Electrophysiological evaluation of pharyngeal phase of swallowing in patients with Parkinson's disease
Identifieur interne : 000011 ( Istex/Corpus ); précédent : 000010; suivant : 000012Electrophysiological evaluation of pharyngeal phase of swallowing in patients with Parkinson's disease
Auteurs : Cumhur Ertekin ; Sultan Tarlaci ; Ibrahim Aydogdu ; Nefati Kiylioglu ; Nur Yuceyar ; A. Bulent Turman ; Yaprak Secil ; Figen EsmeliSource :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
English descriptors
Abstract
We studied the various physiological aspects of oropharyngeal swallowing in Parkinson's disease (PD). Fifty‐eight patients with PD were investigated by clinical and electrophysiological methods that measured the oropharyngeal phase of swallowing. All patients except 1 had mild to moderate degree of disability score. Dysphagia was demonstrated in 53% of all patients in whom the test of dysphagia limit was abnormal. All PD patients with or without dysphagia displayed the following abnormalities: (1) the triggering of the swallowing reflex was prolonged probably due to inadequate bolus control in the mouth and tongue and/or a specific delay in the execution of the swallowing reflex; (2) the duration of the pharyngeal reflex time was extremely prolonged due to slowness of the sequential muscle movements, especially those of the suprahyoid‐submental muscles; (3) cricopharyngeal muscle of the upper oesophageal sphincter was found to be electrophysiologically normal; and (4) the electrophysiological phenomena in PD patients could not be strongly correlated with the degree of the disability and clinical score of the PD. It was concluded that various motor disorders of PD have considerable influence on oropharyngeal swallowing: hypokinesia, reduced rate of spontaneous swallowing, and the slowness of segmented but coordinated sequential movements rather than any abnormalities in the central pattern generator of the bulbar center. Some compensatory mechanisms in the course of PD may explain the benign nature of swallowing disorder until the terminal stage of the disease. Similarly, the swallowing problems of PD are not only related with the dopamine deficiency; some other nondopaminergic mechanisms may also be involved. © 2002 Movement Disorder Society
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DOI: 10.1002/mds.10240
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-09">2002-09</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="942">942</biblScope><biblScope unit="page" to="949">949</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">442C89B4E4F1421B3051AD3379B4621B830F65B7</idno><idno type="DOI">10.1002/mds.10240</idno><idno type="ArticleID">MDS10240</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>cricopharyngeal muscle</term><term>electromyography</term><term>oropharyngeal dysphagia</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We studied the various physiological aspects of oropharyngeal swallowing in Parkinson's disease (PD). Fifty‐eight patients with PD were investigated by clinical and electrophysiological methods that measured the oropharyngeal phase of swallowing. All patients except 1 had mild to moderate degree of disability score. Dysphagia was demonstrated in 53% of all patients in whom the test of dysphagia limit was abnormal. All PD patients with or without dysphagia displayed the following abnormalities: (1) the triggering of the swallowing reflex was prolonged probably due to inadequate bolus control in the mouth and tongue and/or a specific delay in the execution of the swallowing reflex; (2) the duration of the pharyngeal reflex time was extremely prolonged due to slowness of the sequential muscle movements, especially those of the suprahyoid‐submental muscles; (3) cricopharyngeal muscle of the upper oesophageal sphincter was found to be electrophysiologically normal; and (4) the electrophysiological phenomena in PD patients could not be strongly correlated with the degree of the disability and clinical score of the PD. It was concluded that various motor disorders of PD have considerable influence on oropharyngeal swallowing: hypokinesia, reduced rate of spontaneous swallowing, and the slowness of segmented but coordinated sequential movements rather than any abnormalities in the central pattern generator of the bulbar center. Some compensatory mechanisms in the course of PD may explain the benign nature of swallowing disorder until the terminal stage of the disease. Similarly, the swallowing problems of PD are not only related with the dopamine deficiency; some other nondopaminergic mechanisms may also be involved. © 2002 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Cumhur Ertekin MD</name><affiliations><json:string>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string><json:string>Department of Clinical Neurophysiology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string></affiliations></json:item><json:item><name>Sultan Tarlaci MD</name><affiliations><json:string>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string></affiliations></json:item><json:item><name>Ibrahim Aydogdu MD</name><affiliations><json:string>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string><json:string>Department of Clinical Neurophysiology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string></affiliations></json:item><json:item><name>Nefati Kiylioglu MD</name><affiliations><json:string>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string></affiliations></json:item><json:item><name>Nur Yuceyar MD</name><affiliations><json:string>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string></affiliations></json:item><json:item><name>A. Bulent Turman MD</name><affiliations><json:string>Department of Biomedical Sciences, University of Sydney, Australia</json:string></affiliations></json:item><json:item><name>Yaprak Secil MD</name><affiliations><json:string>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string></affiliations></json:item><json:item><name>Figen Esmeli MD</name><affiliations><json:string>Department of Clinical Neurophysiology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</json:string></affiliations></json:item></author><subject><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>oropharyngeal dysphagia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>electromyography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cricopharyngeal muscle</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We studied the various physiological aspects of oropharyngeal swallowing in Parkinson's disease (PD). Fifty‐eight patients with PD were investigated by clinical and electrophysiological methods that measured the oropharyngeal phase of swallowing. All patients except 1 had mild to moderate degree of disability score. Dysphagia was demonstrated in 53% of all patients in whom the test of dysphagia limit was abnormal. All PD patients with or without dysphagia displayed the following abnormalities: (1) the triggering of the swallowing reflex was prolonged probably due to inadequate bolus control in the mouth and tongue and/or a specific delay in the execution of the swallowing reflex; (2) the duration of the pharyngeal reflex time was extremely prolonged due to slowness of the sequential muscle movements, especially those of the suprahyoid‐submental muscles; (3) cricopharyngeal muscle of the upper oesophageal sphincter was found to be electrophysiologically normal; and (4) the electrophysiological phenomena in PD patients could not be strongly correlated with the degree of the disability and clinical score of the PD. It was concluded that various motor disorders of PD have considerable influence on oropharyngeal swallowing: hypokinesia, reduced rate of spontaneous swallowing, and the slowness of segmented but coordinated sequential movements rather than any abnormalities in the central pattern generator of the bulbar center. Some compensatory mechanisms in the course of PD may explain the benign nature of swallowing disorder until the terminal stage of the disease. 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Bulent</forename><surname>Turman</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Biomedical Sciences, University of Sydney, Australia</affiliation></author><author><persName><forename type="first">Yaprak</forename><surname>Secil</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation></author><author><persName><forename type="first">Figen</forename><surname>Esmeli</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Clinical Neurophysiology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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Fifty‐eight patients with PD were investigated by clinical and electrophysiological methods that measured the oropharyngeal phase of swallowing. All patients except 1 had mild to moderate degree of disability score. Dysphagia was demonstrated in 53% of all patients in whom the test of dysphagia limit was abnormal. All PD patients with or without dysphagia displayed the following abnormalities: (1) the triggering of the swallowing reflex was prolonged probably due to inadequate bolus control in the mouth and tongue and/or a specific delay in the execution of the swallowing reflex; (2) the duration of the pharyngeal reflex time was extremely prolonged due to slowness of the sequential muscle movements, especially those of the suprahyoid‐submental muscles; (3) cricopharyngeal muscle of the upper oesophageal sphincter was found to be electrophysiologically normal; and (4) the electrophysiological phenomena in PD patients could not be strongly correlated with the degree of the disability and clinical score of the PD. It was concluded that various motor disorders of PD have considerable influence on oropharyngeal swallowing: hypokinesia, reduced rate of spontaneous swallowing, and the slowness of segmented but coordinated sequential movements rather than any abnormalities in the central pattern generator of the bulbar center. Some compensatory mechanisms in the course of PD may explain the benign nature of swallowing disorder until the terminal stage of the disease. Similarly, the swallowing problems of PD are not only related with the dopamine deficiency; some other nondopaminergic mechanisms may also be involved. © 2002 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>oropharyngeal dysphagia</term></item><item><term>electromyography</term></item><item><term>cricopharyngeal muscle</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-12-10">Received</change><change when="2002-02-26">Registration</change><change when="2002-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/442C89B4E4F1421B3051AD3379B4621B830F65B7/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>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Bulent</givenNames><familyName>Turman</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yaprak</givenNames><familyName>Secil</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Figen</givenNames><familyName>Esmeli</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="TR" type="organization"><unparsedAffiliation>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="TR" type="organization"><unparsedAffiliation>Department of Clinical Neurophysiology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="AU" type="organization"><unparsedAffiliation>Department of Biomedical Sciences, University of Sydney, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">oropharyngeal dysphagia</keyword><keyword xml:id="kwd3">electromyography</keyword><keyword xml:id="kwd4">cricopharyngeal muscle</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We studied the various physiological aspects of oropharyngeal swallowing in Parkinson's disease (PD). Fifty‐eight patients with PD were investigated by clinical and electrophysiological methods that measured the oropharyngeal phase of swallowing. All patients except 1 had mild to moderate degree of disability score. Dysphagia was demonstrated in 53% of all patients in whom the test of dysphagia limit was abnormal. All PD patients with or without dysphagia displayed the following abnormalities: (1) the triggering of the swallowing reflex was prolonged probably due to inadequate bolus control in the mouth and tongue and/or a specific delay in the execution of the swallowing reflex; (2) the duration of the pharyngeal reflex time was extremely prolonged due to slowness of the sequential muscle movements, especially those of the suprahyoid‐submental muscles; (3) cricopharyngeal muscle of the upper oesophageal sphincter was found to be electrophysiologically normal; and (4) the electrophysiological phenomena in PD patients could not be strongly correlated with the degree of the disability and clinical score of the PD. It was concluded that various motor disorders of PD have considerable influence on oropharyngeal swallowing: hypokinesia, reduced rate of spontaneous swallowing, and the slowness of segmented but coordinated sequential movements rather than any abnormalities in the central pattern generator of the bulbar center. Some compensatory mechanisms in the course of PD may explain the benign nature of swallowing disorder until the terminal stage of the disease. Similarly, the swallowing problems of PD are not only related with the dopamine deficiency; some other nondopaminergic mechanisms may also be involved. © 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>Electrophysiological evaluation of pharyngeal phase of swallowing in patients with Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Oropharyngeal Dysfunction in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Electrophysiological evaluation of pharyngeal phase of swallowing in patients with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Cumhur</namePart><namePart type="family">Ertekin</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation><affiliation>Department of Clinical Neurophysiology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation><description>Correspondence: Talatpapa Bulvari, Gönç Apt., No: 12, D3, 35220 Alsancak, Izmir, Turkey</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sultan</namePart><namePart type="family">Tarlaci</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ibrahim</namePart><namePart type="family">Aydogdu</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation><affiliation>Department of Clinical Neurophysiology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nefati</namePart><namePart type="family">Kiylioglu</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nur</namePart><namePart type="family">Yuceyar</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. Bulent</namePart><namePart type="family">Turman</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Biomedical Sciences, University of Sydney, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yaprak</namePart><namePart type="family">Secil</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Figen</namePart><namePart type="family">Esmeli</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neurophysiology, Ege University Medical School Hospital, Bornova, Izmir, Turkey</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">2001-12-10</dateCaptured><dateValid encoding="w3cdtf">2002-02-26</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">4</extent><extent unit="tables">1</extent><extent unit="references">53</extent><extent unit="words">4717</extent></physicalDescription><abstract lang="en">We studied the various physiological aspects of oropharyngeal swallowing in Parkinson's disease (PD). Fifty‐eight patients with PD were investigated by clinical and electrophysiological methods that measured the oropharyngeal phase of swallowing. All patients except 1 had mild to moderate degree of disability score. Dysphagia was demonstrated in 53% of all patients in whom the test of dysphagia limit was abnormal. All PD patients with or without dysphagia displayed the following abnormalities: (1) the triggering of the swallowing reflex was prolonged probably due to inadequate bolus control in the mouth and tongue and/or a specific delay in the execution of the swallowing reflex; (2) the duration of the pharyngeal reflex time was extremely prolonged due to slowness of the sequential muscle movements, especially those of the suprahyoid‐submental muscles; (3) cricopharyngeal muscle of the upper oesophageal sphincter was found to be electrophysiologically normal; and (4) the electrophysiological phenomena in PD patients could not be strongly correlated with the degree of the disability and clinical score of the PD. It was concluded that various motor disorders of PD have considerable influence on oropharyngeal swallowing: hypokinesia, reduced rate of spontaneous swallowing, and the slowness of segmented but coordinated sequential movements rather than any abnormalities in the central pattern generator of the bulbar center. Some compensatory mechanisms in the course of PD may explain the benign nature of swallowing disorder until the terminal stage of the disease. Similarly, the swallowing problems of PD are not only related with the dopamine deficiency; some other nondopaminergic mechanisms may also be involved. © 2002 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>oropharyngeal dysphagia</topic><topic>electromyography</topic><topic>cricopharyngeal muscle</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. 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