SEPs N30 amplitude in Parkinson's disease and in pharmacologically induced rigidity: relationship with the clinical status
Identifieur interne : 002583 ( Main/Corpus ); précédent : 002582; suivant : 002584SEPs N30 amplitude in Parkinson's disease and in pharmacologically induced rigidity: relationship with the clinical status
Auteurs : P. Stanzione ; R. Traversa ; M. Pierantozzi ; R. Semprini ; M. Loberti ; A. Peppe ; A. M. Santilli ; G. BernardiSource :
- European Journal of Neurology [ 1351-5101 ] ; 1997-01.
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- KwdEn :
Abstract
The frontal N30 wave amplitude of somatosensory evoked potentials (SEPs) has been studied in 41 Parkinson's disease (PD) patients (pts) in a basal condition and compared to that of 30 normal subjects; moreover the N30 amplitude and clinical motor score have been evaluated in a subgroup of 30 PD pts before and during apomorphine infusion and in a second subgroup of 22 PD pts also during levodopa chronic therapy. The data show that N30 amplitude is decreased in PD pts in basal condition and increased following both treatments by a percentage proportional to the clinical improvement Analysis by non parametric correlations showed that the increase is well correlated to the clinical score amelioration induced by apomorphine in the more affected side. The best correlation was to rigidity score amelioration in the group of PD pts in medium stage (Hohen and Yahr stage between 2 and 3), suggesting a relationship between the rigidity and N30 amplitude decrease. Non parkinsonian subjects, treated with low (11 aged normal subjects) and high (eight young psychotic pts) doses of antidopaminergic drugs, were studied. N30 amplitude decreases were only found in the group of eight psychotic pts showing clinical extrapyramidal signs, produced by the high dose of drug administered, but not in the group treated with the lower dose not producing extrapyramidal side effects, although this dose was efficacious on different modalities of evoked potentials. We conclude that N30 amplitude decrease in PD reflects the dopaminergic lack paralleled by clinical symptoms. We propose that N30 amplitude variations by dopaminergic agonists may be useful in the clinical evaluation of dopamine related and non related tone alterations.
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DOI: 10.1111/j.1468-1331.1997.tb00296.x
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The data show that N30 amplitude is decreased in PD pts in basal condition and increased following both treatments by a percentage proportional to the clinical improvement Analysis by non parametric correlations showed that the increase is well correlated to the clinical score amelioration induced by apomorphine in the more affected side. The best correlation was to rigidity score amelioration in the group of PD pts in medium stage (Hohen and Yahr stage between 2 and 3), suggesting a relationship between the rigidity and N30 amplitude decrease. Non parkinsonian subjects, treated with low (11 aged normal subjects) and high (eight young psychotic pts) doses of antidopaminergic drugs, were studied. N30 amplitude decreases were only found in the group of eight psychotic pts showing clinical extrapyramidal signs, produced by the high dose of drug administered, but not in the group treated with the lower dose not producing extrapyramidal side effects, although this dose was efficacious on different modalities of evoked potentials. We conclude that N30 amplitude decrease in PD reflects the dopaminergic lack paralleled by clinical symptoms. We propose that N30 amplitude variations by dopaminergic agonists may be useful in the clinical evaluation of dopamine related and non related tone alterations.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>P. Stanzione</name><affiliations><json:string>IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</json:string><json:string>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</json:string></affiliations></json:item><json:item><name>R. Traversa</name><affiliations><json:string>IRCCS Clinica S. 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The data show that N30 amplitude is decreased in PD pts in basal condition and increased following both treatments by a percentage proportional to the clinical improvement Analysis by non parametric correlations showed that the increase is well correlated to the clinical score amelioration induced by apomorphine in the more affected side. The best correlation was to rigidity score amelioration in the group of PD pts in medium stage (Hohen and Yahr stage between 2 and 3), suggesting a relationship between the rigidity and N30 amplitude decrease. Non parkinsonian subjects, treated with low (11 aged normal subjects) and high (eight young psychotic pts) doses of antidopaminergic drugs, were studied. N30 amplitude decreases were only found in the group of eight psychotic pts showing clinical extrapyramidal signs, produced by the high dose of drug administered, but not in the group treated with the lower dose not producing extrapyramidal side effects, although this dose was efficacious on different modalities of evoked potentials. We conclude that N30 amplitude decrease in PD reflects the dopaminergic lack paralleled by clinical symptoms. We propose that N30 amplitude variations by dopaminergic agonists may be useful in the clinical evaluation of dopamine related and non related tone alterations.</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 791.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>8</keywordCount><abstractCharCount>1726</abstractCharCount><pdfWordCount>7221</pdfWordCount><pdfCharCount>45490</pdfCharCount><pdfPageCount>15</pdfPageCount><abstractWordCount>269</abstractWordCount></qualityIndicators><title>SEPs N30 amplitude in Parkinson's disease and in pharmacologically induced rigidity: relationship with the clinical status</title><genre><json:string>article</json:string></genre><host><volume>4</volume><publisherId><json:string>ENE</json:string></publisherId><pages><total>15</total><last>38</last><first>24</first></pages><issn><json:string>1351-5101</json:string></issn><issue>1</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-1331</json:string></eissn><title>European Journal of Neurology</title><doi><json:string>10.1111/(ISSN)1468-1331</json:string></doi></host><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1111/j.1468-1331.1997.tb00296.x</json:string></doi><id>E45E20F5B6D9B231473E8286E07757F557AD4B32</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/E45E20F5B6D9B231473E8286E07757F557AD4B32/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/E45E20F5B6D9B231473E8286E07757F557AD4B32/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/E45E20F5B6D9B231473E8286E07757F557AD4B32/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">SEPs N30 amplitude in Parkinson's disease and in pharmacologically induced rigidity: relationship with the clinical status</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1997</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">SEPs N30 amplitude in Parkinson's disease and in pharmacologically induced rigidity: relationship with the clinical status</title><author><persName><forename type="first">P.</forename><surname>Stanzione</surname></persName><note type="correspondence"><p>Correspondence: IRCCS Clinica S. 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Lucia, Via Ardeatina 306, Rome, Italy</affiliation></author><author><persName><forename type="first">M.</forename><surname>Loberti</surname></persName><affiliation>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</affiliation></author><author><persName><forename type="first">A.</forename><surname>Peppe</surname></persName><affiliation>IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</affiliation></author><author><persName><forename type="first">A. M.</forename><surname>Santilli</surname></persName><affiliation>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</affiliation></author><author><persName><forename type="first">G.</forename><surname>Bernardi</surname></persName><affiliation>IRCCS Clinica S. 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The data show that N30 amplitude is decreased in PD pts in basal condition and increased following both treatments by a percentage proportional to the clinical improvement Analysis by non parametric correlations showed that the increase is well correlated to the clinical score amelioration induced by apomorphine in the more affected side. The best correlation was to rigidity score amelioration in the group of PD pts in medium stage (Hohen and Yahr stage between 2 and 3), suggesting a relationship between the rigidity and N30 amplitude decrease. Non parkinsonian subjects, treated with low (11 aged normal subjects) and high (eight young psychotic pts) doses of antidopaminergic drugs, were studied. N30 amplitude decreases were only found in the group of eight psychotic pts showing clinical extrapyramidal signs, produced by the high dose of drug administered, but not in the group treated with the lower dose not producing extrapyramidal side effects, although this dose was efficacious on different modalities of evoked potentials. We conclude that N30 amplitude decrease in PD reflects the dopaminergic lack paralleled by clinical symptoms. We propose that N30 amplitude variations by dopaminergic agonists may be useful in the clinical evaluation of dopamine related and non related tone alterations.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>Somatosensory evoked potentials</term></item><item><term>Dopamine physiology</term></item><item><term>Levodopa</term></item><item><term>Apomorphine</term></item><item><term>Neuroleptics</term></item><item><term>Rigidity</term></item><item><term>Bradykinesia</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E45E20F5B6D9B231473E8286E07757F557AD4B32/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1468-1331</doi><issn type="print">1351-5101</issn><issn type="electronic">1468-1331</issn><idGroup><id type="product" value="ENE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROLOGY">European Journal of Neurology</title></titleGroup></publicationMeta><publicationMeta level="part" position="01101"><doi origin="wiley">10.1111/ene.1997.4.issue-1</doi><numberingGroup><numbering type="journalVolume" number="4">4</numbering><numbering type="journalIssue" number="1">1</numbering></numberingGroup><coverDate startDate="1997-01">January 1997</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="5" status="forIssue"><doi origin="wiley">10.1111/j.1468-1331.1997.tb00296.x</doi><idGroup><id type="unit" value="ENE296"></id></idGroup><countGroup><count type="pageTotal" number="15"></count></countGroup><titleGroup><title type="tocHeading1">Original Article</title></titleGroup><copyright>1997 Lippincott Williams & Wilkins</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.4.3 mode:FullText" date="2011-01-19"></event><event type="firstOnline" date="2011-01-20"></event><event type="publishedOnlineFinalForm" date="2011-01-20"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="24">24</numbering><numbering type="pageLast" number="38">38</numbering></numberingGroup><correspondenceTo>IRCCS Clinica S. 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M.</givenNames><familyName>Santilli</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1 #a2"><personName><givenNames>G.</givenNames><familyName>Bernardi</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="IT"><unparsedAffiliation>IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="IT"><unparsedAffiliation>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinson's disease</keyword><keyword xml:id="k2">Somatosensory evoked potentials</keyword><keyword xml:id="k3">Dopamine physiology</keyword><keyword xml:id="k4">Levodopa</keyword><keyword xml:id="k5">Apomorphine</keyword><keyword xml:id="k6">Neuroleptics</keyword><keyword xml:id="k7">Rigidity</keyword><keyword xml:id="k8">Bradykinesia</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>The frontal N30 wave amplitude of somatosensory evoked potentials (SEPs) has been studied in 41 Parkinson's disease (PD) patients (pts) in a basal condition and compared to that of 30 normal subjects; moreover the N30 amplitude and clinical motor score have been evaluated in a subgroup of 30 PD pts before and during apomorphine infusion and in a second subgroup of 22 PD pts also during levodopa chronic therapy. The data show that N30 amplitude is decreased in PD pts in basal condition and increased following both treatments by a percentage proportional to the clinical improvement Analysis by non parametric correlations showed that the increase is well correlated to the clinical score amelioration induced by apomorphine in the more affected side. The best correlation was to rigidity score amelioration in the group of PD pts in medium stage (Hohen and Yahr stage between 2 and 3), suggesting a relationship between the rigidity and N30 amplitude decrease. Non parkinsonian subjects, treated with low (11 aged normal subjects) and high (eight young psychotic pts) doses of antidopaminergic drugs, were studied. N30 amplitude decreases were only found in the group of eight psychotic pts showing clinical extrapyramidal signs, produced by the high dose of drug administered, but not in the group treated with the lower dose not producing extrapyramidal side effects, although this dose was efficacious on different modalities of evoked potentials. We conclude that N30 amplitude decrease in PD reflects the dopaminergic lack paralleled by clinical symptoms. We propose that N30 amplitude variations by dopaminergic agonists may be useful in the clinical evaluation of dopamine related and non related tone alterations.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>SEPs N30 amplitude in Parkinson's disease and in pharmacologically induced rigidity: relationship with the clinical status</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>SEPs N30 amplitude in Parkinson's disease and in pharmacologically induced rigidity: relationship with the clinical status</title></titleInfo><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Stanzione</namePart><affiliation>IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</affiliation><affiliation>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</affiliation><description>Correspondence: IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Traversa</namePart><affiliation>IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Pierantozzi</namePart><affiliation>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Semprini</namePart><affiliation>IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Loberti</namePart><affiliation>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Peppe</namePart><affiliation>IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. M.</namePart><namePart type="family">Santilli</namePart><affiliation>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Bernardi</namePart><affiliation>IRCCS Clinica S. Lucia, Via Ardeatina 306, Rome, Italy</affiliation><affiliation>Clinica Neurologica Università di Roma Tor Vergata, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1997-01</dateIssued><edition>Received 10 May 1996; accepted as revised 9 September 1996</edition><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">23</extent></physicalDescription><abstract lang="en">The frontal N30 wave amplitude of somatosensory evoked potentials (SEPs) has been studied in 41 Parkinson's disease (PD) patients (pts) in a basal condition and compared to that of 30 normal subjects; moreover the N30 amplitude and clinical motor score have been evaluated in a subgroup of 30 PD pts before and during apomorphine infusion and in a second subgroup of 22 PD pts also during levodopa chronic therapy. The data show that N30 amplitude is decreased in PD pts in basal condition and increased following both treatments by a percentage proportional to the clinical improvement Analysis by non parametric correlations showed that the increase is well correlated to the clinical score amelioration induced by apomorphine in the more affected side. The best correlation was to rigidity score amelioration in the group of PD pts in medium stage (Hohen and Yahr stage between 2 and 3), suggesting a relationship between the rigidity and N30 amplitude decrease. Non parkinsonian subjects, treated with low (11 aged normal subjects) and high (eight young psychotic pts) doses of antidopaminergic drugs, were studied. N30 amplitude decreases were only found in the group of eight psychotic pts showing clinical extrapyramidal signs, produced by the high dose of drug administered, but not in the group treated with the lower dose not producing extrapyramidal side effects, although this dose was efficacious on different modalities of evoked potentials. We conclude that N30 amplitude decrease in PD reflects the dopaminergic lack paralleled by clinical symptoms. We propose that N30 amplitude variations by dopaminergic agonists may be useful in the clinical evaluation of dopamine related and non related tone alterations.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>Somatosensory evoked potentials</topic><topic>Dopamine physiology</topic><topic>Levodopa</topic><topic>Apomorphine</topic><topic>Neuroleptics</topic><topic>Rigidity</topic><topic>Bradykinesia</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>24</start><end>38</end><total>15</total></extent></part></relatedItem><identifier type="istex">E45E20F5B6D9B231473E8286E07757F557AD4B32</identifier><identifier type="DOI">10.1111/j.1468-1331.1997.tb00296.x</identifier><identifier type="ArticleID">ENE296</identifier><accessCondition type="use and reproduction" contentType="copyright">1997 Lippincott Williams & Wilkins</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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