The pathophysiology of parkinsonism in multiple system atrophy
Identifieur interne : 001C23 ( Istex/Corpus ); précédent : 001C22; suivant : 001C24The pathophysiology of parkinsonism in multiple system atrophy
Auteurs : F. Tison ; G. K. Wenning ; S. E. Daniel ; N. P. QuinnSource :
- European Journal of Neurology [ 1351-5101 ] ; 1995-11.
English descriptors
Abstract
Parkinsonism is the principal motor disorder of multiple system atrophy (MSA). In order to explore the pathophysiology of parkinsonism in MSA, we analysed 182 pathological reports from the literature and 35 from the United Kingdom Parkinson's Disease Society Brain Bank, and have also examined published post‐mortem and in vivo neurochemical data. This review indicates that the brains of MSA patients who had parkinsonism in life show degeneration principally in anatomically related regions of the nigrostriatal dopaminergic pathway and of the striatum as well as in the globus pallidus. This degeneration affects both “direct” and “indirect” striatal outflow pathways. The degree of dopaminergic response in any one subject at any one point in the evolution of the disease probably relates both to the severity and extent of striatal pathology and also to the balance between degeneration in “indirect” and “direct” striatal outflow pathways and in the pallidum, especially its external part Abnormal oligodendroglial cytoplasmic inclusions are also found in large numbers in most of the basal ganglia structures that show cell loss and gliosis. The precise consequences of their additional presence in motor cortex remain unknown, but disturbance of function in supplementary motor area could also contribute to the extrapyramidal syndrome of MSA.
Url:
DOI: 10.1111/j.1468-1331.1995.tb00153.x
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ISTEX:68BB919B221AEE2CC839A7BC8549F1F6557E74D0Le document en format XML
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Daniel</name><affiliation><mods:affiliation>Parkinson's Disease Society Brain Bank, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N. P." last="Quinn">N. P. Quinn</name><affiliation><mods:affiliation>University Department of Clinical Neurology</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:68BB919B221AEE2CC839A7BC8549F1F6557E74D0</idno><date when="1995" year="1995">1995</date><idno type="doi">10.1111/j.1468-1331.1995.tb00153.x</idno><idno type="url">https://api.istex.fr/document/68BB919B221AEE2CC839A7BC8549F1F6557E74D0/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001C23</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001C23</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The pathophysiology of parkinsonism in multiple system atrophy</title><author><name sortKey="Tison, F" sort="Tison, F" uniqKey="Tison F" first="F." last="Tison">F. Tison</name><affiliation><mods:affiliation>University Department of Clinical Neurology</mods:affiliation></affiliation><affiliation><mods:affiliation>Département de Neurologie, Hôpital Pellegrin, Place Amélie Raba‐Léon, 33076 Bordeaux Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G. K." last="Wenning">G. K. Wenning</name><affiliation><mods:affiliation>University Department of Clinical Neurology</mods:affiliation></affiliation></author><author><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S. E." last="Daniel">S. E. Daniel</name><affiliation><mods:affiliation>Parkinson's Disease Society Brain Bank, Institute of Neurology, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N. P." last="Quinn">N. P. Quinn</name><affiliation><mods:affiliation>University Department of Clinical Neurology</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neurology</title><idno type="ISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1995-11">1995-11</date><biblScope unit="volume">2</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="435">435</biblScope><biblScope unit="page" to="444">444</biblScope></imprint><idno type="ISSN">1351-5101</idno></series><idno type="istex">68BB919B221AEE2CC839A7BC8549F1F6557E74D0</idno><idno type="DOI">10.1111/j.1468-1331.1995.tb00153.x</idno><idno type="ArticleID">ENE153</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1351-5101</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Multiple system atrophy</term><term>Parkinsonism</term><term>Pathophysiology</term><term>Response to levodopa</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinsonism is the principal motor disorder of multiple system atrophy (MSA). In order to explore the pathophysiology of parkinsonism in MSA, we analysed 182 pathological reports from the literature and 35 from the United Kingdom Parkinson's Disease Society Brain Bank, and have also examined published post‐mortem and in vivo neurochemical data. This review indicates that the brains of MSA patients who had parkinsonism in life show degeneration principally in anatomically related regions of the nigrostriatal dopaminergic pathway and of the striatum as well as in the globus pallidus. This degeneration affects both “direct” and “indirect” striatal outflow pathways. The degree of dopaminergic response in any one subject at any one point in the evolution of the disease probably relates both to the severity and extent of striatal pathology and also to the balance between degeneration in “indirect” and “direct” striatal outflow pathways and in the pallidum, especially its external part Abnormal oligodendroglial cytoplasmic inclusions are also found in large numbers in most of the basal ganglia structures that show cell loss and gliosis. The precise consequences of their additional presence in motor cortex remain unknown, but disturbance of function in supplementary motor area could also contribute to the extrapyramidal syndrome of MSA.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>F. Tison</name><affiliations><json:string>University Department of Clinical Neurology</json:string><json:string>Département de Neurologie, Hôpital Pellegrin, Place Amélie Raba‐Léon, 33076 Bordeaux Cedex, France</json:string></affiliations></json:item><json:item><name>G.K. Wenning</name><affiliations><json:string>University Department of Clinical Neurology</json:string></affiliations></json:item><json:item><name>S.E. Daniel</name><affiliations><json:string>Parkinson's Disease Society Brain Bank, Institute of Neurology, London, UK</json:string></affiliations></json:item><json:item><name>N.P. Quinn</name><affiliations><json:string>University Department of Clinical Neurology</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinsonism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Multiple system atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Pathophysiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Response to levodopa</value></json:item></subject><articleId><json:string>ENE153</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>reviewArticle</json:string></originalGenre><abstract>Parkinsonism is the principal motor disorder of multiple system atrophy (MSA). In order to explore the pathophysiology of parkinsonism in MSA, we analysed 182 pathological reports from the literature and 35 from the United Kingdom Parkinson's Disease Society Brain Bank, and have also examined published post‐mortem and in vivo neurochemical data. This review indicates that the brains of MSA patients who had parkinsonism in life show degeneration principally in anatomically related regions of the nigrostriatal dopaminergic pathway and of the striatum as well as in the globus pallidus. This degeneration affects both “direct” and “indirect” striatal outflow pathways. The degree of dopaminergic response in any one subject at any one point in the evolution of the disease probably relates both to the severity and extent of striatal pathology and also to the balance between degeneration in “indirect” and “direct” striatal outflow pathways and in the pallidum, especially its external part Abnormal oligodendroglial cytoplasmic inclusions are also found in large numbers in most of the basal ganglia structures that show cell loss and gliosis. The precise consequences of their additional presence in motor cortex remain unknown, but disturbance of function in supplementary motor area could also contribute to the extrapyramidal syndrome of MSA.</abstract><qualityIndicators><score>7.924</score><pdfVersion>1.4</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1351</abstractCharCount><pdfWordCount>6737</pdfWordCount><pdfCharCount>41800</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>202</abstractWordCount></qualityIndicators><title>The pathophysiology of parkinsonism in multiple system atrophy</title><refBibs><json:item><author><json:item><name>GE Alexander</name></json:item><json:item><name>MD Crutcher</name></json:item></author><host><volume>13</volume><pages><last>265</last><first>259</first></pages><author></author><title>Trends in Neuroscience</title></host><title>Functional architecture of basal ganglia circuits: neuronal substrates of parallel processing</title></json:item><json:item><author><json:item><name>DJ Brooks</name></json:item><json:item><name>V Ibanez</name></json:item><json:item><name>GV Sawle</name></json:item><json:item><name>NP Quinn</name></json:item><json:item><name>AJ Lees</name></json:item><json:item><name>CJ Mathias</name></json:item><json:item><name>R Bannister</name></json:item><json:item><name>CD Marsden</name></json:item><json:item><name>RSJ Frackowiak</name></json:item></author><host><volume>28</volume><pages><last>555</last><first>547</first></pages><author></author><title>Annals of Neurology</title></host><title>Differing patterns of striatal 18F‐dopa uptake in Parkinson's disease, multiple system atrophy and progressive supranuclear palsy</title></json:item><json:item><author><json:item><name>DJ Brooks</name></json:item><json:item><name>EP Salmon</name></json:item><json:item><name>CJ Mathias</name></json:item><json:item><name>NP Quinn</name></json:item><json:item><name>KJ Leenders</name></json:item><json:item><name>R Bannister</name></json:item><json:item><name>CD Marsden</name></json:item><json:item><name>RSJ Frackowiack</name></json:item></author><host><volume>113</volume><pages><last>1552</last><first>1539</first></pages><author></author><title>Brain</title></host><title>The relationship between locomotor disability, autonomic dysfunction and the integrity of the striatal dopaminergic system in patients with multiple system atrophy, pure autonomic failure and Parkinson's disease studied by PET</title></json:item><json:item><author><json:item><name>DJ Brooks</name></json:item><json:item><name>V Ibanez</name></json:item><json:item><name>GV Sawle</name></json:item><json:item><name>ED Playford</name></json:item><json:item><name>NP Quinn</name></json:item><json:item><name>CJ Mathias</name></json:item><json:item><name>AJ Lees</name></json:item><json:item><name>CD Marsden</name></json:item><json:item><name>R Bannister</name></json:item><json:item><name>RSJ Frackowiak</name></json:item></author><host><volume>31</volume><pages><last>192</last><first>184</first></pages><author></author><title>Annals of Neurology</title></host><title>Striatal D2 receptor status in patients with Parkinson's disease, striatonigral degeneration and progressive supranuclear palsy, measured with 11C‐raclopride and positron emission tomography</title></json:item><json:item><author><json:item><name>O Bugniani</name></json:item><json:item><name>F Perdelli</name></json:item><json:item><name>S Salvarani</name></json:item><json:item><name>A Leonardi</name></json:item><json:item><name>GL Mancardi</name></json:item></author><host><volume>19</volume><pages><last>344</last><first>339</first></pages><author></author><title>European Neurology</title></host><title>Loss of striatal neurons in Parkinson's disease: a cytometric study</title></json:item><json:item><author><json:item><name>DJ Burn</name></json:item><json:item><name>CJ Mathias</name></json:item><json:item><name>N Quinn</name></json:item><json:item><name>CD Marsden</name></json:item><json:item><name>DJ Brooks</name></json:item></author><host><volume>43</volume><pages><first>270</first></pages><issue>suppl. 2</issue><author></author><title>Neurology</title></host><title>Striatal opiate receptor binding in Parkinson's disease and multiple system atrophy: 11C‐diprenorphine study</title></json:item><json:item><author><json:item><name>DJ Bum</name></json:item><json:item><name>GV Sawle</name></json:item><json:item><name>DJ Brooks</name></json:item></author><host><volume>57</volume><pages><last>284</last><first>278</first></pages><author></author><title>Journal of Neurology, Neurosurgery and Psychiatry</title></host><title>Differential diagnosis of Parkinson's disease, multiple system atrophy, and Steele–Richardson–Olszewski syndrome; discriminant analysis of striatal 18F‐dopa PET data</title></json:item><json:item><host><author></author><title>Carpenter MB (1983) Human Neuroanatomy, 8th edn. 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neurosurgery</json:string></scienceMetrix></categories><publicationDate>1995</publicationDate><copyrightDate>1995</copyrightDate><doi><json:string>10.1111/j.1468-1331.1995.tb00153.x</json:string></doi><id>68BB919B221AEE2CC839A7BC8549F1F6557E74D0</id><score>0.14601302</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/68BB919B221AEE2CC839A7BC8549F1F6557E74D0/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/68BB919B221AEE2CC839A7BC8549F1F6557E74D0/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/68BB919B221AEE2CC839A7BC8549F1F6557E74D0/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">The pathophysiology of parkinsonism in multiple system atrophy</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>1995 Lippincott Williams & Wilkins</p></availability><date>1995</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">The pathophysiology of parkinsonism in multiple system atrophy</title><author xml:id="author-1"><persName><forename type="first">F.</forename><surname>Tison</surname></persName><affiliation>University Department of Clinical Neurology</affiliation><affiliation>Département de Neurologie, Hôpital Pellegrin, Place Amélie Raba‐Léon, 33076 Bordeaux Cedex, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">G.K.</forename><surname>Wenning</surname></persName><affiliation>University Department of Clinical Neurology</affiliation></author><author xml:id="author-3"><persName><forename type="first">S.E.</forename><surname>Daniel</surname></persName><affiliation>Parkinson's Disease Society Brain Bank, Institute of Neurology, London, UK</affiliation></author><author xml:id="author-4"><persName><forename type="first">N.P.</forename><surname>Quinn</surname></persName><affiliation>University Department of Clinical Neurology</affiliation></author></analytic><monogr><title level="j">European Journal of Neurology</title><idno type="pISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><idno type="DOI">10.1111/(ISSN)1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1995-11"></date><biblScope unit="volume">2</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="435">435</biblScope><biblScope unit="page" to="444">444</biblScope></imprint></monogr><idno type="istex">68BB919B221AEE2CC839A7BC8549F1F6557E74D0</idno><idno type="DOI">10.1111/j.1468-1331.1995.tb00153.x</idno><idno type="ArticleID">ENE153</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Parkinsonism is the principal motor disorder of multiple system atrophy (MSA). In order to explore the pathophysiology of parkinsonism in MSA, we analysed 182 pathological reports from the literature and 35 from the United Kingdom Parkinson's Disease Society Brain Bank, and have also examined published post‐mortem and in vivo neurochemical data. This review indicates that the brains of MSA patients who had parkinsonism in life show degeneration principally in anatomically related regions of the nigrostriatal dopaminergic pathway and of the striatum as well as in the globus pallidus. This degeneration affects both “direct” and “indirect” striatal outflow pathways. The degree of dopaminergic response in any one subject at any one point in the evolution of the disease probably relates both to the severity and extent of striatal pathology and also to the balance between degeneration in “indirect” and “direct” striatal outflow pathways and in the pallidum, especially its external part Abnormal oligodendroglial cytoplasmic inclusions are also found in large numbers in most of the basal ganglia structures that show cell loss and gliosis. The precise consequences of their additional presence in motor cortex remain unknown, but disturbance of function in supplementary motor area could also contribute to the extrapyramidal syndrome of MSA.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>Parkinsonism</term></item><item><term>Multiple system atrophy</term></item><item><term>Pathophysiology</term></item><item><term>Response to levodopa</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/68BB919B221AEE2CC839A7BC8549F1F6557E74D0/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="11105"><doi origin="wiley">10.1111/ene.1995.2.issue-5</doi><numberingGroup><numbering type="journalVolume" number="2">2</numbering><numbering type="journalIssue" number="5">5</numbering></numberingGroup><coverDate startDate="1995-11">November 1995</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="5" status="forIssue"><doi origin="wiley">10.1111/j.1468-1331.1995.tb00153.x</doi><idGroup><id type="unit" value="ENE153"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="tocHeading1">Review</title></titleGroup><copyright>1995 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="435">435</numbering><numbering type="pageLast" number="444">444</numbering></numberingGroup><correspondenceTo>Département de Neurologie, Hôpital Pellegrin, Place Amélie Raba‐Léon, 33076 Bordeaux Cedex, France</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE153.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>(Received 27 June 1994; accepted as revised 12 April 1995)</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="62"></count><count type="linksCrossRef" number="5"></count></countGroup><titleGroup><title type="main">The pathophysiology of parkinsonism in multiple system atrophy</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>F.</givenNames><familyName>Tison</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>G.K.</givenNames><familyName>Wenning</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>S.E.</givenNames><familyName>Daniel</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>N.P.</givenNames><familyName>Quinn</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>University Department of Clinical Neurology</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="GB"><unparsedAffiliation>Parkinson's Disease Society Brain Bank, Institute of Neurology, London, UK</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinsonism</keyword><keyword xml:id="k2">Multiple system atrophy</keyword><keyword xml:id="k3">Pathophysiology</keyword><keyword xml:id="k4">Response to levodopa</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Parkinsonism is the principal motor disorder of multiple system atrophy (MSA). In order to explore the pathophysiology of parkinsonism in MSA, we analysed 182 pathological reports from the literature and 35 from the United Kingdom Parkinson's Disease Society Brain Bank, and have also examined published post‐mortem and <i>in vivo</i> neurochemical data. This review indicates that the brains of MSA patients who had parkinsonism in life show degeneration principally in anatomically related regions of the nigrostriatal dopaminergic pathway and of the striatum as well as in the globus pallidus. This degeneration affects both “direct” and “indirect” striatal outflow pathways. The degree of dopaminergic response in any one subject at any one point in the evolution of the disease probably relates both to the severity and extent of striatal pathology and also to the balance between degeneration in “indirect” and “direct” striatal outflow pathways and in the pallidum, especially its external part Abnormal oligodendroglial cytoplasmic inclusions are also found in large numbers in most of the basal ganglia structures that show cell loss and gliosis. The precise consequences of their additional presence in motor cortex remain unknown, but disturbance of function in supplementary motor area could also contribute to the extrapyramidal syndrome of MSA.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The pathophysiology of parkinsonism in multiple system atrophy</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The pathophysiology of parkinsonism in multiple system atrophy</title></titleInfo><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Tison</namePart><affiliation>University Department of Clinical Neurology</affiliation><affiliation>Département de Neurologie, Hôpital Pellegrin, Place Amélie Raba‐Léon, 33076 Bordeaux Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.K.</namePart><namePart type="family">Wenning</namePart><affiliation>University Department of Clinical Neurology</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.E.</namePart><namePart type="family">Daniel</namePart><affiliation>Parkinson's Disease Society Brain Bank, Institute of Neurology, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.P.</namePart><namePart type="family">Quinn</namePart><affiliation>University Department of Clinical Neurology</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1995-11</dateIssued><edition>(Received 27 June 1994; accepted as revised 12 April 1995)</edition><copyrightDate encoding="w3cdtf">1995</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">62</extent></physicalDescription><abstract lang="en">Parkinsonism is the principal motor disorder of multiple system atrophy (MSA). In order to explore the pathophysiology of parkinsonism in MSA, we analysed 182 pathological reports from the literature and 35 from the United Kingdom Parkinson's Disease Society Brain Bank, and have also examined published post‐mortem and in vivo neurochemical data. This review indicates that the brains of MSA patients who had parkinsonism in life show degeneration principally in anatomically related regions of the nigrostriatal dopaminergic pathway and of the striatum as well as in the globus pallidus. This degeneration affects both “direct” and “indirect” striatal outflow pathways. The degree of dopaminergic response in any one subject at any one point in the evolution of the disease probably relates both to the severity and extent of striatal pathology and also to the balance between degeneration in “indirect” and “direct” striatal outflow pathways and in the pallidum, especially its external part Abnormal oligodendroglial cytoplasmic inclusions are also found in large numbers in most of the basal ganglia structures that show cell loss and gliosis. The precise consequences of their additional presence in motor cortex remain unknown, but disturbance of function in supplementary motor area could also contribute to the extrapyramidal syndrome of MSA.</abstract><subject lang="en"><genre>keywords</genre><topic>Parkinsonism</topic><topic>Multiple system atrophy</topic><topic>Pathophysiology</topic><topic>Response to levodopa</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>1995</date><detail type="volume"><caption>vol.</caption><number>2</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>435</start><end>444</end><total>10</total></extent></part></relatedItem><identifier type="istex">68BB919B221AEE2CC839A7BC8549F1F6557E74D0</identifier><identifier type="DOI">10.1111/j.1468-1331.1995.tb00153.x</identifier><identifier type="ArticleID">ENE153</identifier><accessCondition type="use and reproduction" contentType="copyright">1995 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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