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
Links to Exploration step
ISTEX:68BB919B221AEE2CC839A7BC8549F1F6557E74D0Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title 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>
</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. Baltimore, MD: Williams and Wilkins.</title>
</host>
</json:item>
<json:item><author><json:item><name>A Churchyard</name>
</json:item>
<json:item><name>GA Donnan</name>
</json:item>
<json:item><name>A Hughes</name>
</json:item>
<json:item><name>DW Howells</name>
</json:item>
<json:item><name>D Wood‐house</name>
</json:item>
<json:item><name>JYF Wong</name>
</json:item>
<json:item><name>RM Katnias</name>
</json:item>
<json:item><name>FAO Mendelsohn</name>
</json:item>
<json:item><name>G Paxinos</name>
</json:item>
</author>
<host><volume>34</volume>
<pages><last>226</last>
<first>219</first>
</pages>
<author></author>
<title>Annals of Neurology</title>
</host>
<title>Dopa resistance in multiple system atrophy: loss of post‐synaptic D2 receptors</title>
</json:item>
<json:item><author><json:item><name>R Cortes</name>
</json:item>
<json:item><name>M Camps</name>
</json:item>
<json:item><name>B Gueye</name>
</json:item>
<json:item><name>A Probst</name>
</json:item>
<json:item><name>JM Palacios</name>
</json:item>
</author>
<host><volume>483</volume>
<pages><last>38</last>
<first>30</first>
</pages>
<author></author>
<title>Brain Research</title>
</host>
<title>Dopamine receptors in the human brain: autoradiographic distribution of D1 and D2 sites in parkinsonian syndromes of different etiology</title>
</json:item>
<json:item><author><json:item><name>SE Daniel</name>
</json:item>
</author>
<host><pages><last>585</last>
<first>564</first>
</pages>
<author></author>
<title>A Textbook of Clinical Disorders of Autonomic Nervous System</title>
</host>
<title>The neuropathology and neurochemistry of multiple system atrophy</title>
</json:item>
<json:item><author><json:item><name>CA Davie</name>
</json:item>
<json:item><name>GK Wenning</name>
</json:item>
<json:item><name>GJ Barker</name>
</json:item>
<json:item><name>A Brennan</name>
</json:item>
<json:item><name>N Quinn</name>
</json:item>
<json:item><name>DH Miller</name>
</json:item>
</author>
<host><volume>37</volume>
<pages><last>210</last>
<first>204</first>
</pages>
<author></author>
<title>Annals of Neurology</title>
</host>
<title>MRS to differentiate multiple system atrophy from idiopathic Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>AG De Voider</name>
</json:item>
<json:item><name>J Francart</name>
</json:item>
<json:item><name>C Laterne</name>
</json:item>
<json:item><name>G Dooms</name>
</json:item>
<json:item><name>A Bel</name>
</json:item>
<json:item><name>C Michel</name>
</json:item>
<json:item><name>AM Goffinet</name>
</json:item>
</author>
<host><volume>26</volume>
<pages><last>247</last>
<first>239</first>
</pages>
<author></author>
<title>Annals of Neurology</title>
</host>
<title>Decreased glucose utilization in the striatum and frontal lobe in probable striatonigral degeneration</title>
</json:item>
<json:item><author><json:item><name>JPR Dick</name>
</json:item>
<json:item><name>R Benecke</name>
</json:item>
<json:item><name>JC Rothwell</name>
</json:item>
<json:item><name>BL Day</name>
</json:item>
<json:item><name>CD Marsden</name>
</json:item>
</author>
<host><volume>1</volume>
<pages><last>266</last>
<first>255</first>
</pages>
<author></author>
<title>Movement Disorders</title>
</host>
<title>Simple and complex movements in a patient with infarction of the right supplementary motor area</title>
</json:item>
<json:item><author><json:item><name>BP Drayer</name>
</json:item>
<json:item><name>W Olanow</name>
</json:item>
<json:item><name>A Burger</name>
</json:item>
<json:item><name>GA Johnson</name>
</json:item>
<json:item><name>R Herfkens</name>
</json:item>
<json:item><name>S Riederer</name>
</json:item>
</author>
<host><volume>159</volume>
<pages><last>498</last>
<first>493</first>
</pages>
<author></author>
<title>Radiology</title>
</host>
<title>Parkinson plus syndrome: diagnosis using high field MR imaging of brain iron</title>
</json:item>
<json:item><author><json:item><name>MJ Eadie</name>
</json:item>
</author>
<host><volume>21</volume>
<pages><last>431</last>
<first>415</first>
</pages>
<author></author>
<title>Handbook of Clinical Neurology</title>
</host>
<title>Olivo‐ponto‐cerebellar atrophy (Dejerine–Thomas type)</title>
</json:item>
<json:item><author><json:item><name>D Eidelberg</name>
</json:item>
<json:item><name>S Takikawa</name>
</json:item>
<json:item><name>JR Moeller</name>
</json:item>
<json:item><name>V Dhawan</name>
</json:item>
<json:item><name>K Redington</name>
</json:item>
<json:item><name>T Chaly</name>
</json:item>
<json:item><name>W Robeson</name>
</json:item>
<json:item><name>JR Dahl</name>
</json:item>
<json:item><name>D Margouleff</name>
</json:item>
<json:item><name>DO Fazzini</name>
</json:item>
<json:item><name>S Przedborski</name>
</json:item>
<json:item><name>S Fahn</name>
</json:item>
</author>
<host><volume>33</volume>
<pages><last>527</last>
<first>518</first>
</pages>
<author></author>
<title>Annals of Neurology</title>
</host>
<title>Striatal hypometabolism distinguishes striatonigral degeneration from Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>E Fazzini</name>
</json:item>
<json:item><name>M Dogali</name>
</json:item>
<json:item><name>J Eidelberg</name>
</json:item>
<json:item><name>J Gianutsos</name>
</json:item>
<json:item><name>B Newman</name>
</json:item>
<json:item><name>A Beric</name>
</json:item>
<json:item><name>G Stereo</name>
</json:item>
<json:item><name>E Koldony</name>
</json:item>
</author>
<host><volume>43</volume>
<pages><first>222</first>
</pages>
<issue>suppl. 1</issue>
<author></author>
<title>Neurology</title>
</host>
<title>Long‐term follow‐up on patients with Parkinson's disease receiving unilateral ventro‐posterior medial pallidotomy</title>
</json:item>
<json:item><author><json:item><name>JM Fearnley</name>
</json:item>
<json:item><name>AJ Lees</name>
</json:item>
</author>
<host><volume>113</volume>
<pages><last>1842</last>
<first>1823</first>
</pages>
<author></author>
<title>Brain</title>
</host>
<title>Striatonigral degeneration, a clinicopathological study</title>
</json:item>
<json:item><author><json:item><name>RJ Ferrante</name>
</json:item>
<json:item><name>NW Kowall</name>
</json:item>
<json:item><name>MF Beal</name>
</json:item>
<json:item><name>JB Martin</name>
</json:item>
<json:item><name>ED Bird</name>
</json:item>
<json:item><name>EP Richardson</name>
</json:item>
</author>
<host><volume>46</volume>
<pages><last>27</last>
<first>12</first>
</pages>
<author></author>
<title>Journal of Neuropathology and Experimental Neurology</title>
</host>
<title>Morphologic and histochemical characteristics of a spared subset of striatal neurons in Huntington's disease</title>
</json:item>
<json:item><author><json:item><name>I Fujita</name>
</json:item>
<json:item><name>M Doi</name>
</json:item>
<json:item><name>T Ogata</name>
</json:item>
<json:item><name>I Kanazawa</name>
</json:item>
<json:item><name>H Mizusawa</name>
</json:item>
</author>
<host><volume>116</volume>
<pages><last>46</last>
<first>41</first>
</pages>
<author></author>
<title>Journal of Neurological Science</title>
</host>
<title>Cerebral cortical pathology of sporadic olivopontocerebellar atrophy</title>
</json:item>
<json:item><author><json:item><name>MJ Fulham</name>
</json:item>
<json:item><name>RM Dubinsky</name>
</json:item>
<json:item><name>RJ Polinsky</name>
</json:item>
<json:item><name>RA Brooks</name>
</json:item>
<json:item><name>RJ Brown</name>
</json:item>
<json:item><name>MT Carras</name>
</json:item>
<json:item><name>S Boser</name>
</json:item>
<json:item><name>M Hallett</name>
</json:item>
<json:item><name>G Di Chiro</name>
</json:item>
</author>
<host><volume>1</volume>
<pages><last>36</last>
<first>27</first>
</pages>
<author></author>
<title>Clinical Autonomic Research</title>
</host>
<title>Computed tomography, magnetic resonance imaging and positron emission tomography with (18F)‐fluorodeoxyglucose in multiple system atrophy and pure autonomic failure</title>
</json:item>
<json:item><author><json:item><name>S Goto</name>
</json:item>
<json:item><name>A Hirano</name>
</json:item>
<json:item><name>S Matsumoto</name>
</json:item>
</author>
<host><volume>26</volume>
<pages><last>770</last>
<first>766</first>
</pages>
<author></author>
<title>Annals of Neurology</title>
</host>
<title>Subdivisional involvement of nigrostriatal loop in idiopathic Parkinson's disease and nigrostriatal degeneration</title>
</json:item>
<json:item><author><json:item><name>S Goto</name>
</json:item>
<json:item><name>A Hirano</name>
</json:item>
<json:item><name>PR Rojos‐Corona</name>
</json:item>
</author>
<host><volume>78</volume>
<pages><last>550</last>
<first>543</first>
</pages>
<author></author>
<title>Acta Neuropathologica</title>
</host>
<title>Immunohistochemical visualization of afferent nerve terminal in human globus pallidus and its alteration in neostriatal neurodegenerative disorders</title>
</json:item>
<json:item><author><json:item><name>S Goto</name>
</json:item>
<json:item><name>A Hirano</name>
</json:item>
<json:item><name>S Matsumoto</name>
</json:item>
</author>
<host><volume>40</volume>
<pages><last>1056</last>
<first>1051</first>
</pages>
<author></author>
<title>Neurology</title>
</host>
<title>Met‐enkephalin immunoreactivity in the basal ganglia in Parkinson's disease and striatonigral degeneration</title>
</json:item>
<json:item><author><json:item><name>AM Graybiel</name>
</json:item>
</author>
<host><volume>13</volume>
<pages><last>254</last>
<first>244</first>
</pages>
<author></author>
<title>Trends Neuroscience</title>
</host>
<title>Neurotransmitters and neuromodulators in the basal ganglia</title>
</json:item>
<json:item><author><json:item><name>J Guridi</name>
</json:item>
<json:item><name>MR Luquin</name>
</json:item>
<json:item><name>MT Herrero</name>
</json:item>
<json:item><name>JA Obeso</name>
</json:item>
</author>
<host><volume>8</volume>
<pages><last>429</last>
<first>421</first>
</pages>
<author></author>
<title>Movement Disorders</title>
</host>
<title>The subthalamic nucleus: a possible target for stereotaxic surgery in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>M Hallett</name>
</json:item>
</author>
<host><volume>20</volume>
<pages><last>183</last>
<first>177</first>
</pages>
<author></author>
<title>Canadian Journal of Neuroscience</title>
</host>
<title>Physiology of basal ganglia disorders: an overview</title>
</json:item>
<json:item><author><json:item><name>AJ Hughes</name>
</json:item>
<json:item><name>C Colosimo</name>
</json:item>
<json:item><name>B Kleedorfer</name>
</json:item>
<json:item><name>SE Daniel</name>
</json:item>
<json:item><name>AJ Lees</name>
</json:item>
</author>
<host><volume>55</volume>
<pages><last>1013</last>
<first>1009</first>
</pages>
<author></author>
<title>Journal of Neurology, Neurosurgery and Psychiatry</title>
</host>
<title>The dopaminergic response in multiple system atrophy</title>
</json:item>
<json:item><author><json:item><name>SJ Kish</name>
</json:item>
<json:item><name>K Shannak</name>
</json:item>
<json:item><name>O Hornykiewicz</name>
</json:item>
</author>
<host><volume>318</volume>
<pages><last>880</last>
<first>876</first>
</pages>
<author></author>
<title>New England Journal of Medicine</title>
</host>
<title>Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson's disease: pathologic and clinical implications</title>
</json:item>
<json:item><author><json:item><name>A Kume</name>
</json:item>
<json:item><name>A Takahashi</name>
</json:item>
<json:item><name>Y Hashizume</name>
</json:item>
</author>
<host><volume>117</volume>
<pages><last>40</last>
<first>33</first>
</pages>
<author></author>
<title>Journal of Neurological Science</title>
</host>
<title>Neuronal cell loss of the striatonigral system in multiple system atrophy</title>
</json:item>
<json:item><author><json:item><name>LW Laitinen</name>
</json:item>
<json:item><name>AT Bergenheim</name>
</json:item>
<json:item><name>MI Hariz</name>
</json:item>
</author>
<host><volume>76</volume>
<pages><last>61</last>
<first>53</first>
</pages>
<author></author>
<title>Journal of Neurosurgery</title>
</host>
<title>Leksell's posteroventral pallidotomy in the treatment of Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>AE Lang</name>
</json:item>
<json:item><name>T Curran</name>
</json:item>
<json:item><name>J Provias</name>
</json:item>
<json:item><name>C Bergeron</name>
</json:item>
</author>
<host><volume>21</volume>
<pages><last>318</last>
<first>311</first>
</pages>
<author></author>
<title>Canadian Journal of Neurological Science</title>
</host>
<title>Striatonigral degeneration: iron deposition in putamen correlates with the slit‐like void signal in magnetic resonance imaging</title>
</json:item>
<json:item><author><json:item><name>PL Lantos</name>
</json:item>
<json:item><name>MI Papp</name>
</json:item>
</author>
<host><volume>57</volume>
<pages><last>133</last>
<first>129</first>
</pages>
<author></author>
<title>Journal of Neurology. Neurosurgery and Psychiatry</title>
</host>
<title>Cellular pathology of multiple system atrophy: a review</title>
</json:item>
<json:item><author><json:item><name>D Laplane</name>
</json:item>
<json:item><name>J Talairach</name>
</json:item>
<json:item><name>V Meininger</name>
</json:item>
<json:item><name>J Bancaud</name>
</json:item>
<json:item><name>JM Orgogozo</name>
</json:item>
</author>
<host><volume>34</volume>
<pages><last>314</last>
<first>301</first>
</pages>
<author></author>
<title>Journal of Neurological Science</title>
</host>
<title>Clinical consequences of corticectomies involving the supplementary motor area in man</title>
</json:item>
<json:item><author><json:item><name>P Limousin</name>
</json:item>
<json:item><name>P Pollack</name>
</json:item>
<json:item><name>A Benazzouz</name>
</json:item>
<json:item><name>D Hoffmann</name>
</json:item>
<json:item><name>JF LeBas</name>
</json:item>
<json:item><name>E Broussolle</name>
</json:item>
<json:item><name>JE Perret</name>
</json:item>
<json:item><name>AL Benabid</name>
</json:item>
</author>
<host><volume>345</volume>
<pages><last>95</last>
<first>91</first>
</pages>
<author></author>
<title>Lancet</title>
</host>
<title>Effect on parkinsonian signs and symptoms of bilateral subthalamic nucleus stimulation</title>
</json:item>
<json:item><author><json:item><name>CD Marsden</name>
</json:item>
<json:item><name>JA Obeso</name>
</json:item>
</author>
<host><volume>117</volume>
<pages><last>897</last>
<first>877</first>
</pages>
<author></author>
<title>Brain</title>
</host>
<title>The functions of the basal ganglia and the paradox of stereotaxic surgery in Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>JM Miyasaki</name>
</json:item>
<json:item><name>A Lozano</name>
</json:item>
<json:item><name>J Duff</name>
</json:item>
<json:item><name>J Dostrovsky</name>
</json:item>
<json:item><name>J St. Cyr</name>
</json:item>
<json:item><name>AE Lang</name>
</json:item>
</author>
<host><volume>44</volume>
<pages><first>322</first>
</pages>
<issue>suppl. 1</issue>
<author></author>
<title>Neurology</title>
</host>
<title>The role of posteroventral pallidotomy in advanced Parkinson's disease and striatonigral degeneration</title>
</json:item>
<json:item><author><json:item><name>A Nieoullon</name>
</json:item>
<json:item><name>L Kerkerian‐Le Goff</name>
</json:item>
</author>
<host><volume>7</volume>
<pages><last>325</last>
<first>311</first>
</pages>
<author></author>
<title>Movement Disorders</title>
</host>
<title>Cellular interactions in the striatum involving neuronal systems using “classical” neurotransmitters: possible functional implications</title>
</json:item>
<json:item><author><json:item><name>C O'Brien</name>
</json:item>
<json:item><name>JH Sung</name>
</json:item>
<json:item><name>RE McGeache</name>
</json:item>
<json:item><name>MC Lee</name>
</json:item>
</author>
<host><volume>40</volume>
<pages><last>711</last>
<first>710</first>
</pages>
<author></author>
<title>Neurology</title>
</host>
<title>Striatonigral degeneration: clinical, MRI, and pathologic correlation</title>
</json:item>
<json:item><author><json:item><name>CW Olanow</name>
</json:item>
</author>
<host><volume>10</volume>
<pages><last>420</last>
<first>405</first>
</pages>
<author></author>
<title>Neurology Clinics</title>
</host>
<title>Magnetic resonance imaging in parkinsonism</title>
</json:item>
<json:item><author><json:item><name>M Otsuka</name>
</json:item>
<json:item><name>Y Ichiya</name>
</json:item>
<json:item><name>S Husokawa</name>
</json:item>
<json:item><name>Y Kuwabara</name>
</json:item>
<json:item><name>T Tahara</name>
</json:item>
<json:item><name>T Fukumura</name>
</json:item>
<json:item><name>M Kato</name>
</json:item>
<json:item><name>M Matsuda</name>
</json:item>
<json:item><name>I Goto</name>
</json:item>
</author>
<host><volume>54</volume>
<pages><last>904</last>
<first>898</first>
</pages>
<author></author>
<title>Journal of Neurology, Neurosurgery and Psychiatry</title>
</host>
<title>Striatal blood flow, glucose metabolism and 18F‐Dopa uptake: differences in Parkinson's disease and atypical parkinsonism</title>
</json:item>
<json:item><author><json:item><name>MI Papp</name>
</json:item>
<json:item><name>PL Lantos</name>
</json:item>
</author>
<host><volume>117</volume>
<pages><last>243</last>
<first>235</first>
</pages>
<author></author>
<title>Brain</title>
</host>
<title>The distribution of oligodendroglial inclusions in multiple system atrophy and its relevance to clinical symptomatology</title>
</json:item>
<json:item><author><json:item><name>EA Parati</name>
</json:item>
<json:item><name>GC Tetoni</name>
</json:item>
<json:item><name>P Geminiani</name>
</json:item>
<json:item><name>P Saliveri</name>
</json:item>
<json:item><name>P Giovannini</name>
</json:item>
<json:item><name>D Testa</name>
</json:item>
<json:item><name>S Genitini</name>
</json:item>
<json:item><name>F Caraceni Tand Girotti</name>
</json:item>
</author>
<host><volume>16</volume>
<pages><last>144</last>
<first>139</first>
</pages>
<author></author>
<title>Clinica Neuropharmacology</title>
</host>
<title>Response to L‐Dopa in multiple system atrophy</title>
</json:item>
<json:item><author><json:item><name>J Pascual</name>
</json:item>
<json:item><name>A Pazos</name>
</json:item>
<json:item><name>E De Olmo</name>
</json:item>
<json:item><name>J Figols</name>
</json:item>
<json:item><name>C Leno</name>
</json:item>
<json:item><name>J Berciano</name>
</json:item>
</author>
<host><volume>30</volume>
<pages><last>428</last>
<first>425</first>
</pages>
<author></author>
<title>Annals of Neurology</title>
</host>
<title>Presynaptic parkinsonism in olivopontocerebellar atrophy: clinical, pathological, and neurochemical evidence</title>
</json:item>
<json:item><author><json:item><name>ED Playford</name>
</json:item>
<json:item><name>IH Jenkins</name>
</json:item>
<json:item><name>RE Passingham</name>
</json:item>
<json:item><name>J Nutt</name>
</json:item>
<json:item><name>RSJ Frackowiak</name>
</json:item>
<json:item><name>DJ Brooks</name>
</json:item>
</author>
<host><volume>32</volume>
<pages><last>161</last>
<first>151</first>
</pages>
<author></author>
<title>Annals of Neurology</title>
</host>
<title>Impaired mesial frontal and putamen activation in Parkinson's disease: a positron emission tomography study</title>
</json:item>
<json:item><author><json:item><name>M Quik</name>
</json:item>
<json:item><name>E Spokes</name>
</json:item>
<json:item><name>A MacKay</name>
</json:item>
<json:item><name>R Bannister</name>
</json:item>
</author>
<host><volume>43</volume>
<pages><last>437</last>
<first>429</first>
</pages>
<author></author>
<title>Journal of Neurological Science</title>
</host>
<title>Alterations in 3H‐spiperone binding in human caudate nucleus, substantia nigra and frontal cortex in Shy Drager syndrome and Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>N Quinn</name>
</json:item>
</author>
<host><volume>52</volume>
<pages><last>79</last>
<first>78</first>
</pages>
<issue>special suppl.</issue>
<author></author>
<title>Journal of Neurology, Neurosurgery and Psychiatry</title>
</host>
<title>Multiple system atrophy: the nature of the beast</title>
</json:item>
<json:item><author><json:item><name>N Quinn</name>
</json:item>
</author>
<host><volume>3</volume>
<pages><last>275</last>
<first>256</first>
</pages>
<author></author>
<title>Movement Disorders</title>
</host>
<title>Multiple system atrophy.</title>
</json:item>
<json:item><author><json:item><name>N. Quinn</name>
</json:item>
<json:item><name>CD Marsden</name>
</json:item>
</author>
<host><volume>56</volume>
<pages><last>1242</last>
<first>1239</first>
</pages>
<author></author>
<title>Journal of Neurology, Neurosurgery and Psychiatry</title>
</host>
<title>The motor disorder of multiple system atrophy</title>
</json:item>
<json:item><author><json:item><name>AH Rajput</name>
</json:item>
<json:item><name>B Rozdilsky</name>
</json:item>
<json:item><name>A Rajput</name>
</json:item>
<json:item><name>L Ang</name>
</json:item>
</author>
<host><volume>13</volume>
<pages><last>558</last>
<first>553</first>
</pages>
<author></author>
<title>Clinica Neuropharmacologica</title>
</host>
<title>Levodopa efficacy and pathological basis of Parkinson syndrome</title>
</json:item>
<json:item><author><json:item><name>GV Sawle</name>
</json:item>
<json:item><name>ED Playford</name>
</json:item>
<json:item><name>DJ Brooks</name>
</json:item>
<json:item><name>NP Quinn</name>
</json:item>
<json:item><name>RSJ Frackowiak</name>
</json:item>
</author>
<host><volume>116</volume>
<pages><last>867</last>
<first>853</first>
</pages>
<author></author>
<title>Brain</title>
</host>
<title>Asymetrical pre‐synaptic and post‐synaptic changes in the striatal dopamine projection in dopa‐naive parkinsonism. Diagnostic implications of the D2 receptor status</title>
</json:item>
<json:item><author><json:item><name>L Schelosky</name>
</json:item>
<json:item><name>I Hierholzer</name>
</json:item>
<json:item><name>J Wissel</name>
</json:item>
<json:item><name>M Cordes</name>
</json:item>
<json:item><name>W Poewe</name>
</json:item>
</author>
<host><volume>8</volume>
<pages><last>458</last>
<first>453</first>
</pages>
<author></author>
<title>Movement Disorders</title>
</host>
<title>Correlation of clinical response in apomorphine test with D2 receptor status as demonstrated by 123I‐IBZM‐SPECT</title>
</json:item>
<json:item><author><json:item><name>J Schwartz</name>
</json:item>
<json:item><name>K Tatsch</name>
</json:item>
<json:item><name>G Arnold</name>
</json:item>
<json:item><name>M Ott</name>
</json:item>
<json:item><name>C Trenkwalder</name>
</json:item>
<json:item><name>CM Kirsch</name>
</json:item>
<json:item><name>WH Oertel</name>
</json:item>
</author>
<host><volume>43</volume>
<pages><last>20</last>
<first>17</first>
</pages>
<issue>suppl. 6</issue>
<author></author>
<title>Neurology</title>
</host>
<title>123Iodobenzamide‐SPECT in 83 patients with de novo parkinsonism</title>
</json:item>
<json:item><author><json:item><name>H Shinotoh</name>
</json:item>
<json:item><name>A Aotsuka</name>
</json:item>
<json:item><name>H Yonezawa</name>
</json:item>
</author>
<host><volume>2</volume>
<pages><last>110</last>
<first>107</first>
</pages>
<author></author>
<title>Basic, Clinical and Therapeutic Advances in Alzheimer's and Parkinson's Disease</title>
</host>
<title>Striatal dopamine D2 receptors in Parkinson's disease and striatonigral degeneration determined by “PET”</title>
</json:item>
<json:item><author><json:item><name>H Shinotoh</name>
</json:item>
<json:item><name>O Inoue</name>
</json:item>
<json:item><name>K Hirayama</name>
</json:item>
<json:item><name>A Aotsuka</name>
</json:item>
<json:item><name>A Asahina</name>
</json:item>
<json:item><name>T Suhara</name>
</json:item>
<json:item><name>T Yamazaki</name>
</json:item>
<json:item><name>Y Tateno</name>
</json:item>
</author>
<host><volume>56</volume>
<pages><last>472</last>
<first>467</first>
</pages>
<author></author>
<title>Journal of Neurology, Neurosurgery and Psychiatry</title>
</host>
<title>Dopamine D1 receptors in Parkinson's disease and striatonigral degeneration: a positron emission tomography study</title>
</json:item>
<json:item><author><json:item><name>PG Strange</name>
</json:item>
</author>
<host><volume>8</volume>
<pages><last>270</last>
<first>263</first>
</pages>
<author></author>
<title>Movement Disorders</title>
</host>
<title>Dopamine receptors in the basal ganglia: relevance to Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>E Van Royen</name>
</json:item>
<json:item><name>NFLG Verhoeff</name>
</json:item>
<json:item><name>JD Spielman</name>
</json:item>
<json:item><name>EC Wolters</name>
</json:item>
<json:item><name>MA Kuiper</name>
</json:item>
<json:item><name>AGM Janssen</name>
</json:item>
</author>
<host><volume>50</volume>
<pages><last>526</last>
<first>513</first>
</pages>
<author></author>
<title>Archives of Neurology</title>
</host>
<title>Multiple system atrophy and progressive supranuclear palsy: diminished striatal D2 dopamine receptor activity demonstrated by 123IBZM single photon emission computed tomography</title>
</json:item>
<json:item><author><json:item><name>JP Vonsattel</name>
</json:item>
<json:item><name>MH Myers</name>
</json:item>
<json:item><name>TJ Stevens</name>
</json:item>
<json:item><name>RJ Ferrante</name>
</json:item>
<json:item><name>ED Bird</name>
</json:item>
<json:item><name>EP Richardson</name>
</json:item>
</author>
<host><volume>44</volume>
<pages><last>577</last>
<first>559</first>
</pages>
<author></author>
<title>Journal of Neuropathology and Experimental Neurology</title>
</host>
<title>Neuropathological classification of Huntington's disease</title>
</json:item>
<json:item><author><json:item><name>GK Wenning</name>
</json:item>
<json:item><name>Y Ben Shlomo</name>
</json:item>
<json:item><name>M Magalhaes</name>
</json:item>
<json:item><name>SE Daniel</name>
</json:item>
<json:item><name>NP Quinn</name>
</json:item>
</author>
<host><volume>117</volume>
<pages><last>845</last>
<first>835</first>
</pages>
<author></author>
<title>Brain</title>
</host>
<title>Clinical features and natural history of multiple system atrophy</title>
</json:item>
<json:item><author><json:item><name>GK Wenning</name>
</json:item>
<json:item><name>N Quinn</name>
</json:item>
<json:item><name>M Magalhaes</name>
</json:item>
<json:item><name>C Mathias</name>
</json:item>
<json:item><name>SE Daniel</name>
</json:item>
</author>
<host><volume>9</volume>
<pages><last>166</last>
<first>161</first>
</pages>
<author></author>
<title>Movement Disorders</title>
</host>
<title>“Minimal change” multiple sytem atrophy</title>
</json:item>
<json:item><author><json:item><name>GK Wenning</name>
</json:item>
<json:item><name>Y Ben Shlomo</name>
</json:item>
<json:item><name>M Magalhaes</name>
</json:item>
<json:item><name>SE Daniel</name>
</json:item>
<json:item><name>NP Quinn</name>
</json:item>
</author>
<host><volume>58</volume>
<pages><last>166</last>
<first>160</first>
</pages>
<author></author>
<title>Journal of Neurology, Neurosurgery and Psychiatry</title>
</host>
<title>Clinicopathological study of 35 cases of multiple system atrophy</title>
</json:item>
</refBibs>
<genre><json:string>review-article</json:string>
</genre>
<host><volume>2</volume>
<publisherId><json:string>ENE</json:string>
</publisherId>
<pages><total>10</total>
<last>444</last>
<first>435</first>
</pages>
<issn><json:string>1351-5101</json:string>
</issn>
<issue>5</issue>
<genre><json:string>journal</json:string>
</genre>
<language><json:string>unknown</json:string>
</language>
<eissn><json:string>1468-1331</json:string>
</eissn>
<title>European Journal of Neurology</title>
<doi><json:string>10.1111/(ISSN)1468-1331</json:string>
</doi>
</host>
<categories><wos><json:string>science</json:string>
<json:string>neurosciences</json:string>
<json:string>clinical neurology</json:string>
</wos>
<scienceMetrix><json:string>health sciences</json:string>
<json:string>clinical medicine</json:string>
<json:string>neurology & 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)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001C23 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001C23 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= ParkinsonFranceV1 |flux= Istex |étape= Corpus |type= RBID |clé= ISTEX:68BB919B221AEE2CC839A7BC8549F1F6557E74D0 |texte= The pathophysiology of parkinsonism in multiple system atrophy }}
![]() | This area was generated with Dilib version V0.6.29. | ![]() |