Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease
Identifieur interne : 000D23 ( Main/Corpus ); précédent : 000D22; suivant : 000D24Effects 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 ; M. C. Do ; Y. Agid ; M. L. WelterSource :
- Brain [ 0006-8950 ] ; 2009-01.
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:
DOI: 10.1093/brain/awn294
Links to Exploration step
ISTEX:007FA7C896BEE5472BE0D6BD7F7D232EB88F559FLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease</title><author><name sortKey="Chastan, N" sort="Chastan, N" uniqKey="Chastan N" first="N." last="Chastan">N. Chastan</name><affiliation><mods:affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</mods:affiliation></affiliation><affiliation><mods:affiliation>3 Service de Neurophysiologie, Centre Hospitalier Universitaire de Rouen, Rouen F-76000, France</mods:affiliation></affiliation></author><author><name sortKey="Westby, G W M" sort="Westby, G W M" uniqKey="Westby G" first="G. W. M." last="Westby">G. W. M. Westby</name><affiliation><mods:affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Yelnik, J" sort="Yelnik, J" uniqKey="Yelnik J" first="J." last="Yelnik">J. Yelnik</name><affiliation><mods:affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</mods:affiliation></affiliation><affiliation><mods:affiliation>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</mods:affiliation></affiliation></author><author><name sortKey="Bardinet, E" sort="Bardinet, E" uniqKey="Bardinet E" first="E." last="Bardinet">E. Bardinet</name><affiliation><mods:affiliation>5 Centre National de la Recherche Scientifique, UPR 640, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</mods:affiliation></affiliation><affiliation><mods:affiliation>6 Centre de Neuro-Imagerie de Recherche CENIR, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</mods:affiliation></affiliation></author><author><name sortKey="Do, M C" sort="Do, M C" uniqKey="Do M" first="M. C." last="Do">M. C. Do</name><affiliation><mods:affiliation>7 Centre National de la Recherche Scientifique, FRE 2507, Université Pierre et Marie Curie-Paris 6, Institut des Systèmes Intelligents et de Robotique, Paris F-75005, France</mods:affiliation></affiliation><affiliation><mods:affiliation>8 LCMP/UFR STAPS-Orsay, Université Paris-Sud 11, Orsay F-91000, France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Y. Agid</name><affiliation><mods:affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</mods:affiliation></affiliation></author><author><name sortKey="Welter, M L" sort="Welter, M L" uniqKey="Welter M" first="M. L." last="Welter">M. L. Welter</name><affiliation><mods:affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: marie-laure.welter@psl.aphp.fr</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:007FA7C896BEE5472BE0D6BD7F7D232EB88F559F</idno><date when="2008" year="2008">2008</date><idno type="doi">10.1093/brain/awn294</idno><idno type="url">https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000D23</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease</title><author><name sortKey="Chastan, N" sort="Chastan, N" uniqKey="Chastan N" first="N." last="Chastan">N. Chastan</name><affiliation><mods:affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</mods:affiliation></affiliation><affiliation><mods:affiliation>3 Service de Neurophysiologie, Centre Hospitalier Universitaire de Rouen, Rouen F-76000, France</mods:affiliation></affiliation></author><author><name sortKey="Westby, G W M" sort="Westby, G W M" uniqKey="Westby G" first="G. W. M." last="Westby">G. W. M. Westby</name><affiliation><mods:affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Yelnik, J" sort="Yelnik, J" uniqKey="Yelnik J" first="J." last="Yelnik">J. Yelnik</name><affiliation><mods:affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</mods:affiliation></affiliation><affiliation><mods:affiliation>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</mods:affiliation></affiliation></author><author><name sortKey="Bardinet, E" sort="Bardinet, E" uniqKey="Bardinet E" first="E." last="Bardinet">E. Bardinet</name><affiliation><mods:affiliation>5 Centre National de la Recherche Scientifique, UPR 640, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</mods:affiliation></affiliation><affiliation><mods:affiliation>6 Centre de Neuro-Imagerie de Recherche CENIR, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</mods:affiliation></affiliation></author><author><name sortKey="Do, M C" sort="Do, M C" uniqKey="Do M" first="M. C." last="Do">M. C. Do</name><affiliation><mods:affiliation>7 Centre National de la Recherche Scientifique, FRE 2507, Université Pierre et Marie Curie-Paris 6, Institut des Systèmes Intelligents et de Robotique, Paris F-75005, France</mods:affiliation></affiliation><affiliation><mods:affiliation>8 LCMP/UFR STAPS-Orsay, Université Paris-Sud 11, Orsay F-91000, France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Y. Agid</name><affiliation><mods:affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</mods:affiliation></affiliation></author><author><name sortKey="Welter, M L" sort="Welter, M L" uniqKey="Welter M" first="M. L." last="Welter">M. L. Welter</name><affiliation><mods:affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: marie-laure.welter@psl.aphp.fr</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2009-01">2009-01</date><biblScope unit="volume">132</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="172">172</biblScope><biblScope unit="page" to="184">184</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">007FA7C896BEE5472BE0D6BD7F7D232EB88F559F</idno><idno type="DOI">10.1093/brain/awn294</idno><idno type="ArticleID">awn294</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="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.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>N. Chastan</name><affiliations><json:string>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</json:string><json:string>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</json:string><json:string>3 Service de Neurophysiologie, Centre Hospitalier Universitaire de Rouen, Rouen F-76000, France</json:string></affiliations></json:item><json:item><name>G. W. M. Westby</name><affiliations><json:string>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</json:string></affiliations></json:item><json:item><name>J. Yelnik</name><affiliations><json:string>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</json:string><json:string>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</json:string></affiliations></json:item><json:item><name>E. Bardinet</name><affiliations><json:string>5 Centre National de la Recherche Scientifique, UPR 640, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</json:string><json:string>6 Centre de Neuro-Imagerie de Recherche CENIR, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</json:string></affiliations></json:item><json:item><name>M. C. Do</name><affiliations><json:string>7 Centre National de la Recherche Scientifique, FRE 2507, Université Pierre et Marie Curie-Paris 6, Institut des Systèmes Intelligents et de Robotique, Paris F-75005, France</json:string><json:string>8 LCMP/UFR STAPS-Orsay, Université Paris-Sud 11, Orsay F-91000, France</json:string></affiliations></json:item><json:item><name>Y. Agid</name><affiliations><json:string>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</json:string><json:string>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</json:string></affiliations></json:item><json:item><name>M. L. Welter</name><affiliations><json:string>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</json:string><json:string>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</json:string><json:string>E-mail: marie-laure.welter@psl.aphp.fr</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Original Articles</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Gait and balance</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>deep brain stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>substantia nigra</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>subthalamic nucleus</value></json:item></subject><language><json:string>eng</json:string></language><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.</abstract><qualityIndicators><score>8.5</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612.68 x 790.866 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>2797</abstractCharCount><pdfWordCount>8422</pdfWordCount><pdfCharCount>51105</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>404</abstractWordCount></qualityIndicators><title>Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease</title><genre><json:string>research-article</json:string></genre><host><volume>132</volume><pages><last>184</last><first>172</first></pages><issn><json:string>0006-8950</json:string></issn><issue>1</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2156</json:string></eissn><title>Brain</title></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>2009</publicationDate><copyrightDate>2008</copyrightDate><doi><json:string>10.1093/brain/awn294</json:string></doi><id>007FA7C896BEE5472BE0D6BD7F7D232EB88F559F</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>2008-11-11</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease</title><author><persName><forename type="first">N.</forename><surname>Chastan</surname></persName><affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</affiliation><affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</affiliation><affiliation>3 Service de Neurophysiologie, Centre Hospitalier Universitaire de Rouen, Rouen F-76000, France</affiliation></author><author><persName><forename type="first">G. W. M.</forename><surname>Westby</surname></persName><affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</affiliation></author><author><persName><forename type="first">J.</forename><surname>Yelnik</surname></persName><affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</affiliation><affiliation>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</affiliation></author><author><persName><forename type="first">E.</forename><surname>Bardinet</surname></persName><affiliation>5 Centre National de la Recherche Scientifique, UPR 640, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</affiliation><affiliation>6 Centre de Neuro-Imagerie de Recherche CENIR, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</affiliation></author><author><persName><forename type="first">M. C.</forename><surname>Do</surname></persName><affiliation>7 Centre National de la Recherche Scientifique, FRE 2507, Université Pierre et Marie Curie-Paris 6, Institut des Systèmes Intelligents et de Robotique, Paris F-75005, France</affiliation><affiliation>8 LCMP/UFR STAPS-Orsay, Université Paris-Sud 11, Orsay F-91000, France</affiliation></author><author><persName><forename type="first">Y.</forename><surname>Agid</surname></persName><affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</affiliation><affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</affiliation></author><author corresp="yes"><persName><forename type="first">M. L.</forename><surname>Welter</surname></persName><email>marie-laure.welter@psl.aphp.fr</email><affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</affiliation><affiliation>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</affiliation></author></analytic><monogr><title level="j">Brain</title><idno type="pISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2009-01"></date><biblScope unit="volume">132</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="172">172</biblScope><biblScope unit="page" to="184">184</biblScope></imprint></monogr><idno type="istex">007FA7C896BEE5472BE0D6BD7F7D232EB88F559F</idno><idno type="DOI">10.1093/brain/awn294</idno><idno type="ArticleID">awn294</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008-11-11</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>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.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>Original Articles</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Gait and balance</term></item><item><term>Parkinson's disease</term></item><item><term>deep brain stimulation</term></item><item><term>substantia nigra</term></item><item><term>subthalamic nucleus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-11-11">Created</change><change when="2009-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1093/brain/awn294</article-id><article-id pub-id-type="publisher-id">awn294</article-id><article-categories><subj-group><subject>Original Articles</subject></subj-group></article-categories><title-group><article-title>Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Chastan</surname><given-names>N.</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref><xref ref-type="aff" rid="AFF2"><sup>2</sup></xref><xref ref-type="aff" rid="AFF3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Westby</surname><given-names>G. W. M.</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Yelnik</surname><given-names>J.</given-names></name><xref ref-type="aff" rid="AFF2"><sup>2</sup></xref><xref ref-type="aff" rid="AFF4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bardinet</surname><given-names>E.</given-names></name><xref ref-type="aff" rid="AFF5"><sup>5</sup></xref><xref ref-type="aff" rid="AFF6"><sup>6</sup></xref></contrib><contrib contrib-type="author"><name><surname>Do</surname><given-names>M. C.</given-names></name><xref ref-type="aff" rid="AFF7"><sup>7</sup></xref><xref ref-type="aff" rid="AFF8"><sup>8</sup></xref></contrib><contrib contrib-type="author"><name><surname>Agid</surname><given-names>Y.</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref><xref ref-type="aff" rid="AFF2"><sup>2</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Welter</surname><given-names>M. L.</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref><xref ref-type="aff" rid="AFF4"><sup>4</sup></xref></contrib></contrib-group><aff id="AFF1">1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</aff><aff id="AFF2">2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</aff><aff id="AFF3">3 Service de Neurophysiologie, Centre Hospitalier Universitaire de Rouen, Rouen F-76000, France</aff><aff id="AFF4">4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</aff><aff id="AFF5">5 Centre National de la Recherche Scientifique, UPR 640, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</aff><aff id="AFF6">6 Centre de Neuro-Imagerie de Recherche CENIR, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</aff><aff id="AFF7">7 Centre National de la Recherche Scientifique, FRE 2507, Université Pierre et Marie Curie-Paris 6, Institut des Systèmes Intelligents et de Robotique, Paris F-75005, France</aff><aff id="AFF8">8 LCMP/UFR STAPS-Orsay, Université Paris-Sud 11, Orsay F-91000, France</aff><author-notes><corresp>Correspondence to: Marie-Laure Welter, MD, PhD, Fédération des Maladies du Système Nerveux, Centre d’Investigation Clinique, Groupe Hospitalier Pitié-Salpêtrière, 47-83 Boulevard de l’Hôpital, 75651 Paris CEDEX 13, France E-mail: <email>marie-laure.welter@psl.aphp.fr</email></corresp></author-notes><pub-date pub-type="ppub"><month>1</month><year>2009</year></pub-date><pub-date pub-type="epub"><day>11</day><month>11</month><year>2008</year></pub-date><volume>132</volume><issue>1</issue><fpage>172</fpage><lpage>184</lpage><history><date date-type="received"><day>21</day><month>5</month><year>2008</year></date><date date-type="rev-recd"><day>7</day><month>10</month><year>2008</year></date><date date-type="accepted"><day>10</day><month>10</month><year>2008</year></date></history><permissions><copyright-statement>© The Author (2008). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2008</copyright-year></permissions><abstract><p>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.</p></abstract><kwd-group><kwd>Gait and balance</kwd><kwd>Parkinson's disease</kwd><kwd>deep brain stimulation</kwd><kwd>substantia nigra</kwd><kwd>subthalamic nucleus</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Chastan</namePart><affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</affiliation><affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</affiliation><affiliation>3 Service de Neurophysiologie, Centre Hospitalier Universitaire de Rouen, Rouen F-76000, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G. W. M.</namePart><namePart type="family">Westby</namePart><affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Yelnik</namePart><affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</affiliation><affiliation>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Bardinet</namePart><affiliation>5 Centre National de la Recherche Scientifique, UPR 640, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</affiliation><affiliation>6 Centre de Neuro-Imagerie de Recherche CENIR, Université Pierre et Marie Curie-Paris 6, Paris F-75013, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. C.</namePart><namePart type="family">Do</namePart><affiliation>7 Centre National de la Recherche Scientifique, FRE 2507, Université Pierre et Marie Curie-Paris 6, Institut des Systèmes Intelligents et de Robotique, Paris F-75005, France</affiliation><affiliation>8 LCMP/UFR STAPS-Orsay, Université Paris-Sud 11, Orsay F-91000, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Agid</namePart><affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</affiliation><affiliation>2 Institut National de la Santé et de la Recherche Médicale, Unité 679, Université Pierre et Marie Curie-Paris 6, Groupe Hospitalier Pitié-Salpêtrière, Paris F-75013, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">M. L.</namePart><namePart type="family">Welter</namePart><affiliation>1 Centre d’Investigation Clinique, Fédération des Maladies du Système Nerveux, Assistance Publique- Hôpitaux de Paris, France</affiliation><affiliation>4 Groupe AVENIR-IFR 70, Institut National de la Santé et de la Recherche Médicale, Groupe Hospitalier Pitié-Salpêtrière, France</affiliation><affiliation>E-mail: marie-laure.welter@psl.aphp.fr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Original Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2009-01</dateIssued><dateCreated encoding="w3cdtf">2008-11-11</dateCreated><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><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.</abstract><subject><genre>Keywords</genre><topic>Gait and balance</topic><topic>Parkinson's disease</topic><topic>deep brain stimulation</topic><topic>substantia nigra</topic><topic>subthalamic nucleus</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>132</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>172</start><end>184</end></extent></part></relatedItem><identifier type="istex">007FA7C896BEE5472BE0D6BD7F7D232EB88F559F</identifier><identifier type="DOI">10.1093/brain/awn294</identifier><identifier type="ArticleID">awn294</identifier><accessCondition type="use and reproduction" contentType="copyright">© The Author (2008). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</accessCondition><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><covers><json:item><original>true</original><mimetype>image/tiff</mimetype><extension>tiff</extension><uri>https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/covers/tiff</uri></json:item><json:item><original>true</original><mimetype>text/html</mimetype><extension>html</extension><uri>https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/covers/html</uri></json:item></covers><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/annexes/gif</uri></json:item><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/annexes/pdf</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/007FA7C896BEE5472BE0D6BD7F7D232EB88F559F/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000D23 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000D23 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:007FA7C896BEE5472BE0D6BD7F7D232EB88F559F
|texte= Effects of nigral stimulation on locomotion and postural stability in patients with Parkinson's disease
}}
| This area was generated with Dilib version V0.6.23. |  |