Subthalamic nucleus neuronal firing rate increases with Parkinson's disease progression
Identifieur interne : 001425 ( Main/Merge ); précédent : 001424; suivant : 001426Subthalamic nucleus neuronal firing rate increases with Parkinson's disease progression
Auteurs : Michael S. Remple [États-Unis] ; Courtney H. Bradenham [États-Unis] ; C. Chris Kao [États-Unis] ; P. David Charles [États-Unis] ; Joseph S. Neimat [États-Unis] ; Peter E. Konrad [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-08-01.
English descriptors
- KwdEn :
- Action Potentials (physiology), Aged, Deep Brain Stimulation (methods), Disease Progression, Female, Humans, Male, Microelectrodes, Middle Aged, Neurons (physiology), Parkinson Disease (pathology), Parkinson Disease (therapy), Parkinson's disease, Subthalamic Nucleus (pathology), neurodegeneration, neurophysiology, pathophysiology, rate model, subthalamic nucleus.
- MESH :
- methods : Deep Brain Stimulation.
- pathology : Parkinson Disease, Subthalamic Nucleus.
- physiology : Action Potentials, Neurons.
- therapy : Parkinson Disease.
- Aged, Disease Progression, Female, Humans, Male, Microelectrodes, Middle Aged.
Abstract
Parkinson's disease is a neurodegenerative disorder characterized by progressive loss of dopaminergic cells in the central nervous system, in particular the substantia nigra, resulting in an unrelenting loss of motor and nonmotor function. Animal models of Parkinson's disease reveal hyperactive neurons in the subthalamic nucleus that have increased firing rates and bursting activity compared with controls. Although subthalamic nucleus activity has been characterized in patients with advanced‐stage Parkinson's disease, it has not been described in patients with early‐stage Parkinson's disease. Here we present the results of subthalamic nucleus neuronal recordings from patients with early‐stage Parkinson's disease (Hoehn and Yahr stage II) enrolled in an ongoing clinical trial compared with recordings from age‐ and sex‐matched patients with advanced Parkinson's disease. Subthalamic nucleus neurons had a significantly lower firing rate in early versus advanced Parkinson's disease (28.7 vs 36.3 Hz; P < .01). The overall activity of the subthalamic nucleus was also significantly lower in early versus late Parkinson's disease, as measured by background neuronal noise (12.4 vs 14.0 mV; P < .05). No significant difference was identified between groups in the bursting or variability of neuronal firing in the subthalamic nucleus, as measured by a burst index or the interspike interval coefficient of variability. The results suggest that neuronal firing in the subthalamic nucleus increases with Parkinson's disease progression. © 2011 Movement Disorder Society
Url:
- https://api.istex.fr/document/8D72A097114FFCA1D81E255CE6CCC7E2815F73F0/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3151310
DOI: 10.1002/mds.23708
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ISTEX:8D72A097114FFCA1D81E255CE6CCC7E2815F73F0Le document en format XML
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Remple</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurosurgery, Vanderbilt University Medical Center, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Bradenham, Courtney H" sort="Bradenham, Courtney H" uniqKey="Bradenham C" first="Courtney H." last="Bradenham">Courtney H. Bradenham</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Kao, C Chris" sort="Kao, C Chris" uniqKey="Kao C" first="C. Chris" last="Kao">C. 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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="2011-08-01">2011-08-01</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1657">1657</biblScope><biblScope unit="page" to="1662">1662</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">8D72A097114FFCA1D81E255CE6CCC7E2815F73F0</idno><idno type="DOI">10.1002/mds.23708</idno><idno type="ArticleID">MDS23708</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action Potentials (physiology)</term><term>Aged</term><term>Deep Brain Stimulation (methods)</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Microelectrodes</term><term>Middle Aged</term><term>Neurons (physiology)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (therapy)</term><term>Parkinson's disease</term><term>Subthalamic Nucleus (pathology)</term><term>neurodegeneration</term><term>neurophysiology</term><term>pathophysiology</term><term>rate model</term><term>subthalamic nucleus</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Action Potentials</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Microelectrodes</term><term>Middle Aged</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is a neurodegenerative disorder characterized by progressive loss of dopaminergic cells in the central nervous system, in particular the substantia nigra, resulting in an unrelenting loss of motor and nonmotor function. Animal models of Parkinson's disease reveal hyperactive neurons in the subthalamic nucleus that have increased firing rates and bursting activity compared with controls. Although subthalamic nucleus activity has been characterized in patients with advanced‐stage Parkinson's disease, it has not been described in patients with early‐stage Parkinson's disease. Here we present the results of subthalamic nucleus neuronal recordings from patients with early‐stage Parkinson's disease (Hoehn and Yahr stage II) enrolled in an ongoing clinical trial compared with recordings from age‐ and sex‐matched patients with advanced Parkinson's disease. Subthalamic nucleus neurons had a significantly lower firing rate in early versus advanced Parkinson's disease (28.7 vs 36.3 Hz; P < .01). The overall activity of the subthalamic nucleus was also significantly lower in early versus late Parkinson's disease, as measured by background neuronal noise (12.4 vs 14.0 mV; P < .05). No significant difference was identified between groups in the bursting or variability of neuronal firing in the subthalamic nucleus, as measured by a burst index or the interspike interval coefficient of variability. The results suggest that neuronal firing in the subthalamic nucleus increases with Parkinson's disease progression. © 2011 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.23708"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Subthalamic nucleus neuronal firing rate increases with Parkinson's disease progression</title><author><name sortKey="Remple, Michael S" sort="Remple, Michael S" uniqKey="Remple M" first="Michael S." last="Remple">Michael S. Remple</name></author><author><name sortKey="Bradenham, Courtney H" sort="Bradenham, Courtney H" uniqKey="Bradenham C" first="Courtney H." last="Bradenham">Courtney H. Bradenham</name></author><author><name sortKey="Kao, C Chris" sort="Kao, C Chris" uniqKey="Kao C" first="C. Chris" last="Kao">C. Chris Kao</name></author><author><name sortKey="Charles, P David" sort="Charles, P David" uniqKey="Charles P" first="P. David" last="Charles">P. David Charles</name></author><author><name sortKey="Neimat, Joseph S" sort="Neimat, Joseph S" uniqKey="Neimat J" first="Joseph S." last="Neimat">Joseph S. Neimat</name></author><author><name sortKey="Konrad, Peter E" sort="Konrad, Peter E" uniqKey="Konrad P" first="Peter E." last="Konrad">Peter E. Konrad</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8D72A097114FFCA1D81E255CE6CCC7E2815F73F0</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23708</idno><idno type="url">https://api.istex.fr/document/8D72A097114FFCA1D81E255CE6CCC7E2815F73F0/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000C83</idno><idno type="wicri:Area/Istex/Curation">000C83</idno><idno type="wicri:Area/Istex/Checkpoint">000104</idno><idno type="wicri:doubleKey">0885-3185:2011:Remple M:subthalamic:nucleus:neuronal</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Subthalamic nucleus neuronal firing rate increases with Parkinson's disease progression</title><author><name sortKey="Remple, Michael S" sort="Remple, Michael S" uniqKey="Remple M" first="Michael S." last="Remple">Michael S. Remple</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurosurgery, Vanderbilt University Medical Center, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Bradenham, Courtney H" sort="Bradenham, Courtney H" uniqKey="Bradenham C" first="Courtney H." last="Bradenham">Courtney H. Bradenham</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Kao, C Chris" sort="Kao, C Chris" uniqKey="Kao C" first="C. Chris" last="Kao">C. Chris Kao</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurosurgery, Vanderbilt University Medical Center, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Charles, P David" sort="Charles, P David" uniqKey="Charles P" first="P. David" last="Charles">P. David Charles</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Neimat, Joseph S" sort="Neimat, Joseph S" uniqKey="Neimat J" first="Joseph S." last="Neimat">Joseph S. Neimat</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurosurgery, Vanderbilt University Medical Center, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author><author><name sortKey="Konrad, Peter E" sort="Konrad, Peter E" uniqKey="Konrad P" first="Peter E." last="Konrad">Peter E. Konrad</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurosurgery, Vanderbilt University Medical Center, Nashville, Tennessee</wicri:regionArea><placeName><region type="state">Tennessee</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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="2011-08-01">2011-08-01</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1657">1657</biblScope><biblScope unit="page" to="1662">1662</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">8D72A097114FFCA1D81E255CE6CCC7E2815F73F0</idno><idno type="DOI">10.1002/mds.23708</idno><idno type="ArticleID">MDS23708</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>neurodegeneration</term><term>neurophysiology</term><term>pathophysiology</term><term>rate model</term><term>subthalamic nucleus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is a neurodegenerative disorder characterized by progressive loss of dopaminergic cells in the central nervous system, in particular the substantia nigra, resulting in an unrelenting loss of motor and nonmotor function. Animal models of Parkinson's disease reveal hyperactive neurons in the subthalamic nucleus that have increased firing rates and bursting activity compared with controls. Although subthalamic nucleus activity has been characterized in patients with advanced‐stage Parkinson's disease, it has not been described in patients with early‐stage Parkinson's disease. Here we present the results of subthalamic nucleus neuronal recordings from patients with early‐stage Parkinson's disease (Hoehn and Yahr stage II) enrolled in an ongoing clinical trial compared with recordings from age‐ and sex‐matched patients with advanced Parkinson's disease. Subthalamic nucleus neurons had a significantly lower firing rate in early versus advanced Parkinson's disease (28.7 vs 36.3 Hz; P < .01). The overall activity of the subthalamic nucleus was also significantly lower in early versus late Parkinson's disease, as measured by background neuronal noise (12.4 vs 14.0 mV; P < .05). No significant difference was identified between groups in the bursting or variability of neuronal firing in the subthalamic nucleus, as measured by a burst index or the interspike interval coefficient of variability. The results suggest that neuronal firing in the subthalamic nucleus increases with Parkinson's disease progression. © 2011 Movement Disorder Society</div></front></TEI></ISTEX><PMC><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Subthalamic Nucleus Neuronal Firing Rate Increases with Parkinson’s Disease Progression</title><author><name sortKey="Remple, Michael S" sort="Remple, Michael S" uniqKey="Remple M" first="Michael S." last="Remple">Michael S. Remple</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Bradenham, Courtney H" sort="Bradenham, Courtney H" uniqKey="Bradenham C" first="Courtney H." last="Bradenham">Courtney H. Bradenham</name><affiliation><nlm:aff id="A2"> Dept of Neurology, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Kao, C Chris" sort="Kao, C Chris" uniqKey="Kao C" first="C. Chris" last="Kao">C. Chris Kao</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Charles, P David" sort="Charles, P David" uniqKey="Charles P" first="P. David" last="Charles">P. David Charles</name><affiliation><nlm:aff id="A2"> Dept of Neurology, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Neimat, Joseph S" sort="Neimat, Joseph S" uniqKey="Neimat J" first="Joseph S." last="Neimat">Joseph S. Neimat</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Konrad, Peter E" sort="Konrad, Peter E" uniqKey="Konrad P" first="Peter E." last="Konrad">Peter E. 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Remple</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Bradenham, Courtney H" sort="Bradenham, Courtney H" uniqKey="Bradenham C" first="Courtney H." last="Bradenham">Courtney H. Bradenham</name><affiliation><nlm:aff id="A2"> Dept of Neurology, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Kao, C Chris" sort="Kao, C Chris" uniqKey="Kao C" first="C. Chris" last="Kao">C. Chris Kao</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Charles, P David" sort="Charles, P David" uniqKey="Charles P" first="P. David" last="Charles">P. David Charles</name><affiliation><nlm:aff id="A2"> Dept of Neurology, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Neimat, Joseph S" sort="Neimat, Joseph S" uniqKey="Neimat J" first="Joseph S." last="Neimat">Joseph S. Neimat</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author><author><name sortKey="Konrad, Peter E" sort="Konrad, Peter E" uniqKey="Konrad P" first="Peter E." last="Konrad">Peter E. Konrad</name><affiliation><nlm:aff id="A1"> Dept of Neurosurgery, Vanderbilt University Medical Center, Nashville TN</nlm:aff><wicri:noCountry code="subfield">Nashville TN</wicri:noCountry></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action Potentials (physiology)</term><term>Aged</term><term>Deep Brain Stimulation (methods)</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Microelectrodes</term><term>Middle Aged</term><term>Neurons (physiology)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (therapy)</term><term>Subthalamic Nucleus (pathology)</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Action Potentials</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Microelectrodes</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic cells in the central nervous system, in particular the substantia nigra, resulting in an unrelenting loss of motor and non-motor function. Animal models of PD reveal hyperactive neurons in the subthalamic nucleus (STN) that have increased firing rates and bursting activity compared to controls. Although STN activity has been characterized in advanced stage PD patients, it has not been described in early stage PD patients. Here we present the results of STN neuronal recordings from early stage PD patients (Hoehn and Yahr stage II) enrolled in an ongoing clinical trial compared to recordings from age and sex matched advanced PD patients. STN neurons had a significantly lower firing rate in early versus advanced PD (28.7Hz vs. 36.3Hz; p<0.01). The overall activity of the STN was also significantly lower in early versus late PD, as measured by background neuronal noise (12.4mV vs. 14.0mV; p <0.05). No significant difference was identified between groups in the bursting or variability of neuronal firing in the STN, as measured by a burst index or the interspike interval coefficient of variability. The results suggest that neuronal firing in STN increases with PD progression.</p></div></front></TEI></PMC></double></record>Pour manipuler ce document sous Unix (Dilib)
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