Cerebellar sensory processing alterations impact motor cortical plasticity in Parkinson's disease: clues from dyskinetic patients.
Identifieur interne : 000A37 ( Main/Exploration ); précédent : 000A36; suivant : 000A38Cerebellar sensory processing alterations impact motor cortical plasticity in Parkinson's disease: clues from dyskinetic patients.
Auteurs : Asha Kishore [Inde] ; Traian Popa [France] ; Ammu Balachandran [Inde] ; Shyambabu Chandran [Inde] ; Salini Pradeep [Inde] ; Febina Backer [Inde] ; Syam Krishnan [Inde] ; Sabine Meunier [France]Source :
- Cerebral cortex (New York, N.Y. : 1991) [ 1460-2199 ] ; 2014.
English descriptors
- KwdEn :
- Adult, Aged, Antiparkinson Agents (adverse effects), Antiparkinson Agents (therapeutic use), Cerebellum (drug effects), Cerebellum (physiopathology), Dyskinesia, Drug-Induced (diagnosis), Dyskinesia, Drug-Induced (physiopathology), Dyskinesia, Drug-Induced (therapy), Electromyography, Evoked Potentials, Motor, Female, Follow-Up Studies, Functional Laterality, Humans, Levodopa (adverse effects), Levodopa (therapeutic use), Male, Middle Aged, Motor Cortex (drug effects), Motor Cortex (physiopathology), Muscle, Skeletal (drug effects), Muscle, Skeletal (physiopathology), Neuronal Plasticity (drug effects), Neuronal Plasticity (physiology), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Severity of Illness Index, Transcranial Magnetic Stimulation (methods).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- diagnosis : Dyskinesia, Drug-Induced.
- drug effects : Cerebellum, Motor Cortex, Muscle, Skeletal, Neuronal Plasticity.
- drug therapy : Parkinson Disease.
- methods : Transcranial Magnetic Stimulation.
- physiology : Neuronal Plasticity.
- physiopathology : Cerebellum, Dyskinesia, Drug-Induced, Motor Cortex, Muscle, Skeletal, Parkinson Disease.
- therapy : Dyskinesia, Drug-Induced.
- Adult, Aged, Electromyography, Evoked Potentials, Motor, Female, Follow-Up Studies, Functional Laterality, Humans, Male, Middle Aged, Severity of Illness Index.
Abstract
The plasticity of primary motor cortex (M1) in patients with Parkinson's disease (PD) and levodopa-induced dyskinesias (LIDs) is severely impaired. We recently reported in young healthy subjects that inhibitory cerebellar stimulation enhanced the sensorimotor plasticity of M1 that was induced by paired associative stimulation (PAS). This study demonstrates that the deficient sensorimotor M1 plasticity in 16 patients with LIDs could be reinstated by a single session of real inhibitory cerebellar stimulation but not sham stimulation. This was evident only when a sensory component was involved in the induction of plasticity, indicating that cerebellar sensory processing function is involved in the resurgence of M1 plasticity. The benefit of inhibitory cerebellar stimulation on LIDs is known. To explore whether this benefit is linked to the restoration of sensorimotor plasticity of M1, we conducted an additional study looking at changes in LIDs and PAS-induced plasticity after 10 sessions of either bilateral, real inhibitory cerebellar stimulation or sham stimulation. Only real and not sham stimulation had an antidyskinetic effect and it was paralleled by a resurgence in the sensorimotor plasticity of M1. These results suggest that alterations in cerebellar sensory processing function, occurring secondary to abnormal basal ganglia signals reaching it, may be an important element contributing to the maladaptive sensorimotor plasticity of M1 and the emergence of abnormal involuntary movements.
DOI: 10.1093/cercor/bht058
PubMed: 23535177
Affiliations:
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695011</wicri:regionArea><wicri:noRegion>Kerala 695011</wicri:noRegion></affiliation></author><author><name sortKey="Popa, Traian" sort="Popa, Traian" uniqKey="Popa T" first="Traian" last="Popa">Traian Popa</name><affiliation wicri:level="4"><nlm:affiliation>Université Pierre et Marie Curie, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, UMR-S975, Paris 75013, France CNRS, UMR 7225, Paris 75013, France INSERM, U975, Paris 75013, France ICM-Institut du Cerveau et de la Moëlle épinière, Paris 75013, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université Pierre et Marie Curie, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, UMR-S975, Paris 75013, France CNRS, UMR 7225, Paris 75013, France INSERM, U975, Paris 75013, France ICM-Institut du Cerveau et de la Moëlle épinière, Paris 75013</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="university">Université Pierre-et-Marie-Curie</orgName></affiliation></author><author><name sortKey="Balachandran, Ammu" sort="Balachandran, Ammu" uniqKey="Balachandran A" first="Ammu" last="Balachandran">Ammu Balachandran</name><affiliation wicri:level="1"><nlm:affiliation>Comprehensive Care Centre for Movement Disorders, Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala 695011, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Comprehensive Care Centre for Movement Disorders, Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala 695011</wicri:regionArea><wicri:noRegion>Kerala 695011</wicri:noRegion></affiliation></author><author><name sortKey="Chandran, Shyambabu" sort="Chandran, Shyambabu" uniqKey="Chandran S" first="Shyambabu" last="Chandran">Shyambabu Chandran</name><affiliation wicri:level="1"><nlm:affiliation>Comprehensive Care Centre for Movement Disorders, Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala 695011, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Comprehensive Care Centre for Movement Disorders, Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala 695011</wicri:regionArea><wicri:noRegion>Kerala 695011</wicri:noRegion></affiliation></author><author><name sortKey="Pradeep, Salini" sort="Pradeep, Salini" uniqKey="Pradeep S" first="Salini" last="Pradeep">Salini Pradeep</name><affiliation wicri:level="1"><nlm:affiliation>Comprehensive Care Centre for Movement Disorders, Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala 695011, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Comprehensive Care Centre for Movement Disorders, Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, 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Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala 695011, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Comprehensive Care Centre for Movement Disorders, Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala 695011</wicri:regionArea><wicri:noRegion>Kerala 695011</wicri:noRegion></affiliation></author><author><name sortKey="Meunier, Sabine" sort="Meunier, Sabine" uniqKey="Meunier S" first="Sabine" last="Meunier">Sabine Meunier</name><affiliation wicri:level="4"><nlm:affiliation>Université Pierre et Marie Curie, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, UMR-S975, Paris 75013, France CNRS, UMR 7225, Paris 75013, France INSERM, U975, Paris 75013, France ICM-Institut du Cerveau et de la Moëlle épinière, Paris 75013, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université Pierre et Marie Curie, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière, UMR-S975, Paris 75013, France CNRS, UMR 7225, Paris 75013, France INSERM, U975, Paris 75013, France ICM-Institut du Cerveau et de la Moëlle épinière, Paris 75013</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="university">Université Pierre-et-Marie-Curie</orgName></affiliation></author></analytic><series><title level="j">Cerebral cortex (New York, N.Y. : 1991)</title><idno type="eISSN">1460-2199</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Cerebellum (drug effects)</term><term>Cerebellum (physiopathology)</term><term>Dyskinesia, Drug-Induced (diagnosis)</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Dyskinesia, Drug-Induced (therapy)</term><term>Electromyography</term><term>Evoked Potentials, Motor</term><term>Female</term><term>Follow-Up Studies</term><term>Functional Laterality</term><term>Humans</term><term>Levodopa (adverse effects)</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>Muscle, Skeletal (drug effects)</term><term>Muscle, Skeletal (physiopathology)</term><term>Neuronal Plasticity (drug effects)</term><term>Neuronal Plasticity (physiology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Severity of Illness Index</term><term>Transcranial Magnetic Stimulation (methods)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" 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="diagnosis" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cerebellum</term><term>Motor Cortex</term><term>Muscle, Skeletal</term><term>Neuronal Plasticity</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Transcranial Magnetic Stimulation</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neuronal Plasticity</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebellum</term><term>Dyskinesia, Drug-Induced</term><term>Motor Cortex</term><term>Muscle, Skeletal</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Electromyography</term><term>Evoked Potentials, Motor</term><term>Female</term><term>Follow-Up Studies</term><term>Functional Laterality</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The plasticity of primary motor cortex (M1) in patients with Parkinson's disease (PD) and levodopa-induced dyskinesias (LIDs) is severely impaired. We recently reported in young healthy subjects that inhibitory cerebellar stimulation enhanced the sensorimotor plasticity of M1 that was induced by paired associative stimulation (PAS). This study demonstrates that the deficient sensorimotor M1 plasticity in 16 patients with LIDs could be reinstated by a single session of real inhibitory cerebellar stimulation but not sham stimulation. This was evident only when a sensory component was involved in the induction of plasticity, indicating that cerebellar sensory processing function is involved in the resurgence of M1 plasticity. The benefit of inhibitory cerebellar stimulation on LIDs is known. To explore whether this benefit is linked to the restoration of sensorimotor plasticity of M1, we conducted an additional study looking at changes in LIDs and PAS-induced plasticity after 10 sessions of either bilateral, real inhibitory cerebellar stimulation or sham stimulation. Only real and not sham stimulation had an antidyskinetic effect and it was paralleled by a resurgence in the sensorimotor plasticity of M1. These results suggest that alterations in cerebellar sensory processing function, occurring secondary to abnormal basal ganglia signals reaching it, may be an important element contributing to the maladaptive sensorimotor plasticity of M1 and the emergence of abnormal involuntary movements.</div></front></TEI><affiliations><list><country><li>France</li><li>Inde</li></country><region><li>Île-de-France</li></region><orgName><li>Université Pierre-et-Marie-Curie</li></orgName></list><tree><country name="Inde"><noRegion><name sortKey="Kishore, Asha" sort="Kishore, Asha" uniqKey="Kishore A" first="Asha" last="Kishore">Asha Kishore</name></noRegion><name sortKey="Backer, Febina" sort="Backer, Febina" uniqKey="Backer F" first="Febina" last="Backer">Febina Backer</name><name sortKey="Balachandran, Ammu" sort="Balachandran, Ammu" uniqKey="Balachandran A" first="Ammu" last="Balachandran">Ammu Balachandran</name><name sortKey="Chandran, Shyambabu" sort="Chandran, Shyambabu" uniqKey="Chandran S" first="Shyambabu" last="Chandran">Shyambabu Chandran</name><name sortKey="Krishnan, Syam" sort="Krishnan, Syam" uniqKey="Krishnan S" first="Syam" last="Krishnan">Syam Krishnan</name><name sortKey="Pradeep, Salini" sort="Pradeep, Salini" uniqKey="Pradeep S" first="Salini" last="Pradeep">Salini Pradeep</name></country><country name="France"><region name="Île-de-France"><name sortKey="Popa, Traian" sort="Popa, Traian" uniqKey="Popa T" first="Traian" last="Popa">Traian Popa</name></region><name sortKey="Meunier, Sabine" sort="Meunier, Sabine" uniqKey="Meunier S" first="Sabine" last="Meunier">Sabine Meunier</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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