Deep brain stimulation effects in dystonia: Time course of electrophysiological changes in early treatment
Identifieur interne : 001718 ( Main/Exploration ); précédent : 001717; suivant : 001719Deep brain stimulation effects in dystonia: Time course of electrophysiological changes in early treatment
Auteurs : Diane Ruge [Royaume-Uni] ; Stephen Tisch [Royaume-Uni, Australie] ; Marwan I. Hariz [Royaume-Uni] ; Ludvic Zrinzo [Royaume-Uni] ; Kailash P. Bhatia [Royaume-Uni] ; Niall P. Quinn [Royaume-Uni] ; Marjan Jahanshahi [Royaume-Uni] ; Patricia Limousin [Royaume-Uni] ; John C. Rothwell [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-08-15.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Adult, Deep Brain Stimulation (methods), Deep brain stimulation, Dystonia, Dystonia (physiopathology), Dystonia (therapy), Electromyography, Evoked Potentials, Motor (physiology), Excitability, Female, Globus Pallidus (physiology), Human, Humans, Male, Middle Aged, Nervous system diseases, Neural Inhibition, Plasticity, Severity of Illness Index, Time Factors, Transcranial Magnetic Stimulation, Treatment, Treatment Outcome, deep brain stimulation, dystonia, excitability, human, longitudinal, mechanism, plasticity.
- MESH :
- methods : Deep Brain Stimulation.
- physiology : Evoked Potentials, Motor, Globus Pallidus.
- physiopathology : Dystonia.
- therapy : Dystonia.
- Adult, Electromyography, Female, Humans, Male, Middle Aged, Neural Inhibition, Severity of Illness Index, Time Factors, Transcranial Magnetic Stimulation, Treatment Outcome.
Abstract
Deep brain stimulation to the internal globus pallidus is an effective treatment for primary dystonia. The optimal clinical effect often occurs only weeks to months after starting stimulation. To better understand the underlying electrophysiological changes in this period, we assessed longitudinally 2 pathophysiological markers of dystonia in patients prior to and in the early treatment period (1, 3, 6 months) after deep brain stimulation surgery. Transcranial magnetic stimulation was used to track changes in short‐latency intracortical inhibition, a measure of excitability of GABAA‐ergic corticocortical connections and long‐term potentiation‐like synaptic plasticity (as a response to paired associative stimulation). Deep brain stimulation remained on for the duration of the study. Prior to surgery, inhibition was reduced and plasticity increased in patients compared with healthy controls. Following surgery and commencement of deep brain stimulation, short‐latency intracortical inhibition increased toward normal levels over the following months with the same monotonic time course as the patients' clinical benefit. In contrast, synaptic plasticity changed rapidly, following a nonmonotonic time course: it was absent early (1 month) after surgery, and then over the following months increased toward levels observed in healthy individuals. We postulate that before surgery preexisting high levels of plasticity form strong memories of dystonic movement patterns. When deep brain stimulation is turned on, it disrupts abnormal basal ganglia signals, resulting in the absent response to paired associative stimulation at 1 month. Clinical benefit is delayed because engrams of abnormal movement persist and take time to normalize. Our observations suggest that plasticity may be a driver of long‐term therapeutic effects of deep brain stimulation in dystonia. © 2011 Movement Disorder Society
Url:
- https://api.istex.fr/document/0CFC8235EC8D0EED5AD51A8158677D675BDD72D6/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174341
DOI: 10.1002/mds.23731
Affiliations:
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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="2011-08-15">2011-08-15</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1913">1913</biblScope><biblScope unit="page" to="1921">1921</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">0CFC8235EC8D0EED5AD51A8158677D675BDD72D6</idno><idno type="DOI">10.1002/mds.23731</idno><idno type="ArticleID">MDS23731</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Deep Brain Stimulation (methods)</term><term>Deep brain stimulation</term><term>Dystonia</term><term>Dystonia (physiopathology)</term><term>Dystonia (therapy)</term><term>Electromyography</term><term>Evoked Potentials, Motor (physiology)</term><term>Excitability</term><term>Female</term><term>Globus Pallidus (physiology)</term><term>Human</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Nervous system diseases</term><term>Neural Inhibition</term><term>Plasticity</term><term>Severity of Illness Index</term><term>Time Factors</term><term>Transcranial Magnetic Stimulation</term><term>Treatment</term><term>Treatment Outcome</term><term>deep brain stimulation</term><term>dystonia</term><term>excitability</term><term>human</term><term>longitudinal</term><term>mechanism</term><term>plasticity</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Evoked Potentials, Motor</term><term>Globus Pallidus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dystonia</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Dystonia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neural Inhibition</term><term>Severity of Illness Index</term><term>Time Factors</term><term>Transcranial Magnetic Stimulation</term><term>Treatment Outcome</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dystonie</term><term>Excitabilité</term><term>Homme</term><term>Pathologie du système nerveux</term><term>Plasticité</term><term>Stimulation cérébrale profonde</term><term>Traitement</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">Deep brain stimulation to the internal globus pallidus is an effective treatment for primary dystonia. The optimal clinical effect often occurs only weeks to months after starting stimulation. To better understand the underlying electrophysiological changes in this period, we assessed longitudinally 2 pathophysiological markers of dystonia in patients prior to and in the early treatment period (1, 3, 6 months) after deep brain stimulation surgery. Transcranial magnetic stimulation was used to track changes in short‐latency intracortical inhibition, a measure of excitability of GABAA‐ergic corticocortical connections and long‐term potentiation‐like synaptic plasticity (as a response to paired associative stimulation). Deep brain stimulation remained on for the duration of the study. Prior to surgery, inhibition was reduced and plasticity increased in patients compared with healthy controls. Following surgery and commencement of deep brain stimulation, short‐latency intracortical inhibition increased toward normal levels over the following months with the same monotonic time course as the patients' clinical benefit. In contrast, synaptic plasticity changed rapidly, following a nonmonotonic time course: it was absent early (1 month) after surgery, and then over the following months increased toward levels observed in healthy individuals. We postulate that before surgery preexisting high levels of plasticity form strong memories of dystonic movement patterns. When deep brain stimulation is turned on, it disrupts abnormal basal ganglia signals, resulting in the absent response to paired associative stimulation at 1 month. Clinical benefit is delayed because engrams of abnormal movement persist and take time to normalize. Our observations suggest that plasticity may be a driver of long‐term therapeutic effects of deep brain stimulation in dystonia. © 2011 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Australie</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li><li>Sydney</li></settlement></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Ruge, Diane" sort="Ruge, Diane" uniqKey="Ruge D" first="Diane" last="Ruge">Diane Ruge</name></region><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name><name sortKey="Hariz, Marwan I" sort="Hariz, Marwan I" uniqKey="Hariz M" first="Marwan I." last="Hariz">Marwan I. Hariz</name><name sortKey="Jahanshahi, Marjan" sort="Jahanshahi, Marjan" uniqKey="Jahanshahi M" first="Marjan" last="Jahanshahi">Marjan Jahanshahi</name><name sortKey="Limousin, Patricia" sort="Limousin, Patricia" uniqKey="Limousin P" first="Patricia" last="Limousin">Patricia Limousin</name><name sortKey="Quinn, Niall P" sort="Quinn, Niall P" uniqKey="Quinn N" first="Niall P." last="Quinn">Niall P. Quinn</name><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C." last="Rothwell">John C. Rothwell</name><name sortKey="Tisch, Stephen" sort="Tisch, Stephen" uniqKey="Tisch S" first="Stephen" last="Tisch">Stephen Tisch</name><name sortKey="Zrinzo, Ludvic" sort="Zrinzo, Ludvic" uniqKey="Zrinzo L" first="Ludvic" last="Zrinzo">Ludvic Zrinzo</name></country><country name="Australie"><noRegion><name sortKey="Tisch, Stephen" sort="Tisch, Stephen" uniqKey="Tisch S" first="Stephen" last="Tisch">Stephen Tisch</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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