ParkinsonFranceV1, Hal, Corpus, bibRecord, 000373

Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease.

Identifieur interne : 000373 ( Hal/Corpus ); précédent : 000372; suivant : 000374

Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease.

Auteurs : N. Chastan ; G. W. M. Westby ; J. Yelnik ; E. Bardinet ; Manh-Cuong Do ; Y. Agid ; M. L. Welter

Source :

Brain - A Journal of Neurology [ 0006-8950 ] ; 2009-01.

RBID : Hal:hal-00583628

Abstract

The physiopathology of gait and balance disorders in Parkinson's disease patients is still poorly understood. Levodopa treatment and subthalamic nucleus (STN) stimulation improve step length and walking speed, with less effect on postural instability. These disorders have been linked to dysfunction of the descending basal ganglia outputs to brainstem structures. In this study, we evaluated the effects of stimulation of the substantia nigra pars reticulata (SNr), on locomotion and balance in Parkinson's disease patients. Biomechanical parameters and leg muscle activity were recorded during gait initiation in seven selected patients operated for bilateral STN stimulation, out of 204 stimulated patients, with one contact of each electrode located within the SNr. Step length, anteroposterior and vertical velocities of the centre of gravity were studied, with special reference to the subjects' ability to brake the centre of gravity fall before foot-contact, and compared to seven controls. In Parkinson's disease patients, five treatment conditions were tested: (i) no treatment, (ii) levodopa treatment, (iii) STN stimulation, (iv) SNr stimulation and (v) combined levodopa treatment and STN stimulation. The effects of these treatments on motor parkinsonian disability were assessed with the UPDRS III scale, separated into 'axial' (rising from chair, posture, postural stability and gait) and 'distal' scores. Whereas levodopa and/or STN stimulation improved 'axial' and 'distal' motor symptoms, SNr stimulation improved only the 'axial' symptoms. Compared to controls, untreated Parkinson's disease patients showed reduced step length and velocity, and poor braking just prior to foot-contact, with a decrease in both soleus (S) and anterior tibialis (AT) muscle activity. Step length and velocity significantly increased with levodopa treatment alone or in combination with STN stimulation in both natural and fast gait conditions, and with STN stimulation alone in the fast gait condition. Conversely, SNr stimulation had no significant effect on these measures in either condition. In the natural gait condition, no fall in the centre of gravity occurred as step length was low and active braking was unnecessary. In the fast gait condition, braking was improved with STN or SNr stimulation but not with levodopa treatment, with an increase in the stance leg S muscle activity. These results suggest that anteroposterior (length and velocity) and vertical (braking capacity) gait parameters are controlled by two distinct systems within the basal ganglia circuitry, representing respectively locomotion and balance. The SNr, a major basal ganglia output known to project to pontomesencephalic structures, is postulated as being particularly involved in balance control during gait.

Url:

https://hal.archives-ouvertes.fr/hal-00583628

DOI: 10.1093/brain/awn294

Links to Exploration step

Hal:hal-00583628

Le document en format XML

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<front><div type="abstract" xml:lang="en">The physiopathology of gait and balance disorders in Parkinson's disease patients is still poorly understood. Levodopa treatment and subthalamic nucleus (STN) stimulation improve step length and walking speed, with less effect on postural instability. These disorders have been linked to dysfunction of the descending basal ganglia outputs to brainstem structures. In this study, we evaluated the effects of stimulation of the substantia nigra pars reticulata (SNr), on locomotion and balance in Parkinson's disease patients. Biomechanical parameters and leg muscle activity were recorded during gait initiation in seven selected patients operated for bilateral STN stimulation, out of 204 stimulated patients, with one contact of each electrode located within the SNr. Step length, anteroposterior and vertical velocities of the centre of gravity were studied, with special reference to the subjects' ability to brake the centre of gravity fall before foot-contact, and compared to seven controls. In Parkinson's disease patients, five treatment conditions were tested: (i) no treatment, (ii) levodopa treatment, (iii) STN stimulation, (iv) SNr stimulation and (v) combined levodopa treatment and STN stimulation. The effects of these treatments on motor parkinsonian disability were assessed with the UPDRS III scale, separated into 'axial' (rising from chair, posture, postural stability and gait) and 'distal' scores. Whereas levodopa and/or STN stimulation improved 'axial' and 'distal' motor symptoms, SNr stimulation improved only the 'axial' symptoms. Compared to controls, untreated Parkinson's disease patients showed reduced step length and velocity, and poor braking just prior to foot-contact, with a decrease in both soleus (S) and anterior tibialis (AT) muscle activity. Step length and velocity significantly increased with levodopa treatment alone or in combination with STN stimulation in both natural and fast gait conditions, and with STN stimulation alone in the fast gait condition. Conversely, SNr stimulation had no significant effect on these measures in either condition. In the natural gait condition, no fall in the centre of gravity occurred as step length was low and active braking was unnecessary. In the fast gait condition, braking was improved with STN or SNr stimulation but not with levodopa treatment, with an increase in the stance leg S muscle activity. These results suggest that anteroposterior (length and velocity) and vertical (braking capacity) gait parameters are controlled by two distinct systems within the basal ganglia circuitry, representing respectively locomotion and balance. The SNr, a major basal ganglia output known to project to pontomesencephalic structures, is postulated as being particularly involved in balance control during gait.</div>
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              </persName>
              <idno type="halauthorid">456954</idno>
            </author>
            <editor role="depositor">              <persName>                <forename>Jeuvrey</forename>
                <surname>Jean</surname>
              </persName>
              <email type="md5">38761549c0ea5bff0d63a419822a6fdc</email>
              <email type="domain">u-psud.fr</email>
            </editor>
          </titleStmt>
          <editionStmt>            <edition n="v1" type="current">              <date type="whenSubmitted">2011-04-06 10:32:19</date>
              <date type="whenModified">2017-02-09 15:54:57</date>
              <date type="whenReleased">2011-04-06 10:32:19</date>
              <date type="whenProduced">2009-01</date>
            </edition>
            <respStmt>              <resp>contributor</resp>
              <name key="159855">                <persName>                  <forename>Jeuvrey</forename>
                  <surname>Jean</surname>
                </persName>
                <email type="md5">38761549c0ea5bff0d63a419822a6fdc</email>
                <email type="domain">u-psud.fr</email>
              </name>
            </respStmt>
          </editionStmt>
          <publicationStmt>            <distributor>CCSD</distributor>
            <idno type="halId">hal-00583628</idno>
            <idno type="halUri">https://hal.archives-ouvertes.fr/hal-00583628</idno>
            <idno type="halBibtex">chastan:hal-00583628</idno>
            <idno type="halRefHtml">Brain - A Journal of Neurology , Oxford University Press (OUP), 2009, 132 (Pt 1), pp.172-84. <10.1093/brain/awn294></idno>
            <idno type="halRef">Brain - A Journal of Neurology , Oxford University Press (OUP), 2009, 132 (Pt 1), pp.172-84. <10.1093/brain/awn294></idno>
          </publicationStmt>
          <seriesStmt>            <idno type="stamp" n="CIAMS">Complexité, Innovation, Activités Motrices et Sportives</idno>
            <idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno>
            <idno type="stamp" n="UNIV-PSUD">Université Paris Sud - Paris XI</idno>
            <idno type="stamp" n="UPMC">Université Pierre et Marie Curie</idno>
            <idno type="stamp" n="ICM" p="UPMC">Institut du Cerveau et de la Moëlle Epinière</idno>
            <idno type="stamp" n="APHP" p="INSERM">AP-HP</idno>
          </seriesStmt>
          <notesStmt>            <note type="audience" n="2">International</note>
            <note type="popular" n="0">No</note>
            <note type="peer" n="1">Yes</note>
          </notesStmt>
          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="en">Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease.</title>
                <author role="aut">                  <persName>                    <forename type="first">N.</forename>
                    <surname>Chastan</surname>
                  </persName>
                  <idno type="halauthorid">598332</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">G. W. M.</forename>
                    <surname>Westby</surname>
                  </persName>
                  <idno type="halauthorid">598333</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">J.</forename>
                    <surname>Yelnik</surname>
                  </persName>
                  <idno type="halauthorid">456951</idno>
                  <affiliation ref="#struct-81470"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">E.</forename>
                    <surname>Bardinet</surname>
                  </persName>
                  <idno type="halauthorid">121866</idno>
                  <affiliation ref="#struct-81470"></affiliation>
                  <affiliation ref="#struct-106232"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Manh-Cuong</forename>
                    <surname>Do</surname>
                  </persName>
                  <email type="md5">5d99d125931dc1e819b77230a3d6ca80</email>
                  <email type="domain">u-psud.fr</email>
                  <idno type="halauthorid">595322</idno>
                  <affiliation ref="#struct-148375"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Y.</forename>
                    <surname>Agid</surname>
                  </persName>
                  <idno type="halauthorid">375934</idno>
                  <affiliation ref="#struct-16845"></affiliation>
                  <affiliation ref="#struct-3037"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">M. L.</forename>
                    <surname>Welter</surname>
                  </persName>
                  <idno type="halauthorid">456954</idno>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">11274</idno>
                <idno type="issn">0006-8950</idno>
                <idno type="eissn">1460-2156</idno>
                <title level="j">Brain - A Journal of Neurology </title>
                <imprint>                  <publisher>Oxford University Press (OUP)</publisher>
                  <biblScope unit="volume">132</biblScope>
                  <biblScope unit="issue">Pt 1</biblScope>
                  <biblScope unit="pp">172-84</biblScope>
                  <date type="datePub">2009-01</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1093/brain/awn294</idno>
              <idno type="pubmed">19001482</idno>
            </biblStruct>
          </sourceDesc>
          <profileDesc>            <langUsage>              <language ident="en">English</language>
            </langUsage>
            <textClass>              <classCode scheme="halDomain" n="spi.meca.biom">Engineering Sciences [physics]/Mechanics [physics.med-ph]/Biomechanics [physics.med-ph]</classCode>
              <classCode scheme="halDomain" n="phys.meca.biom">Physics [physics]/Mechanics [physics]/Biomechanics [physics.med-ph]</classCode>
              <classCode scheme="halDomain" n="scco.psyc">Cognitive science/Psychology</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
            </textClass>
            <abstract xml:lang="en">The physiopathology of gait and balance disorders in Parkinson's disease patients is still poorly understood. Levodopa treatment and subthalamic nucleus (STN) stimulation improve step length and walking speed, with less effect on postural instability. These disorders have been linked to dysfunction of the descending basal ganglia outputs to brainstem structures. In this study, we evaluated the effects of stimulation of the substantia nigra pars reticulata (SNr), on locomotion and balance in Parkinson's disease patients. Biomechanical parameters and leg muscle activity were recorded during gait initiation in seven selected patients operated for bilateral STN stimulation, out of 204 stimulated patients, with one contact of each electrode located within the SNr. Step length, anteroposterior and vertical velocities of the centre of gravity were studied, with special reference to the subjects' ability to brake the centre of gravity fall before foot-contact, and compared to seven controls. In Parkinson's disease patients, five treatment conditions were tested: (i) no treatment, (ii) levodopa treatment, (iii) STN stimulation, (iv) SNr stimulation and (v) combined levodopa treatment and STN stimulation. The effects of these treatments on motor parkinsonian disability were assessed with the UPDRS III scale, separated into 'axial' (rising from chair, posture, postural stability and gait) and 'distal' scores. Whereas levodopa and/or STN stimulation improved 'axial' and 'distal' motor symptoms, SNr stimulation improved only the 'axial' symptoms. Compared to controls, untreated Parkinson's disease patients showed reduced step length and velocity, and poor braking just prior to foot-contact, with a decrease in both soleus (S) and anterior tibialis (AT) muscle activity. Step length and velocity significantly increased with levodopa treatment alone or in combination with STN stimulation in both natural and fast gait conditions, and with STN stimulation alone in the fast gait condition. Conversely, SNr stimulation had no significant effect on these measures in either condition. In the natural gait condition, no fall in the centre of gravity occurred as step length was low and active braking was unnecessary. In the fast gait condition, braking was improved with STN or SNr stimulation but not with levodopa treatment, with an increase in the stance leg S muscle activity. These results suggest that anteroposterior (length and velocity) and vertical (braking capacity) gait parameters are controlled by two distinct systems within the basal ganglia circuitry, representing respectively locomotion and balance. The SNr, a major basal ganglia output known to project to pontomesencephalic structures, is postulated as being particularly involved in balance control during gait.</abstract>
          </profileDesc>
        </hal>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease.

Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease.

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