Progressive subcortical gliosis and progressive supranuclear palsy can have similar clinical and PET abnormalities.
Identifieur interne : 000B81 ( Istex/Corpus ); précédent : 000B80; suivant : 000B82Progressive subcortical gliosis and progressive supranuclear palsy can have similar clinical and PET abnormalities.
Auteurs : N Foster ; S. Gilman ; S. Berent ; A Sima ; C. D ; R Koeppe ; S HicksSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 1992-08.
Abstract
In studies of cerebral glucose metabolism utilising positron emission tomography (PET) with 18F-fluoro-2-deoxy-D-glucose, patients with the clinical picture of progressive supranuclear palsy (PSP) have shown predominantly frontal glucose hypometabolism. This is presumed to represent deafferentation of cerebral cortical from subcortical structures. In these studies, however, the diagnosis of PSP has not been verified by pathological examination. Necropsy examinations were performed in three patients with the clinical features of PSP in whom PET had demonstrated predominantly frontal hypometabolism. In two of these patients the diagnosis of PSP was confirmed pathologically, and no morphological abnormalities were found in the cerebral cortex. The third patient had extensive cortical and subcortical neuronal loss and gliosis without neurofibrillary tangles, consistent with the diagnosis of progressive subcortical gliosis (PSG). Even in retrospect no unique clinical neurological abnormality or finding on laboratory investigation could be identified that distinguished this latter patient from those with pathologically confirmed PSP. We conclude that PSG and PSP may be indistinguishable during life, and necropsy confirmation is needed for definite diagnosis.
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DOI: 10.1136/jnnp.55.8.707
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Berent</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="Sima, A A" sort="Sima, A A" uniqKey="Sima A" first="A" last="Sima">A Sima</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="D Amato, C" sort="D Amato, C" uniqKey="D Amato C" first="C" last="D">C. D</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="Koeppe, R A" sort="Koeppe, R A" uniqKey="Koeppe R" first="R" last="Koeppe">R Koeppe</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="Hicks, S P" sort="Hicks, S P" uniqKey="Hicks S" first="S" last="Hicks">S Hicks</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:82D2FDCC83FADEA94BF65F4DDD26BE7E031BF854</idno><date when="1992-08-01" year="1992">1992-08-01</date><idno type="doi">10.1136/jnnp.55.8.707</idno><idno type="url">https://api.istex.fr/document/82D2FDCC83FADEA94BF65F4DDD26BE7E031BF854/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000B81</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Progressive subcortical gliosis and progressive supranuclear palsy can have similar clinical and PET abnormalities.</title><author><name sortKey="Foster, N L" sort="Foster, N L" uniqKey="Foster N" first="N" last="Foster">N Foster</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="Gilman, S" sort="Gilman, S" uniqKey="Gilman S" first="S" last="Gilman">S. Gilman</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="Berent, S" sort="Berent, S" uniqKey="Berent S" first="S" last="Berent">S. Berent</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="Sima, A A" sort="Sima, A A" uniqKey="Sima A" first="A" last="Sima">A Sima</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="D Amato, C" sort="D Amato, C" uniqKey="D Amato C" first="C" last="D">C. D</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="Koeppe, R A" sort="Koeppe, R A" uniqKey="Koeppe R" first="R" last="Koeppe">R Koeppe</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author><author><name sortKey="Hicks, S P" sort="Hicks, S P" uniqKey="Hicks S" first="S" last="Hicks">S Hicks</name><affiliation><mods:affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="1992-08">1992-08</date><biblScope unit="volume">55</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="707">707</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">82D2FDCC83FADEA94BF65F4DDD26BE7E031BF854</idno><idno type="DOI">10.1136/jnnp.55.8.707</idno><idno type="href">jnnp-55-707.pdf</idno><idno type="PMID">1527543</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In studies of cerebral glucose metabolism utilising positron emission tomography (PET) with 18F-fluoro-2-deoxy-D-glucose, patients with the clinical picture of progressive supranuclear palsy (PSP) have shown predominantly frontal glucose hypometabolism. This is presumed to represent deafferentation of cerebral cortical from subcortical structures. In these studies, however, the diagnosis of PSP has not been verified by pathological examination. Necropsy examinations were performed in three patients with the clinical features of PSP in whom PET had demonstrated predominantly frontal hypometabolism. In two of these patients the diagnosis of PSP was confirmed pathologically, and no morphological abnormalities were found in the cerebral cortex. The third patient had extensive cortical and subcortical neuronal loss and gliosis without neurofibrillary tangles, consistent with the diagnosis of progressive subcortical gliosis (PSG). Even in retrospect no unique clinical neurological abnormality or finding on laboratory investigation could be identified that distinguished this latter patient from those with pathologically confirmed PSP. We conclude that PSG and PSP may be indistinguishable during life, and necropsy confirmation is needed for definite diagnosis.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>N L Foster</name><affiliations><json:string>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</json:string></affiliations></json:item><json:item><name>S Gilman</name><affiliations><json:string>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</json:string></affiliations></json:item><json:item><name>S Berent</name><affiliations><json:string>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</json:string></affiliations></json:item><json:item><name>A A Sima</name><affiliations><json:string>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</json:string></affiliations></json:item><json:item><name>C D'Amato</name><affiliations><json:string>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</json:string></affiliations></json:item><json:item><name>R A Koeppe</name><affiliations><json:string>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</json:string></affiliations></json:item><json:item><name>S P Hicks</name><affiliations><json:string>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Research Article</value></json:item></subject><language><json:string>eng</json:string></language><abstract>In studies of cerebral glucose metabolism utilising positron emission tomography (PET) with 18F-fluoro-2-deoxy-D-glucose, patients with the clinical picture of progressive supranuclear palsy (PSP) have shown predominantly frontal glucose hypometabolism. This is presumed to represent deafferentation of cerebral cortical from subcortical structures. In these studies, however, the diagnosis of PSP has not been verified by pathological examination. Necropsy examinations were performed in three patients with the clinical features of PSP in whom PET had demonstrated predominantly frontal hypometabolism. In two of these patients the diagnosis of PSP was confirmed pathologically, and no morphological abnormalities were found in the cerebral cortex. The third patient had extensive cortical and subcortical neuronal loss and gliosis without neurofibrillary tangles, consistent with the diagnosis of progressive subcortical gliosis (PSG). Even in retrospect no unique clinical neurological abnormality or finding on laboratory investigation could be identified that distinguished this latter patient from those with pathologically confirmed PSP. 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type="first">S</forename><surname>Berent</surname></persName><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation></author><author><persName><forename type="first">A A</forename><surname>Sima</surname></persName><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation></author><author><persName><forename type="first">C</forename><surname>D'Amato</surname></persName><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation></author><author><persName><forename type="first">R A</forename><surname>Koeppe</surname></persName><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation></author><author><persName><forename type="first">S P</forename><surname>Hicks</surname></persName><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="1992-08"></date><biblScope unit="volume">55</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="707">707</biblScope></imprint></monogr><idno type="istex">82D2FDCC83FADEA94BF65F4DDD26BE7E031BF854</idno><idno type="DOI">10.1136/jnnp.55.8.707</idno><idno type="href">jnnp-55-707.pdf</idno><idno type="PMID">1527543</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1992-08-01</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In studies of cerebral glucose metabolism utilising positron emission tomography (PET) with 18F-fluoro-2-deoxy-D-glucose, patients with the clinical picture of progressive supranuclear palsy (PSP) have shown predominantly frontal glucose hypometabolism. This is presumed to represent deafferentation of cerebral cortical from subcortical structures. In these studies, however, the diagnosis of PSP has not been verified by pathological examination. Necropsy examinations were performed in three patients with the clinical features of PSP in whom PET had demonstrated predominantly frontal hypometabolism. In two of these patients the diagnosis of PSP was confirmed pathologically, and no morphological abnormalities were found in the cerebral cortex. The third patient had extensive cortical and subcortical neuronal loss and gliosis without neurofibrillary tangles, consistent with the diagnosis of progressive subcortical gliosis (PSG). Even in retrospect no unique clinical neurological abnormality or finding on laboratory investigation could be identified that distinguished this latter patient from those with pathologically confirmed PSP. We conclude that PSG and PSP may be indistinguishable during life, and necropsy confirmation is needed for definite diagnosis.</p></abstract><textClass><keywords scheme="keyword"><list><head>heading</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1992-08-01">Created</change><change when="1992-08">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-0-25">References added</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-1-3">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/82D2FDCC83FADEA94BF65F4DDD26BE7E031BF854/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article" xml:lang="EN"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">1527543</article-id><article-id pub-id-type="other">jnnp;55/8/707</article-id><article-id pub-id-type="doi">10.1136/jnnp.55.8.707</article-id><article-id pub-id-type="other">707</article-id><article-id pub-id-type="other">jnnp.55.8.707</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Progressive subcortical gliosis and progressive supranuclear palsy can have similar clinical and PET abnormalities.</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Foster</surname><given-names>N L</given-names></name></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Gilman</surname><given-names>S</given-names></name></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Berent</surname><given-names>S</given-names></name></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Sima</surname><given-names>A A</given-names></name></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>D'Amato</surname><given-names>C</given-names></name></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Koeppe</surname><given-names>R A</given-names></name></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Hicks</surname><given-names>S P</given-names></name></contrib></contrib-group><aff>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</aff><pub-date pub-type="ppub"><month>8</month><year>1992</year></pub-date><pub-date pub-type="epub"><day>1</day><month>8</month><year>1992</year></pub-date><volume>55</volume><volume-id pub-id-type="other">55</volume-id><volume-id pub-id-type="other">55</volume-id><issue>8</issue><issue-id pub-id-type="other">jnnp;55/8</issue-id><issue-id pub-id-type="other">8</issue-id><issue-id pub-id-type="other">55/8</issue-id><fpage>707</fpage><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-55-707.pdf"></self-uri><abstract><p>In studies of cerebral glucose metabolism utilising positron emission tomography (PET) with 18F-fluoro-2-deoxy-D-glucose, patients with the clinical picture of progressive supranuclear palsy (PSP) have shown predominantly frontal glucose hypometabolism. This is presumed to represent deafferentation of cerebral cortical from subcortical structures. In these studies, however, the diagnosis of PSP has not been verified by pathological examination. Necropsy examinations were performed in three patients with the clinical features of PSP in whom PET had demonstrated predominantly frontal hypometabolism. In two of these patients the diagnosis of PSP was confirmed pathologically, and no morphological abnormalities were found in the cerebral cortex. The third patient had extensive cortical and subcortical neuronal loss and gliosis without neurofibrillary tangles, consistent with the diagnosis of progressive subcortical gliosis (PSG). Even in retrospect no unique clinical neurological abnormality or finding on laboratory investigation could be identified that distinguished this latter patient from those with pathologically confirmed PSP. We conclude that PSG and PSP may be indistinguishable during life, and necropsy confirmation is needed for definite diagnosis.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Progressive subcortical gliosis and progressive supranuclear palsy can have similar clinical and PET abnormalities.</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Progressive subcortical gliosis and progressive supranuclear palsy can have similar clinical and PET abnormalities.</title></titleInfo><name type="personal"><namePart type="given">N L</namePart><namePart type="family">Foster</namePart><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Gilman</namePart><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Berent</namePart><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A A</namePart><namePart type="family">Sima</namePart><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">D'Amato</namePart><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R A</namePart><namePart type="family">Koeppe</namePart><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S P</namePart><namePart type="family">Hicks</namePart><affiliation>Department of Neurology, University of Michigan Medical Center, Ann Arbor 48109-0316.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article">research-article</genre><subject><genre>heading</genre><topic>Research Article</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">1992-08</dateIssued><dateCreated encoding="w3cdtf">1992-08-01</dateCreated></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">In studies of cerebral glucose metabolism utilising positron emission tomography (PET) with 18F-fluoro-2-deoxy-D-glucose, patients with the clinical picture of progressive supranuclear palsy (PSP) have shown predominantly frontal glucose hypometabolism. This is presumed to represent deafferentation of cerebral cortical from subcortical structures. In these studies, however, the diagnosis of PSP has not been verified by pathological examination. Necropsy examinations were performed in three patients with the clinical features of PSP in whom PET had demonstrated predominantly frontal hypometabolism. In two of these patients the diagnosis of PSP was confirmed pathologically, and no morphological abnormalities were found in the cerebral cortex. The third patient had extensive cortical and subcortical neuronal loss and gliosis without neurofibrillary tangles, consistent with the diagnosis of progressive subcortical gliosis (PSG). Even in retrospect no unique clinical neurological abnormality or finding on laboratory investigation could be identified that distinguished this latter patient from those with pathologically confirmed PSP. We conclude that PSG and PSP may be indistinguishable during life, and necropsy confirmation is needed for definite diagnosis.</abstract><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="JournalID-hwp">jnnp</identifier><identifier type="JournalID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>1992</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>707</start></extent></part></relatedItem><identifier type="istex">82D2FDCC83FADEA94BF65F4DDD26BE7E031BF854</identifier><identifier type="DOI">10.1136/jnnp.55.8.707</identifier><identifier type="href">jnnp-55-707.pdf</identifier><identifier type="PMID">1527543</identifier><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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