiological (physiology)</term><term>Sensory Thresholds</term><term>TMS</term><term>Transcranial Magnetic Stimulation (methods)</term><term>Ubiquitin-Protein Ligases (genetics)</term><term>carrier/asymptomatic</term><term>neurophysiology</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Transcranial Magnetic Stimulation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Evoked Potentials, Motor</term><term>Neural Conduction</term><term>Reaction Time</term><term>Recruitment, Neurophysiological</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Motor Cortex</term><term>Parkinson Disease</term><term>Pyramidal Tracts</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Analysis of Variance</term><term>Case-Control Studies</term><term>Electric Stimulation</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Sensory Thresholds</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Asymptomatique</term><term>Homme</term><term>Maladie de Parkinson</term><term>Mutation</term><term>Neurophysiologie</term><term>Parkine</term><term>Parkinsonisme</term><term>Pathologie du système nerveux</term><term>Physiologie</term><term>Porteur</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autosomal recessive parkin (PARK2) gene‐related parkinsonism may be phenotypically and pathophysiologically distinct from idiopathic Parkinson's disease (PD). Furthermore, asymptomatic subjects carrying a single parkin mutation (“parkin carriers”) may show striatal dopaminergic dysfunction and increased cortical movement‐related activation. Here, we used transcranial magnetic stimulation (TMS) to study corticospinal and intracortical excitability in manifesting parkin patients and asymptomatic carriers. We studied resting and active motor thresholds (RMT/AMT), central motor conduction time (CMCT), active recruitment curves, short‐interval intracortical inhibition (SICI) and facilitation (ICF), SICI recruitment curve, and cortical silent period (CSP) in 8 patients “off” medication, 7 carriers, and two groups of age‐matched controls (n = 21). Patients had longer CMCTs compared to controls with a significant negative correlation between CMCT duration and onset age (r = −0.83, P = 0.04). Carriers had increased RMT/AMT; the time course of SICI/ICF and the duration of CSP were normal in both patients and carriers; however slight abnormalities in the recruitment of SICI were found in the carriers. Prolonged CMCT and normal cortical inhibitory mechanisms in parkin patients may be of value in the differentiation from idiopathic PD. The subclinical electrophysiological abnormalities found in carriers may represent underlying compensatory mechanisms. © 2008 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Schneider, Susanne A" sort="Schneider, Susanne A" uniqKey="Schneider S" first="Susanne A." last="Schneider">Susanne A. Schneider</name></noRegion><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name><name sortKey="Cheeran, Binith J" sort="Cheeran, Binith J" uniqKey="Cheeran B" first="Binith J." last="Cheeran">Binith J. Cheeran</name><name sortKey="Khan, Naheed L" sort="Khan, Naheed L" uniqKey="Khan N" first="Naheed L." last="Khan">Naheed L. Khan</name><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. Rothwell</name><name sortKey="Talelli, Penelope" sort="Talelli, Penelope" uniqKey="Talelli P" first="Penelope" last="Talelli">Penelope Talelli</name><name sortKey="Wood, Nicholas W" sort="Wood, Nicholas W" uniqKey="Wood N" first="Nicholas W." last="Wood">Nicholas W. Wood</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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