Levodopa affects functional brain networks in parkinsonian resting tremor
Identifieur interne : 002235 ( Main/Exploration ); précédent : 002234; suivant : 002236Levodopa affects functional brain networks in parkinsonian resting tremor
Auteurs : Bettina Pollok [Allemagne] ; Houssain Makhloufi [Allemagne] ; Markus Butz [Allemagne] ; Joachim Gross [Royaume-Uni] ; Lars Timmermann [Allemagne] ; Lars Wojtecki [Allemagne] ; Alfons Schnitzler [Allemagne]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-01-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Brain (drug effects), Brain (physiopathology), Brain Mapping, Cerebellum (drug effects), Cerebellum (physiopathology), Coherence, Coupling, Electromyography, Encephalon, Female, Humans, Levodopa, Levodopa (pharmacology), Levodopa (therapeutic use), Male, Middle Aged, Motor Cortex (drug effects), Motor Cortex (physiopathology), Nerve Net (drug effects), Nervous system diseases, Oscillation, Parietal Lobe (drug effects), Parietal Lobe (physiopathology), Parkinson disease, Parkinsonian Disorders (complications), Parkinsonian Disorders (drug therapy), Parkinsonian Disorders (physiopathology), Parkinsonian disease, Resting tremor, Somatosensory Cortex (drug effects), Somatosensory Cortex (physiopathology), Thalamus (drug effects), Thalamus (physiopathology), Tremor (etiology), Tremor (physiopathology), coherence, coupling, network, oscillations, resting tremor.
- MESH :
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- complications : Parkinsonian Disorders.
- drug effects : Brain, Cerebellum, Motor Cortex, Nerve Net, Parietal Lobe, Somatosensory Cortex, Thalamus.
- drug therapy : Parkinsonian Disorders.
- etiology : Tremor.
- physiopathology : Brain, Cerebellum, Motor Cortex, Parietal Lobe, Parkinsonian Disorders, Somatosensory Cortex, Thalamus, Tremor.
- Brain Mapping, Electromyography, Female, Humans, Male, Middle Aged.
Abstract
Resting tremor in idiopathic Parkinson's disease (PD) is associated with an oscillatory network comprising cortical as well as subcortical brain areas. To shed light on the effect of levodopa on these network interactions, we investigated 10 patients with tremor‐dominant PD and reanalyzed data in 11 healthy volunteers mimicking PD resting tremor. To this end, we recorded surface electromyograms of forearm muscles and neuromagnetic activity using a 122‐channel whole‐head magnetometer (MEG). Measurements were performed after overnight withdrawal of levodopa (OFF) and 30 min after oral application of fast‐acting levodopa (ON). During OFF, patients showed the typical antagonistic resting tremor. Using the analysis tool Dynamic Imaging of Coherent Sources, we identified the oscillatory network associated with tremor comprising contralateral primary sensorimotor cortex (S1/M1), supplementary motor area (SMA), contralateral premotor cortex (PMC), thalamus, secondary somatosensory cortex (S2), posterior parietal cortex (PPC), and ipsilateral cerebellum oscillating at 8 to 10 Hz. After intake of levodopa, we found a significant decrease of cerebro‐cerebral coupling between thalamus and motor cortical areas. Similarly, in healthy controls mimicking resting tremor, we found a significant decrease of functional interaction within a thalamus–premotor–motor network during rest. However, in patients with PD, decrease of functional interaction between thalamus and PMC was significantly stronger when compared with healthy controls. These data support the hypothesis that (1) in patients with PD the basal ganglia and motor cortical structures become more closely entrained and (2) levodopa is associated with normalization of the functional interaction between thalamus and motor cortical areas. © 2008 Movement Disorder Society
Url:
DOI: 10.1002/mds.22318
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="2009-01-15">2009-01-15</date><biblScope unit="vol">24</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="91">91</biblScope><biblScope unit="page" to="98">98</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">7FF7F26F358FFADCDD03F7A8508BDA553DD76253</idno><idno type="DOI">10.1002/mds.22318</idno><idno type="ArticleID">MDS22318</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Brain (drug effects)</term><term>Brain (physiopathology)</term><term>Brain Mapping</term><term>Cerebellum (drug effects)</term><term>Cerebellum (physiopathology)</term><term>Coherence</term><term>Coupling</term><term>Electromyography</term><term>Encephalon</term><term>Female</term><term>Humans</term><term>Levodopa</term><term>Levodopa (pharmacology)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Motor Cortex (drug effects)</term><term>Motor Cortex (physiopathology)</term><term>Nerve Net (drug effects)</term><term>Nervous system diseases</term><term>Oscillation</term><term>Parietal Lobe (drug effects)</term><term>Parietal Lobe (physiopathology)</term><term>Parkinson disease</term><term>Parkinsonian Disorders (complications)</term><term>Parkinsonian Disorders (drug therapy)</term><term>Parkinsonian Disorders (physiopathology)</term><term>Parkinsonian disease</term><term>Resting tremor</term><term>Somatosensory Cortex (drug effects)</term><term>Somatosensory Cortex (physiopathology)</term><term>Thalamus (drug effects)</term><term>Thalamus (physiopathology)</term><term>Tremor (etiology)</term><term>Tremor (physiopathology)</term><term>coherence</term><term>coupling</term><term>network</term><term>oscillations</term><term>resting tremor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term><term>Cerebellum</term><term>Motor Cortex</term><term>Nerve Net</term><term>Parietal Lobe</term><term>Somatosensory Cortex</term><term>Thalamus</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Tremor</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Cerebellum</term><term>Motor Cortex</term><term>Parietal Lobe</term><term>Parkinsonian Disorders</term><term>Somatosensory Cortex</term><term>Thalamus</term><term>Tremor</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Brain Mapping</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Cohérence</term><term>Couplage</term><term>Encéphale</term><term>Lévodopa</term><term>Maladie de Parkinson</term><term>Oscillation</term><term>Pathologie du système nerveux</term><term>Tremblement de repos</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Resting tremor in idiopathic Parkinson's disease (PD) is associated with an oscillatory network comprising cortical as well as subcortical brain areas. To shed light on the effect of levodopa on these network interactions, we investigated 10 patients with tremor‐dominant PD and reanalyzed data in 11 healthy volunteers mimicking PD resting tremor. To this end, we recorded surface electromyograms of forearm muscles and neuromagnetic activity using a 122‐channel whole‐head magnetometer (MEG). Measurements were performed after overnight withdrawal of levodopa (OFF) and 30 min after oral application of fast‐acting levodopa (ON). During OFF, patients showed the typical antagonistic resting tremor. Using the analysis tool Dynamic Imaging of Coherent Sources, we identified the oscillatory network associated with tremor comprising contralateral primary sensorimotor cortex (S1/M1), supplementary motor area (SMA), contralateral premotor cortex (PMC), thalamus, secondary somatosensory cortex (S2), posterior parietal cortex (PPC), and ipsilateral cerebellum oscillating at 8 to 10 Hz. After intake of levodopa, we found a significant decrease of cerebro‐cerebral coupling between thalamus and motor cortical areas. Similarly, in healthy controls mimicking resting tremor, we found a significant decrease of functional interaction within a thalamus–premotor–motor network during rest. However, in patients with PD, decrease of functional interaction between thalamus and PMC was significantly stronger when compared with healthy controls. These data support the hypothesis that (1) in patients with PD the basal ganglia and motor cortical structures become more closely entrained and (2) levodopa is associated with normalization of the functional interaction between thalamus and motor cortical areas. © 2008 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Royaume-Uni</li></country><region><li>Écosse</li></region><settlement><li>Glasgow</li></settlement><orgName><li>Université de Glasgow</li></orgName></list><tree><country name="Allemagne"><noRegion><name sortKey="Pollok, Bettina" sort="Pollok, Bettina" uniqKey="Pollok B" first="Bettina" last="Pollok">Bettina Pollok</name></noRegion><name sortKey="Butz, Markus" sort="Butz, Markus" uniqKey="Butz M" first="Markus" last="Butz">Markus Butz</name><name sortKey="Butz, Markus" sort="Butz, Markus" uniqKey="Butz M" first="Markus" last="Butz">Markus Butz</name><name sortKey="Makhloufi, Houssain" sort="Makhloufi, Houssain" uniqKey="Makhloufi H" first="Houssain" last="Makhloufi">Houssain Makhloufi</name><name sortKey="Pollok, Bettina" sort="Pollok, Bettina" uniqKey="Pollok B" first="Bettina" last="Pollok">Bettina Pollok</name><name sortKey="Schnitzler, Alfons" sort="Schnitzler, Alfons" uniqKey="Schnitzler A" first="Alfons" last="Schnitzler">Alfons Schnitzler</name><name sortKey="Schnitzler, Alfons" sort="Schnitzler, Alfons" uniqKey="Schnitzler A" first="Alfons" last="Schnitzler">Alfons Schnitzler</name><name sortKey="Timmermann, Lars" sort="Timmermann, Lars" uniqKey="Timmermann L" first="Lars" last="Timmermann">Lars Timmermann</name><name sortKey="Wojtecki, Lars" sort="Wojtecki, Lars" uniqKey="Wojtecki L" first="Lars" last="Wojtecki">Lars Wojtecki</name><name sortKey="Wojtecki, Lars" sort="Wojtecki, Lars" uniqKey="Wojtecki L" first="Lars" last="Wojtecki">Lars Wojtecki</name></country><country name="Royaume-Uni"><region name="Écosse"><name sortKey="Gross, Joachim" sort="Gross, Joachim" uniqKey="Gross J" first="Joachim" last="Gross">Joachim Gross</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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