Electrophysiological studies of early stage corticobasal degeneration
Identifieur interne : 001865 ( Istex/Corpus ); précédent : 001864; suivant : 001866Electrophysiological studies of early stage corticobasal degeneration
Auteurs : C. S. Lu ; A. Ikeda ; K. Terada ; T. Mima ; T. Nagamine ; H. Fukuyama ; N. Kohara ; Y. Kojima ; Y. Yonekura ; R. S. Chen ; C. H. Tsai ; N. S. Chu ; J. Kimura ; ShibasakiSource :
- Movement Disorders [ 0885-3185 ] ; 1998-01.
English descriptors
Abstract
We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.
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DOI: 10.1002/mds.870130126
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Terada</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Mima, T" sort="Mima, T" uniqKey="Mima T" first="T." last="Mima">T. Mima</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nagamine, T" sort="Nagamine, T" uniqKey="Nagamine T" first="T." last="Nagamine">T. Nagamine</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Fukuyama, H" sort="Fukuyama, H" uniqKey="Fukuyama H" first="H." last="Fukuyama">H. 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Chu</name><affiliation><mods:affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Kimura, J" sort="Kimura, J" uniqKey="Kimura J" first="J." last="Kimura">J. 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S." last="Lu">C. S. Lu</name><affiliation><mods:affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Ikeda, A" sort="Ikeda, A" uniqKey="Ikeda A" first="A." last="Ikeda">A. Ikeda</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Terada, K" sort="Terada, K" uniqKey="Terada K" first="K." last="Terada">K. Terada</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Mima, T" sort="Mima, T" uniqKey="Mima T" first="T." last="Mima">T. Mima</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nagamine, T" sort="Nagamine, T" uniqKey="Nagamine T" first="T." last="Nagamine">T. Nagamine</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Fukuyama, H" sort="Fukuyama, H" uniqKey="Fukuyama H" first="H." last="Fukuyama">H. Fukuyama</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kohara, N" sort="Kohara, N" uniqKey="Kohara N" first="N." last="Kohara">N. Kohara</name><affiliation><mods:affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kojima, Y" sort="Kojima, Y" uniqKey="Kojima Y" first="Y." last="Kojima">Y. Kojima</name><affiliation><mods:affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yonekura, Y" sort="Yonekura, Y" uniqKey="Yonekura Y" first="Y." last="Yonekura">Y. Yonekura</name><affiliation><mods:affiliation>High Energy Medical Research Center, Fukui Medical School, Fukui, Japan</mods:affiliation></affiliation></author><author><name sortKey="Chen, R S" sort="Chen, R S" uniqKey="Chen R" first="R. S." last="Chen">R. S. Chen</name><affiliation><mods:affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Tsai, C H" sort="Tsai, C H" uniqKey="Tsai C" first="C. H." last="Tsai">C. H. Tsai</name><affiliation><mods:affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Chu, N S" sort="Chu, N S" uniqKey="Chu N" first="N. S." last="Chu">N. S. Chu</name><affiliation><mods:affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</mods:affiliation></affiliation></author><author><name sortKey="Kimura, J" sort="Kimura, J" uniqKey="Kimura J" first="J." last="Kimura">J. Kimura</name><affiliation><mods:affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author><author><name sortKey="Shibasaki" sort="Shibasaki" uniqKey="Shibasaki" last="Shibasaki">Shibasaki</name><affiliation><mods:affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><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. 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>Hoboken</pubPlace><date type="published" when="1998-01">1998-01</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="140">140</biblScope><biblScope unit="page" to="146">146</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">50D8C2B0832A6AB1C96F96850090CDFCF8700710</idno><idno type="DOI">10.1002/mds.870130126</idno><idno type="ArticleID">MDS870130126</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action myoclonus</term><term>Corticobasal degeneration</term><term>MEP</term><term>SPECT</term><term>electrophysiology</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>C. S. Lu</name><affiliations><json:string>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>A. Ikeda</name><affiliations><json:string>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>K. Terada</name><affiliations><json:string>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>T. Mima</name><affiliations><json:string>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>T. Nagamine</name><affiliations><json:string>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>H. Fukuyama</name><affiliations><json:string>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>N. Kohara</name><affiliations><json:string>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Y. Kojima</name><affiliations><json:string>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Y. Yonekura</name><affiliations><json:string>High Energy Medical Research Center, Fukui Medical School, Fukui, Japan</json:string></affiliations></json:item><json:item><name>R. S. Chen</name><affiliations><json:string>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>C. H. Tsai</name><affiliations><json:string>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>N. S. Chu</name><affiliations><json:string>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</json:string></affiliations></json:item><json:item><name>J. Kimura</name><affiliations><json:string>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item><json:item><name>Dr. Shibasaki</name><affiliations><json:string>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Corticobasal degeneration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>electrophysiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Action myoclonus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MEP</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SPECT</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.</abstract><qualityIndicators><score>5.941</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1359</abstractCharCount><pdfWordCount>3757</pdfWordCount><pdfCharCount>23518</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>182</abstractWordCount></qualityIndicators><title>Electrophysiological studies of early stage corticobasal degeneration</title><genre><json:string>Serial article</json:string></genre><host><volume>13</volume><pages><total>7</total><last>146</last><first>140</first></pages><issn><json:string>0885-3185</json:string></issn><issue>1</issue><subject><json:item><value>Brief Report</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1002/mds.870130126</json:string></doi><id>50D8C2B0832A6AB1C96F96850090CDFCF8700710</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/50D8C2B0832A6AB1C96F96850090CDFCF8700710/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/50D8C2B0832A6AB1C96F96850090CDFCF8700710/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/50D8C2B0832A6AB1C96F96850090CDFCF8700710/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Electrophysiological studies of early stage corticobasal degeneration</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>1998</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Electrophysiological studies of early stage corticobasal degeneration</title><author><persName><forename type="first">C. S.</forename><surname>Lu</surname></persName><affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</affiliation></author><author><persName><forename type="first">A.</forename><surname>Ikeda</surname></persName><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation></author><author><persName><forename type="first">K.</forename><surname>Terada</surname></persName><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation></author><author><persName><forename type="first">T.</forename><surname>Mima</surname></persName><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation></author><author><persName><forename type="first">T.</forename><surname>Nagamine</surname></persName><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation></author><author><persName><forename type="first">H.</forename><surname>Fukuyama</surname></persName><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation></author><author><persName><forename type="first">N.</forename><surname>Kohara</surname></persName><affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Y.</forename><surname>Kojima</surname></persName><affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation></author><author><persName><forename type="first">Y.</forename><surname>Yonekura</surname></persName><affiliation>High Energy Medical Research Center, Fukui Medical School, Fukui, Japan</affiliation></author><author><persName><forename type="first">R. S.</forename><surname>Chen</surname></persName><affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</affiliation></author><author><persName><forename type="first">C. H.</forename><surname>Tsai</surname></persName><affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</affiliation></author><author><persName><forename type="first">N. S.</forename><surname>Chu</surname></persName><affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</affiliation></author><author><persName><forename type="first">J.</forename><surname>Kimura</surname></persName><affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation></author><author><persName><surname>Shibasaki</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Department of Brain pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, 606‐01 Japan</p></note><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</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. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-01"></date><biblScope unit="vol">13</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="140">140</biblScope><biblScope unit="page" to="146">146</biblScope></imprint></monogr><idno type="istex">50D8C2B0832A6AB1C96F96850090CDFCF8700710</idno><idno type="DOI">10.1002/mds.870130126</idno><idno type="ArticleID">MDS870130126</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Corticobasal degeneration</term></item><item><term>electrophysiology</term></item><item><term>Action myoclonus</term></item><item><term>MEP</term></item><item><term>SPECT</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-01-12">Received</change><change when="1997-04-28">Registration</change><change when="1998-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/50D8C2B0832A6AB1C96F96850090CDFCF8700710/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>Hoboken</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="tocForm">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/mds.v13:1</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="1998-01">January 1998</coverDate></publicationMeta><publicationMeta level="unit" type="shortCommunication" position="26" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870130126</doi><idGroup><id type="unit" value="MDS870130126"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Brief Report</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 1998 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1996-01-12"></event><event type="manuscriptRevised" date="1997-04-28"></event><event type="manuscriptAccepted" date="1997-04-28"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">140</numbering><numbering type="pageLast">146</numbering></numberingGroup><correspondenceTo>Department of Brain pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, 606‐01 Japan</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870130126.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="19"></count></countGroup><titleGroup><title type="main" xml:lang="en">Electrophysiological studies of early stage corticobasal degeneration</title><title type="short" xml:lang="en">ELECTROPHYSIOLOGICAL STUDIES OF CBD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>C. S.</givenNames><familyName>Lu</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>A.</givenNames><familyName>Ikeda</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>K.</givenNames><familyName>Terada</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>T.</givenNames><familyName>Mima</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>T.</givenNames><familyName>Nagamine</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>H.</givenNames><familyName>Fukuyama</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>N.</givenNames><familyName>Kohara</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Y.</givenNames><familyName>Kojima</familyName></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Y.</givenNames><familyName>Yonekura</familyName></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1"><personName><givenNames>R. S.</givenNames><familyName>Chen</familyName></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af1"><personName><givenNames>C. H.</givenNames><familyName>Tsai</familyName></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af1"><personName><givenNames>N. S.</givenNames><familyName>Chu</familyName></personName></creator><creator xml:id="au13" creatorRole="author" affiliationRef="#af3"><personName><givenNames>J.</givenNames><familyName>Kimura</familyName></personName></creator><creator xml:id="au14" creatorRole="author" affiliationRef="#af2" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>H.</givenNames><familyName>Shibasaki</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="TW" type="organization"><unparsedAffiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="JP" type="organization"><unparsedAffiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="JP" type="organization"><unparsedAffiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="JP" type="organization"><unparsedAffiliation>High Energy Medical Research Center, Fukui Medical School, Fukui, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Corticobasal degeneration</keyword><keyword xml:id="kwd2">electrophysiology</keyword><keyword xml:id="kwd3">Action myoclonus</keyword><keyword xml:id="kwd4">MEP</keyword><keyword xml:id="kwd5">SPECT</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Electrophysiological studies of early stage corticobasal degeneration</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>ELECTROPHYSIOLOGICAL STUDIES OF CBD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Electrophysiological studies of early stage corticobasal degeneration</title></titleInfo><name type="personal"><namePart type="given">C. S.</namePart><namePart type="family">Lu</namePart><affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Ikeda</namePart><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Terada</namePart><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Mima</namePart><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Nagamine</namePart><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Fukuyama</namePart><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Kohara</namePart><affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Kojima</namePart><affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Yonekura</namePart><affiliation>High Energy Medical Research Center, Fukui Medical School, Fukui, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. S.</namePart><namePart type="family">Chen</namePart><affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. H.</namePart><namePart type="family">Tsai</namePart><affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N. S.</namePart><namePart type="family">Chu</namePart><affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Kimura</namePart><affiliation>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Shibasaki</namePart><affiliation>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, Japan</affiliation><description>Correspondence: Department of Brain pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto, 606‐01 Japan</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">shortCommunication</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-01</dateIssued><dateCaptured encoding="w3cdtf">1996-01-12</dateCaptured><dateValid encoding="w3cdtf">1997-04-28</dateValid><copyrightDate encoding="w3cdtf">1998</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">3</extent><extent unit="tables">2</extent><extent unit="references">19</extent></physicalDescription><abstract lang="en">We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.</abstract><subject lang="en"><genre>Keywords</genre><topic>Corticobasal degeneration</topic><topic>electrophysiology</topic><topic>Action myoclonus</topic><topic>MEP</topic><topic>SPECT</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>Brief Report</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>1998</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>140</start><end>146</end><total>7</total></extent></part></relatedItem><identifier type="istex">50D8C2B0832A6AB1C96F96850090CDFCF8700710</identifier><identifier type="DOI">10.1002/mds.870130126</identifier><identifier type="ArticleID">MDS870130126</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Movement Disorder 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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