Levodopa raises objective pain threshold in Parkinson’s disease: a RIII reflex study
Identifieur interne : 001167 ( Istex/Corpus ); précédent : 001166; suivant : 001168Levodopa raises objective pain threshold in Parkinson’s disease: a RIII reflex study
Auteurs : A. Gerdelat-Mas ; M. Simonetta-Moreau ; C. Thalamas ; F. Ory-Magne ; T. Slaoui ; O. Rascol ; C. Brefel-CourbonSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2007-10.
Abstract
Background: Patients suffering from Parkinson’s disease (PD) describe painful sensations that could be related to neuropathic pain. Experimental data have indicated the involvement of basal ganglia and dopaminergic pathways in central nociceptive processing. Aim: The objective of this study was to assess and compare the effect of levodopa on the objective pain threshold in patients with PD and healthy subjects. Methods: The objective pain threshold was assessed by the nociceptive flexion reflex (RIII) in 13 PD patients and 10 healthy subjects. Patients and healthy subjects were evaluated under two randomised conditions: with levodopa (ON) and without (OFF). Results: Levodopa significantly increased the RIII threshold of PD patients (6.9 (1.2) mA in the OFF condition vs 8 (1.1) mA in the ON position; p = 0.02). RIII threshold was significantly lower in PD patients than in healthy subjects in the OFF condition (6.9 (1.2) mA vs 9.7 (3.4) mA; p = 0.02). RIII threshold did not change after levodopa administration in healthy subjects. Conclusion: These results provide evidence of a dopaminergic modulation of objective pain threshold in PD patients. In addition, the decrease in RIII threshold in PD patients, in the OFF condition, compared with controls, confirms the existence of an objective pain perception disturbance in PD.
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DOI: 10.1136/jnnp.2007.120212
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Thalamas</name><affiliation><mods:affiliation>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Ory Magne, F" sort="Ory Magne, F" uniqKey="Ory Magne F" first="F" last="Ory-Magne">F. Ory-Magne</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Slaoui, T" sort="Slaoui, T" uniqKey="Slaoui T" first="T" last="Slaoui">T. Slaoui</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Rascol, O" sort="Rascol, O" uniqKey="Rascol O" first="O" last="Rascol">O. Rascol</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Brefel Courbon, C" sort="Brefel Courbon, C" uniqKey="Brefel Courbon C" first="C" last="Brefel-Courbon">C. 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Gerdelat-Mas</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Simonetta Moreau, M" sort="Simonetta Moreau, M" uniqKey="Simonetta Moreau M" first="M" last="Simonetta-Moreau">M. Simonetta-Moreau</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Thalamas, C" sort="Thalamas, C" uniqKey="Thalamas C" first="C" last="Thalamas">C. Thalamas</name><affiliation><mods:affiliation>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Ory Magne, F" sort="Ory Magne, F" uniqKey="Ory Magne F" first="F" last="Ory-Magne">F. Ory-Magne</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Slaoui, T" sort="Slaoui, T" uniqKey="Slaoui T" first="T" last="Slaoui">T. Slaoui</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Rascol, O" sort="Rascol, O" uniqKey="Rascol O" first="O" last="Rascol">O. Rascol</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Brefel Courbon, C" sort="Brefel Courbon, C" uniqKey="Brefel Courbon C" first="C" last="Brefel-Courbon">C. Brefel-Courbon</name><affiliation><mods:affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</mods:affiliation></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="2007-10">2007-10</date><biblScope unit="volume">78</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1140">1140</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">7D39F07A82984C94805F0F629B6E82B87A59DCD6</idno><idno type="DOI">10.1136/jnnp.2007.120212</idno><idno type="href">jnnp-78-1140.pdf</idno><idno type="ArticleID">jn120212</idno><idno type="PMID">17504881</idno><idno type="local">jnnp;78/10/1140</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background: Patients suffering from Parkinson’s disease (PD) describe painful sensations that could be related to neuropathic pain. Experimental data have indicated the involvement of basal ganglia and dopaminergic pathways in central nociceptive processing. Aim: The objective of this study was to assess and compare the effect of levodopa on the objective pain threshold in patients with PD and healthy subjects. Methods: The objective pain threshold was assessed by the nociceptive flexion reflex (RIII) in 13 PD patients and 10 healthy subjects. Patients and healthy subjects were evaluated under two randomised conditions: with levodopa (ON) and without (OFF). Results: Levodopa significantly increased the RIII threshold of PD patients (6.9 (1.2) mA in the OFF condition vs 8 (1.1) mA in the ON position; p = 0.02). RIII threshold was significantly lower in PD patients than in healthy subjects in the OFF condition (6.9 (1.2) mA vs 9.7 (3.4) mA; p = 0.02). RIII threshold did not change after levodopa administration in healthy subjects. Conclusion: These results provide evidence of a dopaminergic modulation of objective pain threshold in PD patients. In addition, the decrease in RIII threshold in PD patients, in the OFF condition, compared with controls, confirms the existence of an objective pain perception disturbance in PD.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>A Gerdelat-Mas</name><affiliations><json:string>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</json:string></affiliations></json:item><json:item><name>M Simonetta-Moreau</name><affiliations><json:string>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</json:string><json:string>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</json:string></affiliations></json:item><json:item><name>C Thalamas</name><affiliations><json:string>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</json:string></affiliations></json:item><json:item><name>F Ory-Magne</name><affiliations><json:string>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</json:string></affiliations></json:item><json:item><name>T Slaoui</name><affiliations><json:string>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</json:string></affiliations></json:item><json:item><name>O Rascol</name><affiliations><json:string>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</json:string><json:string>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</json:string><json:string>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</json:string><json:string>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</json:string></affiliations></json:item><json:item><name>C Brefel-Courbon</name><affiliations><json:string>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</json:string><json:string>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</json:string><json:string>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Pain (neurology)</value></json:item></subject><articleId><json:string>jn120212</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Background: Patients suffering from Parkinson’s disease (PD) describe painful sensations that could be related to neuropathic pain. Experimental data have indicated the involvement of basal ganglia and dopaminergic pathways in central nociceptive processing. Aim: The objective of this study was to assess and compare the effect of levodopa on the objective pain threshold in patients with PD and healthy subjects. Methods: The objective pain threshold was assessed by the nociceptive flexion reflex (RIII) in 13 PD patients and 10 healthy subjects. Patients and healthy subjects were evaluated under two randomised conditions: with levodopa (ON) and without (OFF). Results: Levodopa significantly increased the RIII threshold of PD patients (6.9 (1.2) mA in the OFF condition vs 8 (1.1) mA in the ON position; p = 0.02). RIII threshold was significantly lower in PD patients than in healthy subjects in the OFF condition (6.9 (1.2) mA vs 9.7 (3.4) mA; p = 0.02). RIII threshold did not change after levodopa administration in healthy subjects. Conclusion: These results provide evidence of a dopaminergic modulation of objective pain threshold in PD patients. In addition, the decrease in RIII threshold in PD patients, in the OFF condition, compared with controls, confirms the existence of an objective pain perception disturbance in PD.</abstract><qualityIndicators><score>6.549</score><pdfVersion>1.2</pdfVersion><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>1340</abstractCharCount><pdfWordCount>2125</pdfWordCount><pdfCharCount>14112</pdfCharCount><pdfPageCount>3</pdfPageCount><abstractWordCount>202</abstractWordCount></qualityIndicators><title>Levodopa raises objective pain threshold in Parkinson’s disease: a RIII reflex study</title><pmid><json:string>17504881</json:string></pmid><refBibs><json:item><author><json:item><name>RVF Guiffrida</name></json:item><json:item><name>J Bogousslavsky</name></json:item><json:item><name>J Ghika</name></json:item></author><host><volume>161</volume><author></author><title>Rev Neurol (Paris)</title></host><title>Pain in 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France</affiliation></author><author xml:id="author-3"><persName><forename type="first">C</forename><surname>Thalamas</surname></persName><affiliation>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">F</forename><surname>Ory-Magne</surname></persName><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation></author><author xml:id="author-5"><persName><forename type="first">T</forename><surname>Slaoui</surname></persName><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation></author><author xml:id="author-6"><persName><forename type="first">O</forename><surname>Rascol</surname></persName><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation><affiliation>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</affiliation><affiliation>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</affiliation><affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</affiliation></author><author xml:id="author-7"><persName><forename type="first">C</forename><surname>Brefel-Courbon</surname></persName><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation><affiliation>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</affiliation><affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</affiliation></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2007-10"></date><biblScope unit="volume">78</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1140">1140</biblScope></imprint></monogr><idno type="istex">7D39F07A82984C94805F0F629B6E82B87A59DCD6</idno><idno type="DOI">10.1136/jnnp.2007.120212</idno><idno type="href">jnnp-78-1140.pdf</idno><idno type="ArticleID">jn120212</idno><idno type="PMID">17504881</idno><idno type="local">jnnp;78/10/1140</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007-05-15</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Background: Patients suffering from Parkinson’s disease (PD) describe painful sensations that could be related to neuropathic pain. Experimental data have indicated the involvement of basal ganglia and dopaminergic pathways in central nociceptive processing. Aim: The objective of this study was to assess and compare the effect of levodopa on the objective pain threshold in patients with PD and healthy subjects. Methods: The objective pain threshold was assessed by the nociceptive flexion reflex (RIII) in 13 PD patients and 10 healthy subjects. Patients and healthy subjects were evaluated under two randomised conditions: with levodopa (ON) and without (OFF). Results: Levodopa significantly increased the RIII threshold of PD patients (6.9 (1.2) mA in the OFF condition vs 8 (1.1) mA in the ON position; p = 0.02). RIII threshold was significantly lower in PD patients than in healthy subjects in the OFF condition (6.9 (1.2) mA vs 9.7 (3.4) mA; p = 0.02). RIII threshold did not change after levodopa administration in healthy subjects. Conclusion: These results provide evidence of a dopaminergic modulation of objective pain threshold in PD patients. In addition, the decrease in RIII threshold in PD patients, in the OFF condition, compared with controls, confirms the existence of an objective pain perception disturbance in PD.</p></abstract><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Pain (neurology)</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-05-15">Created</change><change when="2007-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/7D39F07A82984C94805F0F629B6E82B87A59DCD6/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article" xml:lang="EN"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-id journal-id-type="publisher-id">jnnp</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">jn120212</article-id><article-id pub-id-type="doi">10.1136/jnnp.2007.120212</article-id><article-id pub-id-type="other">jnnp;78/10/1140</article-id><article-id pub-id-type="other">jnnp;jnnp.2007.120212</article-id><article-id pub-id-type="pmid">17504881</article-id><article-id pub-id-type="other">1140</article-id><article-id pub-id-type="other">jnnp.2007.120212</article-id><article-categories><subj-group subj-group-type="heading"><subject content-type="original">Short reports</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Pain (neurology)</subject></subj-group></article-categories><title-group><article-title>Levodopa raises objective pain threshold in Parkinson’s disease: a RIII reflex study</article-title><alt-title alt-title-type="running-head">Levodopa and objective pain threshold</alt-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Gerdelat-Mas</surname><given-names>A</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Simonetta-Moreau</surname><given-names>M</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff4">4</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Thalamas</surname><given-names>C</given-names></name><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Ory-Magne</surname><given-names>F</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Slaoui</surname><given-names>T</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Rascol</surname><given-names>O</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref><xref ref-type="aff" rid="aff3">3</xref><xref ref-type="aff" rid="aff4">4</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Brefel-Courbon</surname><given-names>C</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff3">3</xref><xref ref-type="aff" rid="aff4">4</xref></contrib></contrib-group><aff id="aff1"><label>1</label> <addr-line>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</addr-line> </aff><aff id="aff2"><label>2</label> <addr-line>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</addr-line> </aff><aff id="aff3"><label>3</label> <addr-line>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</addr-line> </aff><aff id="aff4"><label>4</label> <addr-line>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</addr-line> </aff><author-notes><corresp>Dr Angélique Gerdelat-Mas, Service de Neurologie, Hôpital Purpan, Pavillon Riser, Place du Dr Baylac, Toulouse 31059, France; <email xlink:type="simple">gerdelat-mas.a@chu-toulouse.fr</email></corresp></author-notes><pub-date pub-type="ppub"><month>10</month><year>2007</year></pub-date><pub-date pub-type="epub-original"><day>15</day><month>5</month><year>2007</year></pub-date><pub-date pub-type="epub"><day>15</day><month>5</month><year>2007</year></pub-date><volume>78</volume><volume-id pub-id-type="other">78</volume-id><volume-id pub-id-type="other">78</volume-id><issue>10</issue><issue-id pub-id-type="other">jnnp;78/10</issue-id><issue-id pub-id-type="other">10</issue-id><issue-id pub-id-type="other">78/10</issue-id><fpage>1140</fpage><history><date date-type="received"><day>11</day><month>3</month><year>2007</year></date><date date-type="rev-recd"><day>24</day><month>4</month><year>2007</year></date><date date-type="accepted"><day>4</day><month>5</month><year>2007</year></date></history><permissions><copyright-statement>2007 BMJ Publishing Group</copyright-statement><copyright-year>2007</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-78-1140.pdf"></self-uri><abstract><sec><title>Background:</title><p>Patients suffering from Parkinson’s disease (PD) describe painful sensations that could be related to neuropathic pain. Experimental data have indicated the involvement of basal ganglia and dopaminergic pathways in central nociceptive processing.</p></sec><sec><title>Aim:</title><p>The objective of this study was to assess and compare the effect of levodopa on the objective pain threshold in patients with PD and healthy subjects.</p></sec><sec><title>Methods:</title><p>The objective pain threshold was assessed by the nociceptive flexion reflex (RIII) in 13 PD patients and 10 healthy subjects. Patients and healthy subjects were evaluated under two randomised conditions: with levodopa (ON) and without (OFF).</p></sec><sec><title>Results:</title><p>Levodopa significantly increased the RIII threshold of PD patients (6.9 (1.2) mA in the OFF condition vs 8 (1.1) mA in the ON position; p = 0.02). RIII threshold was significantly lower in PD patients than in healthy subjects in the OFF condition (6.9 (1.2) mA vs 9.7 (3.4) mA; p = 0.02). RIII threshold did not change after levodopa administration in healthy subjects.</p></sec><sec><title>Conclusion:</title><p>These results provide evidence of a dopaminergic modulation of objective pain threshold in PD patients. In addition, the decrease in RIII threshold in PD patients, in the OFF condition, compared with controls, confirms the existence of an objective pain perception disturbance in PD.</p></sec></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Levodopa raises objective pain threshold in Parkinson’s disease: a RIII reflex study</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Levodopa raises objective pain threshold in Parkinson’s disease: a RIII reflex study</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Gerdelat-Mas</namePart><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Simonetta-Moreau</namePart><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation><affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Thalamas</namePart><affiliation>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Ory-Magne</namePart><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Slaoui</namePart><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Rascol</namePart><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation><affiliation>Centre d’Investigation Clinique, Hôpital Purpan, Toulouse, France</affiliation><affiliation>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</affiliation><affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Brefel-Courbon</namePart><affiliation>Fédération de Neuroscience, Hôpital Purpan, Toulouse, France</affiliation><affiliation>Departement de Pharmacologie Clinique, Hôpital Purpan, Toulouse, France</affiliation><affiliation>INSERM, U825, Université Toulouse III Paul Sabatier, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><genre>hwp-journal-coll</genre><topic>Pain (neurology)</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2007-10</dateIssued><dateCreated encoding="w3cdtf">2007-05-15</dateCreated><copyrightDate encoding="w3cdtf">2007</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>Background: Patients suffering from Parkinson’s disease (PD) describe painful sensations that could be related to neuropathic pain. Experimental data have indicated the involvement of basal ganglia and dopaminergic pathways in central nociceptive processing. Aim: The objective of this study was to assess and compare the effect of levodopa on the objective pain threshold in patients with PD and healthy subjects. Methods: The objective pain threshold was assessed by the nociceptive flexion reflex (RIII) in 13 PD patients and 10 healthy subjects. Patients and healthy subjects were evaluated under two randomised conditions: with levodopa (ON) and without (OFF). Results: Levodopa significantly increased the RIII threshold of PD patients (6.9 (1.2) mA in the OFF condition vs 8 (1.1) mA in the ON position; p = 0.02). RIII threshold was significantly lower in PD patients than in healthy subjects in the OFF condition (6.9 (1.2) mA vs 9.7 (3.4) mA; p = 0.02). RIII threshold did not change after levodopa administration in healthy subjects. Conclusion: These results provide evidence of a dopaminergic modulation of objective pain threshold in PD patients. In addition, the decrease in RIII threshold in PD patients, in the OFF condition, compared with controls, confirms the existence of an objective pain perception disturbance in PD.</abstract><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID">jnnp</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>78</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1140</start></extent></part></relatedItem><identifier type="istex">7D39F07A82984C94805F0F629B6E82B87A59DCD6</identifier><identifier type="DOI">10.1136/jnnp.2007.120212</identifier><identifier type="href">jnnp-78-1140.pdf</identifier><identifier type="ArticleID">jn120212</identifier><identifier type="PMID">17504881</identifier><identifier type="local">jnnp;78/10/1140</identifier><accessCondition type="use and reproduction" contentType="copyright">2007 BMJ Publishing Group</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><extension>jpeg</extension><original>true</original><mimetype>image/jpeg</mimetype><uri>https://api.istex.fr/document/7D39F07A82984C94805F0F629B6E82B87A59DCD6/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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