Subthalamic nucleus stimulation modulates motor cortex oscillatory activity in Parkinson's disease
Identifieur interne : 000D76 ( PascalFrancis/Corpus ); précédent : 000D75; suivant : 000D77Subthalamic nucleus stimulation modulates motor cortex oscillatory activity in Parkinson's disease
Auteurs : D. Devos ; E. Labyt ; P. Derambure ; J. L. Bourriez ; F. Cassim ; N. Reyns ; S. Blond ; J. D. Guieu ; A. Destee ; L. DefebvreSource :
- Brain [ 0006-8950 ] ; 2004.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
In Parkinson's disease, impaired motor preparation has been related to an increased latency in the appearance of movement-related desynchronization (MRD) throughout the contralateral primary sensorimotor (PSM) cortex. Internal globus pallidus (GPi) stimulation improved movement desynchronization over the PSM cortex during movement execution but failed to improve impaired motor preparation. PET studies indicate that subthalamic nucleus (STN) stimulation partly reverses the abnormal premotor pattern of brain activation during movement. By monitoring MRD, we aimed to assess changes in premotor and PSM cortex oscillatory activity induced by bilateral STN stimulation and to compare these changes with those induced by L-dopa. Ten Parkinson's disease patients and a group of healthy, age-matched controls performed self-paced wrist flexions in each of four conditions: without either stimulation or L-dopa (the 'off' condition), with stimulation and without L-dopa (On Stim), with L-dopa and without stimulation ('on drug'), and with both stimulation and L-dopa (On Both). Compared with the Off condition, in both the On Stim and the On Drug condition the Unified Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% and in the On Both condition it decreased by 80%. The desynchronization latency over central regions contralateral to movement and the movement desynchronization over bilateral central regions were significantly increased by stimulation and by L-dopa, with a maximal effect when the two were associated. Furthermore, desynchronization latency significantly decreased over bilateral frontocentral regions in the three treatment conditions compared with the Off condition. In Parkinson's disease, STN stimulation may induce a change in abnormal cortical oscillatory activity patterns (similar to that produced by L-dopa) by decreasing the abnormal spreading of desynchronization over frontocentral regions and increasing PSM cortex activity during movement preparation and execution, with a correlated improvement in bradykinesia. Parkinsonians under treatment displayed a desynchronization pattern close to that seen in healthy, age-matched controls, although central latencies remained shorter. The study indicates that it is possible to influence cortical reactivity related to the planning and execution of voluntary movement through the basal ganglia, and furthermore that the oscillatory activity of the PSM cortex (in addition to that of premotor areas) could be of major importance in the control of movement-associated, neural activity in Parkinson's disease.
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Format Inist (serveur)
NO : | PASCAL 04-0453729 INIST |
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ET : | Subthalamic nucleus stimulation modulates motor cortex oscillatory activity in Parkinson's disease |
AU : | DEVOS (D.); LABYT (E.); DERAMBURE (P.); BOURRIEZ (J. L.); CASSIM (F.); REYNS (N.); BLOND (S.); GUIEU (J. D.); DESTEE (A.); DEFEBVRE (L.) |
AF : | Department of Neurology, EA2683, Lille University Medical Centre/Lille/France (1 aut., 9 aut., 10 aut.); Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre/Lille/France (2 aut., 3 aut., 4 aut., 5 aut., 8 aut.); Department of Neurosurgery, EA2683, Lille University Medical Centre/Lille/France (6 aut., 7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Brain; ISSN 0006-8950; Royaume-Uni; Da. 2004; Vol. 127; No. p.2; Pp. 408-419; Bibl. 1 p.3/4 |
LA : | Anglais |
EA : | In Parkinson's disease, impaired motor preparation has been related to an increased latency in the appearance of movement-related desynchronization (MRD) throughout the contralateral primary sensorimotor (PSM) cortex. Internal globus pallidus (GPi) stimulation improved movement desynchronization over the PSM cortex during movement execution but failed to improve impaired motor preparation. PET studies indicate that subthalamic nucleus (STN) stimulation partly reverses the abnormal premotor pattern of brain activation during movement. By monitoring MRD, we aimed to assess changes in premotor and PSM cortex oscillatory activity induced by bilateral STN stimulation and to compare these changes with those induced by L-dopa. Ten Parkinson's disease patients and a group of healthy, age-matched controls performed self-paced wrist flexions in each of four conditions: without either stimulation or L-dopa (the 'off' condition), with stimulation and without L-dopa (On Stim), with L-dopa and without stimulation ('on drug'), and with both stimulation and L-dopa (On Both). Compared with the Off condition, in both the On Stim and the On Drug condition the Unified Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% and in the On Both condition it decreased by 80%. The desynchronization latency over central regions contralateral to movement and the movement desynchronization over bilateral central regions were significantly increased by stimulation and by L-dopa, with a maximal effect when the two were associated. Furthermore, desynchronization latency significantly decreased over bilateral frontocentral regions in the three treatment conditions compared with the Off condition. In Parkinson's disease, STN stimulation may induce a change in abnormal cortical oscillatory activity patterns (similar to that produced by L-dopa) by decreasing the abnormal spreading of desynchronization over frontocentral regions and increasing PSM cortex activity during movement preparation and execution, with a correlated improvement in bradykinesia. Parkinsonians under treatment displayed a desynchronization pattern close to that seen in healthy, age-matched controls, although central latencies remained shorter. The study indicates that it is possible to influence cortical reactivity related to the planning and execution of voluntary movement through the basal ganglia, and furthermore that the oscillatory activity of the PSM cortex (in addition to that of premotor areas) could be of major importance in the control of movement-associated, neural activity in Parkinson's disease. |
CC : | 002B17 |
FD : | Parkinson maladie; Noyau sousthalamique; Noyau moteur; Système nerveux pathologie; Cortex moteur; Electroencéphalographie; Désynchronisation |
FG : | Encéphale pathologie; Système nerveux central; Voie motrice; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Electrophysiologie; Electrodiagnostic |
ED : | Parkinson disease; Subthalamic nucleus; Motor nucleus; Nervous system diseases; Motor cortex; Electroencephalography; Desynchronization |
EG : | Cerebral disorder; Central nervous system; Motor pathway; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Electrophysiology; Electrodiagnosis |
SD : | Parkinson enfermedad; Núcleo subtalámico; Núcleo motor; Sistema nervioso patología; Corteza motora; Electroencefalografía; Desincronización |
LO : | INIST-998.354000116430960170 |
ID : | 04-0453729 |
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Desynchronization</term>
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<front><div type="abstract" xml:lang="en">In Parkinson's disease, impaired motor preparation has been related to an increased latency in the appearance of movement-related desynchronization (MRD) throughout the contralateral primary sensorimotor (PSM) cortex. Internal globus pallidus (GPi) stimulation improved movement desynchronization over the PSM cortex during movement execution but failed to improve impaired motor preparation. PET studies indicate that subthalamic nucleus (STN) stimulation partly reverses the abnormal premotor pattern of brain activation during movement. By monitoring MRD, we aimed to assess changes in premotor and PSM cortex oscillatory activity induced by bilateral STN stimulation and to compare these changes with those induced by L-dopa. Ten Parkinson's disease patients and a group of healthy, age-matched controls performed self-paced wrist flexions in each of four conditions: without either stimulation or L-dopa (the 'off' condition), with stimulation and without L-dopa (On Stim), with L-dopa and without stimulation ('on drug'), and with both stimulation and L-dopa (On Both). Compared with the Off condition, in both the On Stim and the On Drug condition the Unified Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% and in the On Both condition it decreased by 80%. The desynchronization latency over central regions contralateral to movement and the movement desynchronization over bilateral central regions were significantly increased by stimulation and by L-dopa, with a maximal effect when the two were associated. Furthermore, desynchronization latency significantly decreased over bilateral frontocentral regions in the three treatment conditions compared with the Off condition. In Parkinson's disease, STN stimulation may induce a change in abnormal cortical oscillatory activity patterns (similar to that produced by L-dopa) by decreasing the abnormal spreading of desynchronization over frontocentral regions and increasing PSM cortex activity during movement preparation and execution, with a correlated improvement in bradykinesia. Parkinsonians under treatment displayed a desynchronization pattern close to that seen in healthy, age-matched controls, although central latencies remained shorter. The study indicates that it is possible to influence cortical reactivity related to the planning and execution of voluntary movement through the basal ganglia, and furthermore that the oscillatory activity of the PSM cortex (in addition to that of premotor areas) could be of major importance in the control of movement-associated, neural activity in Parkinson's disease.</div>
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<fC01 i1="01" l="ENG"><s0>In Parkinson's disease, impaired motor preparation has been related to an increased latency in the appearance of movement-related desynchronization (MRD) throughout the contralateral primary sensorimotor (PSM) cortex. Internal globus pallidus (GPi) stimulation improved movement desynchronization over the PSM cortex during movement execution but failed to improve impaired motor preparation. PET studies indicate that subthalamic nucleus (STN) stimulation partly reverses the abnormal premotor pattern of brain activation during movement. By monitoring MRD, we aimed to assess changes in premotor and PSM cortex oscillatory activity induced by bilateral STN stimulation and to compare these changes with those induced by L-dopa. Ten Parkinson's disease patients and a group of healthy, age-matched controls performed self-paced wrist flexions in each of four conditions: without either stimulation or L-dopa (the 'off' condition), with stimulation and without L-dopa (On Stim), with L-dopa and without stimulation ('on drug'), and with both stimulation and L-dopa (On Both). Compared with the Off condition, in both the On Stim and the On Drug condition the Unified Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% and in the On Both condition it decreased by 80%. The desynchronization latency over central regions contralateral to movement and the movement desynchronization over bilateral central regions were significantly increased by stimulation and by L-dopa, with a maximal effect when the two were associated. Furthermore, desynchronization latency significantly decreased over bilateral frontocentral regions in the three treatment conditions compared with the Off condition. In Parkinson's disease, STN stimulation may induce a change in abnormal cortical oscillatory activity patterns (similar to that produced by L-dopa) by decreasing the abnormal spreading of desynchronization over frontocentral regions and increasing PSM cortex activity during movement preparation and execution, with a correlated improvement in bradykinesia. Parkinsonians under treatment displayed a desynchronization pattern close to that seen in healthy, age-matched controls, although central latencies remained shorter. The study indicates that it is possible to influence cortical reactivity related to the planning and execution of voluntary movement through the basal ganglia, and furthermore that the oscillatory activity of the PSM cortex (in addition to that of premotor areas) could be of major importance in the control of movement-associated, neural activity in Parkinson's disease.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Noyau sousthalamique</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Subthalamic nucleus</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Núcleo subtalámico</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Noyau moteur</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Motor nucleus</s0>
<s5>03</s5>
</fC03>
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<s5>03</s5>
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<s5>04</s5>
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<s5>04</s5>
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<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Cortex moteur</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Motor cortex</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Corteza motora</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Electroencéphalographie</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Electroencephalography</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Electroencefalografía</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Désynchronisation</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Desynchronization</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Desincronización</s0>
<s5>08</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Voie motrice</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Motor pathway</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vía motora</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>42</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Electrophysiologie</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Electrophysiology</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Electrofisiología</s0>
<s5>43</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Electrodiagnostic</s0>
<s5>45</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Electrodiagnosis</s0>
<s5>45</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Electrodiagnóstico</s0>
<s5>45</s5>
</fC07>
<fN21><s1>257</s1>
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<fN82><s1>OTO</s1>
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<server><NO>PASCAL 04-0453729 INIST</NO>
<ET>Subthalamic nucleus stimulation modulates motor cortex oscillatory activity in Parkinson's disease</ET>
<AU>DEVOS (D.); LABYT (E.); DERAMBURE (P.); BOURRIEZ (J. L.); CASSIM (F.); REYNS (N.); BLOND (S.); GUIEU (J. D.); DESTEE (A.); DEFEBVRE (L.)</AU>
<AF>Department of Neurology, EA2683, Lille University Medical Centre/Lille/France (1 aut., 9 aut., 10 aut.); Department of Clinical Neurophysiology, EA2683, Lille University Medical Centre/Lille/France (2 aut., 3 aut., 4 aut., 5 aut., 8 aut.); Department of Neurosurgery, EA2683, Lille University Medical Centre/Lille/France (6 aut., 7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Brain; ISSN 0006-8950; Royaume-Uni; Da. 2004; Vol. 127; No. p.2; Pp. 408-419; Bibl. 1 p.3/4</SO>
<LA>Anglais</LA>
<EA>In Parkinson's disease, impaired motor preparation has been related to an increased latency in the appearance of movement-related desynchronization (MRD) throughout the contralateral primary sensorimotor (PSM) cortex. Internal globus pallidus (GPi) stimulation improved movement desynchronization over the PSM cortex during movement execution but failed to improve impaired motor preparation. PET studies indicate that subthalamic nucleus (STN) stimulation partly reverses the abnormal premotor pattern of brain activation during movement. By monitoring MRD, we aimed to assess changes in premotor and PSM cortex oscillatory activity induced by bilateral STN stimulation and to compare these changes with those induced by L-dopa. Ten Parkinson's disease patients and a group of healthy, age-matched controls performed self-paced wrist flexions in each of four conditions: without either stimulation or L-dopa (the 'off' condition), with stimulation and without L-dopa (On Stim), with L-dopa and without stimulation ('on drug'), and with both stimulation and L-dopa (On Both). Compared with the Off condition, in both the On Stim and the On Drug condition the Unified Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% and in the On Both condition it decreased by 80%. The desynchronization latency over central regions contralateral to movement and the movement desynchronization over bilateral central regions were significantly increased by stimulation and by L-dopa, with a maximal effect when the two were associated. Furthermore, desynchronization latency significantly decreased over bilateral frontocentral regions in the three treatment conditions compared with the Off condition. In Parkinson's disease, STN stimulation may induce a change in abnormal cortical oscillatory activity patterns (similar to that produced by L-dopa) by decreasing the abnormal spreading of desynchronization over frontocentral regions and increasing PSM cortex activity during movement preparation and execution, with a correlated improvement in bradykinesia. Parkinsonians under treatment displayed a desynchronization pattern close to that seen in healthy, age-matched controls, although central latencies remained shorter. The study indicates that it is possible to influence cortical reactivity related to the planning and execution of voluntary movement through the basal ganglia, and furthermore that the oscillatory activity of the PSM cortex (in addition to that of premotor areas) could be of major importance in the control of movement-associated, neural activity in Parkinson's disease.</EA>
<CC>002B17</CC>
<FD>Parkinson maladie; Noyau sousthalamique; Noyau moteur; Système nerveux pathologie; Cortex moteur; Electroencéphalographie; Désynchronisation</FD>
<FG>Encéphale pathologie; Système nerveux central; Voie motrice; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Electrophysiologie; Electrodiagnostic</FG>
<ED>Parkinson disease; Subthalamic nucleus; Motor nucleus; Nervous system diseases; Motor cortex; Electroencephalography; Desynchronization</ED>
<EG>Cerebral disorder; Central nervous system; Motor pathway; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Electrophysiology; Electrodiagnosis</EG>
<SD>Parkinson enfermedad; Núcleo subtalámico; Núcleo motor; Sistema nervioso patología; Corteza motora; Electroencefalografía; Desincronización</SD>
<LO>INIST-998.354000116430960170</LO>
<ID>04-0453729</ID>
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