Effect of medication on EMG patterns in individuals with Parkinson's disease
Identifieur interne : 000258 ( Istex/Corpus ); précédent : 000257; suivant : 000259Effect of medication on EMG patterns in individuals with Parkinson's disease
Auteurs : Julie A. Robichaud ; Kerstin D. Pfann ; Cynthia L. Comella ; Daniel M. CorcosSource :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
English descriptors
Abstract
Individuals with Parkinson's disease show dramatic improvements in their ability to move when medicated. However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while off and on antiparkinsonian medication. When the subjects were off medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. These results show that medication does not alter the temporal profile of EMG activation. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10218
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ISTEX:915FB92AA301FDE6D0E2075B8CA207A1DC9EB778Le document en format XML
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However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while off and on antiparkinsonian medication. When the subjects were off medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. 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Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. 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Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. 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However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while <i>off</i> and <i>on</i> antiparkinsonian medication. When the subjects were <i>off</i> medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. These results show that medication does not alter the temporal profile of EMG activation. © 2002 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Effect of medication on EMG patterns in individuals with Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Medication, Movement, and Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effect of medication on EMG patterns in individuals with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Julie A.</namePart><namePart type="family">Robichaud</namePart><namePart type="termsOfAddress">PT, PhD</namePart><affiliation>School of Kinesiology, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><description>Correspondence: School of Kinesiology (M/C 194), University of Illinois at Chicago, 901 West Roosevelt Road, Chicago, IL 60608</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kerstin D.</namePart><namePart type="family">Pfann</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>School of Kinesiology, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cynthia L.</namePart><namePart type="family">Comella</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, Rush Medical Center, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daniel M.</namePart><namePart type="family">Corcos</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>School of Kinesiology, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Physical Therapy, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><affiliation>Department of Neurological Sciences, Rush Medical Center, Chicago, Illinois, USA</affiliation><affiliation>Department of Psychology, University of Illinois at Chicago, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002-09</dateIssued><dateCaptured encoding="w3cdtf">2001-06-07</dateCaptured><dateValid encoding="w3cdtf">2002-02-20</dateValid><copyrightDate encoding="w3cdtf">2002</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="figures">8</extent><extent unit="tables">2</extent><extent unit="references">27</extent><extent unit="words">5436</extent></physicalDescription><abstract lang="en">Individuals with Parkinson's disease show dramatic improvements in their ability to move when medicated. However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while off and on antiparkinsonian medication. When the subjects were off medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. These results show that medication does not alter the temporal profile of EMG activation. © 2002 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>medication</topic><topic>EMG patterns</topic><topic>movement control</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>950</start><end>960</end><total>11</total></extent></part></relatedItem><identifier type="istex">915FB92AA301FDE6D0E2075B8CA207A1DC9EB778</identifier><identifier type="DOI">10.1002/mds.10218</identifier><identifier type="ArticleID">MDS10218</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Movement Disorders Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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