Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception
Identifieur interne : 000F01 ( Main/Exploration ); précédent : 000F00; suivant : 000F02Long-term subthalamic nucleus stimulation improves sensorimotor integration and proprioception
Auteurs : Aparna Wagle Shukla [États-Unis] ; Elena Moro [Canada] ; Carolyn Gunraj [Canada] ; Andres Lozano [Canada] ; Mojgan Hodaie [Canada] ; Anthony Lang [Canada] ; Robert Chen [Canada]Source :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2013-09.
English descriptors
- KwdEn :
- Adult, Aged, Antiparkinson Agents (therapeutic use), Deep Brain Stimulation (methods), Electrodes, Implanted, Female, Functional Laterality, Hand, Humans, Male, Middle Aged, Movement, Neurosurgical Procedures, Parkinson Disease (physiopathology), Parkinson Disease (therapy), Proprioception, Psychomotor Performance, Sensation, Subthalamic Nucleus (physiology), Treatment Outcome.
- MESH :
- chemical , therapeutic use : Antiparkinson Agents.
- methods : Deep Brain Stimulation.
- physiology : Subthalamic Nucleus.
- physiopathology : Parkinson Disease.
- therapy : Parkinson Disease.
- Adult, Aged, Electrodes, Implanted, Female, Functional Laterality, Hand, Humans, Male, Middle Aged, Movement, Neurosurgical Procedures, Proprioception, Psychomotor Performance, Sensation, Treatment Outcome.
Abstract
Objective Sensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used to measure sensorimotor integration. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been found to restore these abnormalities, but the time course of these changes is not known. We prospectively evaluated the short-term and long-term effects of STN DBS on SAI, LAI and proprioception. We hypothesised plasticity changes induced by chronic stimulation are necessary to normalise sensorimotor integration and proprioception. Methods Patients with PD were studied preoperatively, at 1 month and more than 6 months postoperatively. SAI was tested with median nerve stimulation to the wrist preceding TMS pulse to motor cortex by ∼20 ms and LAI by 200 ms. Proprioception (distance and spatial errors) in the arm was quantitatively assessed. For postoperative assessments, patients were studied in the medication-off/stimulator-off, medication-off/stimulator-on, medication-on/stimulator-off and medication-on/stimulator-on conditions. Results 11 patients with PD and 10 controls were enrolled. Preoperatively, SAI and proprioception was abnormal during the medication-on conditions and LAI was reduced regardless of the medication status. STN DBS had no significant effect on SAI, LAI and proprioception at 1 month. However, at 6 months SAI, LAI and distance errors were normalised in the medication-on/stimulator-on condition. Spatial error was normalised with DBS on and off. Conclusions Chronic STN DBS in PD normalises sensorimotor integration and proprioception, likely through long-term plastic changes in the basal ganglia thalamocortical circuit.
Url:
DOI: 10.1136/jnnp-2012-304102
Affiliations:
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Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Gunraj, Carolyn" sort="Gunraj, Carolyn" uniqKey="Gunraj C" first="Carolyn" last="Gunraj">Carolyn Gunraj</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Hodaie, Mojgan" sort="Hodaie, Mojgan" uniqKey="Hodaie M" first="Mojgan" last="Hodaie">Mojgan Hodaie</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurosurgery, Department of Surgery, University Health Network, University of Toronto, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Lang, Anthony" sort="Lang, Anthony" uniqKey="Lang A" first="Anthony" last="Lang">Anthony Lang</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Edmond J. Safra Program, Parkinson's Disease and National Parkinson's Disease Centre of Excellence, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Brain Imaging and Behavior Systems—Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2013-09">2013-09</date><biblScope unit="volume">84</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1020">1020</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">506F9AB25F7D5CD115DADA0F56E9B21AF94C1E30</idno><idno type="DOI">10.1136/jnnp-2012-304102</idno><idno type="href">jnnp-84-1020.pdf</idno><idno type="ArticleID">jnnp-2012-304102</idno><idno type="PMID">23616568</idno><idno type="local">jnnp;84/9/1020</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Antiparkinson Agents (therapeutic use)</term><term>Deep Brain Stimulation (methods)</term><term>Electrodes, Implanted</term><term>Female</term><term>Functional Laterality</term><term>Hand</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Movement</term><term>Neurosurgical Procedures</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Proprioception</term><term>Psychomotor Performance</term><term>Sensation</term><term>Subthalamic Nucleus (physiology)</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</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>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Electrodes, Implanted</term><term>Female</term><term>Functional Laterality</term><term>Hand</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Movement</term><term>Neurosurgical Procedures</term><term>Proprioception</term><term>Psychomotor Performance</term><term>Sensation</term><term>Treatment Outcome</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Objective Sensorimotor integration is impaired in patients with Parkinson's disease (PD). Short latency afferent inhibition (SAI) and long latency afferent inhibition (LAI) measured with transcranial magnetic stimulation (TMS) can be used to measure sensorimotor integration. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been found to restore these abnormalities, but the time course of these changes is not known. We prospectively evaluated the short-term and long-term effects of STN DBS on SAI, LAI and proprioception. We hypothesised plasticity changes induced by chronic stimulation are necessary to normalise sensorimotor integration and proprioception. Methods Patients with PD were studied preoperatively, at 1 month and more than 6 months postoperatively. SAI was tested with median nerve stimulation to the wrist preceding TMS pulse to motor cortex by ∼20 ms and LAI by 200 ms. Proprioception (distance and spatial errors) in the arm was quantitatively assessed. For postoperative assessments, patients were studied in the medication-off/stimulator-off, medication-off/stimulator-on, medication-on/stimulator-off and medication-on/stimulator-on conditions. Results 11 patients with PD and 10 controls were enrolled. Preoperatively, SAI and proprioception was abnormal during the medication-on conditions and LAI was reduced regardless of the medication status. STN DBS had no significant effect on SAI, LAI and proprioception at 1 month. However, at 6 months SAI, LAI and distance errors were normalised in the medication-on/stimulator-on condition. Spatial error was normalised with DBS on and off. Conclusions Chronic STN DBS in PD normalises sensorimotor integration and proprioception, likely through long-term plastic changes in the basal ganglia thalamocortical circuit.</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>Floride</li></region></list><tree><country name="États-Unis"><region name="Floride"><name sortKey="Wagle Shukla, Aparna" sort="Wagle Shukla, Aparna" uniqKey="Wagle Shukla A" first="Aparna" last="Wagle Shukla">Aparna Wagle Shukla</name></region></country><country name="Canada"><noRegion><name sortKey="Moro, Elena" sort="Moro, Elena" uniqKey="Moro E" first="Elena" last="Moro">Elena Moro</name></noRegion><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name><name sortKey="Gunraj, Carolyn" sort="Gunraj, Carolyn" uniqKey="Gunraj C" first="Carolyn" last="Gunraj">Carolyn Gunraj</name><name sortKey="Hodaie, Mojgan" sort="Hodaie, Mojgan" uniqKey="Hodaie M" first="Mojgan" last="Hodaie">Mojgan Hodaie</name><name sortKey="Lang, Anthony" sort="Lang, Anthony" uniqKey="Lang A" first="Anthony" last="Lang">Anthony Lang</name><name sortKey="Lang, Anthony" sort="Lang, Anthony" uniqKey="Lang A" first="Anthony" last="Lang">Anthony Lang</name><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name><name sortKey="Moro, Elena" sort="Moro, Elena" uniqKey="Moro E" first="Elena" last="Moro">Elena Moro</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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