The pathogenesis of multiple sclerosis
Identifieur interne : 000690 ( Istex/Corpus ); précédent : 000689; suivant : 000691The pathogenesis of multiple sclerosis
Auteurs : Charles M. PoserSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1993.
English descriptors
- Teeft :
- Acta, Acta neurol, Acta neuropathol, Acute lesions, Beth israel hospital, Blood vessel wall, Blood vessels, Brain inflammation, Brain injury, Brain lesions, Bystander demyelination, Cell membrane, Cerebrospinal fluid, Cervical cord, Cervical spondylosis, Churchill livingstone, Clinical manifestations, Compston, Concussion, Concussional trauma, Convincing evidence, Crucial role, Demyelinating, Demyelination, Disease process, Edema, Electrolytic lesion, Encephalomyelitis, Endothelial cells, Entire life, Esiri, Exact mechanism, Experimental evidence, Familial subclinical, Gadolinium enhancement, Genetic susceptibility, Head injury, Hickey, Humoral, Humoral mediators, Hyperactive immunocompetent responsiveness, Imaging, Immune, Immune complexes, Immune reaction, Immune response, Immune system, Immunocompetent cells, Immunological, Impermeability, Important role, Inflammation, Inflammatory, Inflammatory cells, Inflammatory changes, Inflammatory reaction, Influenza, Lesion, Lesion development, Local breakdown, Lymphocyte, Magnetic resonance imaging, Magnetization transfer imaging, Many investigators, Many studies, Many years, Mediator, Mimicry, Molecular mimicry, Multiple sclerosis, Myelin, Myelin components, Myelin proteolipid protein, Myelin sheath, Nervous system, Neurol, Neurology, Neuropathol, Neurosurg, Obligatory step, Oligoclonal bands, Other hand, Other words, Pathogenesis, Peripheral blood, Perivascular spaces, Permeability, Personal communication, Personal communications, Pivotal role, Plaque, Poser, Possible importance, Primary event, Primary target, Progression, Psychiat, Safety margin, Same patient, Sclerosis, Several mechanisms, Single event, Systemic condition, Target organ, Trait, Trauma, Unaffected siblings, Unanswered questions, Vaccination, Vaccine, Viral, Viral antibodies, Viral infection, Viral proteins, White matter, White matter lesions.
Abstract
Abstract: Multiple sclerosis (MS) is acquired as a systemic “trait” by individuals who are genetically susceptible. This condition does not involve the central nervous system (CNS) and is characterized by a state of hyperactive immunocompetent responsiveness. It develops as the result of an antigenic challenge by a viral protein, either from a viral infection or a vaccination. In order for MS to become a disease affecting the CNS, it is necessary for the blood-brain barrier's (BBB) impermeability to be altered. This is now a fully recognized fact. As a result of this change, the MS lesion, which consists of edema and inflammation occurs. It may but need not lead to demyelination. Several mechanisms can cause this increased permeability of the BBB. The role of the immune system, and in particular of T lymphocytes in initiating and continuing the process of lesion formation remains extremely controversial. In fact, there are unanswered questions regarding the actual target of MS: is it the myelin sheath itself or its forming cell, the oligodendrocyte, or is it the BBB itself leading to bystander demyelination? The role of mild, concussional trauma to the CNS in producing the alteration of the BBB and therefore acting as a trigger or facilitator in the development or enlargement of MS lesions in the CNS, is based on considerable clinical, neuropathological and experimental evidence. Along with another viral infection, it must be one of the commonest causes of progression of MS, and quite often leads to the onset of the clinical manifestations of an hitherto asymptomatic condition.
Url:
DOI: 10.1016/0022-510X(93)90203-B
Links to Exploration step
ISTEX:51A24426A511CBC197A5CA23DE968EA6A7D49E92Le document en format XML
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This condition does not involve the central nervous system (CNS) and is characterized by a state of hyperactive immunocompetent responsiveness. It develops as the result of an antigenic challenge by a viral protein, either from a viral infection or a vaccination. In order for MS to become a disease affecting the CNS, it is necessary for the blood-brain barrier's (BBB) impermeability to be altered. This is now a fully recognized fact. As a result of this change, the MS lesion, which consists of edema and inflammation occurs. It may but need not lead to demyelination. Several mechanisms can cause this increased permeability of the BBB. The role of the immune system, and in particular of T lymphocytes in initiating and continuing the process of lesion formation remains extremely controversial. In fact, there are unanswered questions regarding the actual target of MS: is it the myelin sheath itself or its forming cell, the oligodendrocyte, or is it the BBB itself leading to bystander demyelination? The role of mild, concussional trauma to the CNS in producing the alteration of the BBB and therefore acting as a trigger or facilitator in the development or enlargement of MS lesions in the CNS, is based on considerable clinical, neuropathological and experimental evidence. Along with another viral infection, it must be one of the commonest causes of progression of MS, and quite often leads to the onset of the clinical manifestations of an hitherto asymptomatic condition.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>myelin</json:string><json:string>neurol</json:string><json:string>poser</json:string><json:string>lesion</json:string><json:string>demyelination</json:string><json:string>immune</json:string><json:string>viral</json:string><json:string>encephalomyelitis</json:string><json:string>trauma</json:string><json:string>neurosurg</json:string><json:string>neurology</json:string><json:string>multiple 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injury</json:string><json:string>single event</json:string><json:string>inflammatory cells</json:string><json:string>acta neurol</json:string><json:string>cerebrospinal fluid</json:string><json:string>immune reaction</json:string><json:string>familial subclinical</json:string><json:string>brain lesions</json:string><json:string>brain inflammation</json:string><json:string>imaging</json:string><json:string>influenza</json:string></teeft></keywords><author><json:item><name>Charles M. Poser</name><affiliations><json:string>Department of Neurology, Harvard Medical School and Neurological Unit, Beth Israel Hospital, Boston, MA, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Multiple sclerosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Pathogenesis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Blood-brain barrier</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Trauma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Disease progression</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Multiple sclerosis trait</value></json:item></subject><arkIstex>ark:/67375/6H6-V3F6SPRX-M</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Multiple sclerosis (MS) is acquired as a systemic “trait” by individuals who are genetically susceptible. This condition does not involve the central nervous system (CNS) and is characterized by a state of hyperactive immunocompetent responsiveness. It develops as the result of an antigenic challenge by a viral protein, either from a viral infection or a vaccination. In order for MS to become a disease affecting the CNS, it is necessary for the blood-brain barrier's (BBB) impermeability to be altered. This is now a fully recognized fact. As a result of this change, the MS lesion, which consists of edema and inflammation occurs. It may but need not lead to demyelination. Several mechanisms can cause this increased permeability of the BBB. The role of the immune system, and in particular of T lymphocytes in initiating and continuing the process of lesion formation remains extremely controversial. In fact, there are unanswered questions regarding the actual target of MS: is it the myelin sheath itself or its forming cell, the oligodendrocyte, or is it the BBB itself leading to bystander demyelination? The role of mild, concussional trauma to the CNS in producing the alteration of the BBB and therefore acting as a trigger or facilitator in the development or enlargement of MS lesions in the CNS, is based on considerable clinical, neuropathological and experimental evidence. Along with another viral infection, it must be one of the commonest causes of progression of MS, and quite often leads to the onset of the clinical manifestations of an hitherto asymptomatic condition.</abstract><qualityIndicators><score>10</score><pdfWordCount>9368</pdfWordCount><pdfCharCount>55151</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>13</pdfPageCount><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>256</abstractWordCount><abstractCharCount>1604</abstractCharCount><keywordCount>6</keywordCount></qualityIndicators><title>The pathogenesis of multiple sclerosis</title><pmid><json:string>7688036</json:string></pmid><pii><json:string>0022-510X(93)90203-B</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Handbook of Neurology: Demyelinating diseases</title><language><json:string>unknown</json:string></language><volume>vol. 3</volume><pages><first>429</first><last>466</last></pages></serie><host><title>Journal of the Neurological Sciences</title><language><json:string>unknown</json:string></language><publicationDate>1993</publicationDate><issn><json:string>0022-510X</json:string></issn><pii><json:string>S0022-510X(00)X0304-8</json:string></pii><volume>115</volume><pages><first>S3</first><last>S15</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1950s</json:string><json:string>1992</json:string><json:string>1968</json:string><json:string>1986</json:string><json:string>1993</json:string><json:string>1976</json:string><json:string>1959</json:string><json:string>1977</json:string><json:string>1949</json:string></date><geogName></geogName><orgName><json:string>Beth Israel Hospital, Boston, MA, USA Key</json:string><json:string>Beth Israel Hospital</json:string><json:string>Colchester General Hospital, Essex, UK</json:string><json:string>University of Iceland School of Medicine, Reykjavik, Iceland</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Scott Zamvil</json:string><json:string>Luigi Pugnetti</json:string><json:string>Derek Gay</json:string><json:string>Charles M. Poser</json:string><json:string>Gtmnar Gudmtmdsson</json:string></persName><placeName><json:string>Colombia</json:string><json:string>Boston</json:string><json:string>Europe</json:string><json:string>USA</json:string><json:string>Japan</json:string><json:string>MA</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Ommaya et al.</json:string><json:string>Jingzu et al. (1992)</json:string><json:string>Gay and Esiri (1992)</json:string><json:string>Wadia et al. 1974</json:string><json:string>Jahnke et al. 1985</json:string><json:string>Barnes et al. (1991)</json:string><json:string>Poser et al. (1987)</json:string><json:string>Thompson et al. 1991</json:string><json:string>Levin et al. (1987, 1988, 1992)</json:string><json:string>Gyorkey et al. 1987</json:string><json:string>Kelly et al. (1991)</json:string><json:string>Murray et al. 1992</json:string><json:string>Amon et al. 1980</json:string><json:string>Toro et al. 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(1991)</json:string><json:string>Wisniewski and Bloom (1985)</json:string><json:string>Adams 1985</json:string><json:string>Clark and Bogdanove (1955)</json:string><json:string>Jenkins et al. (1986)</json:string><json:string>Riechert et al. (1975)</json:string><json:string>Rosenberg et al. 1988</json:string><json:string>Naqvi et al. 1988</json:string><json:string>Gay and Esiri (1991)</json:string><json:string>Xu and McFarlin 1984</json:string><json:string>Rimel et al.</json:string><json:string>Levine and Hoenig (1968)</json:string><json:string>Woyciechowska et al. 1985</json:string><json:string>Poser 1992a</json:string><json:string>Axthelm and Krakowka 1987</json:string><json:string>Rudge 1991</json:string><json:string>Poser 1985</json:string><json:string>Domer et al. (1979)</json:string><json:string>Coyle et al. (1980)</json:string><json:string>Estes et al. 1990</json:string><json:string>Filley et al. 1990</json:string><json:string>Kapadia (1984)</json:string><json:string>Poser 1979</json:string><json:string>Davison (1992)</json:string><json:string>Jahnke et al. (1985)</json:string><json:string>Poser 1986, 1987, 1992a</json:string><json:string>Adams et al. (1985)</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-V3F6SPRX-M</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - neurosciences</json:string><json:string>2 - clinical neurology</json:string></wos><scienceMetrix></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Clinical Neurology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Neuroscience</json:string><json:string>3 - Neurology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1993</publicationDate><copyrightDate>1993</copyrightDate><doi><json:string>10.1016/0022-510X(93)90203-B</json:string></doi><id>51A24426A511CBC197A5CA23DE968EA6A7D49E92</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-V3F6SPRX-M/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-V3F6SPRX-M/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-V3F6SPRX-M/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">The pathogenesis of multiple sclerosis</title><title level="a" type="sub">Additional considerations</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1993</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">The pathogenesis of multiple sclerosis</title><title level="a" type="sub">Additional considerations</title><author xml:id="author-0000"><persName><forename type="first">Charles M.</forename><surname>Poser</surname></persName><note type="correspondence"><p>Correspondence to: Charles M. Poser, MD, Neurological Unit, Harvard Medical School, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215, USA. Fax: (617) 735-5216.</p></note><affiliation>Department of Neurology, Harvard Medical School and Neurological Unit, Beth Israel Hospital, Boston, MA, USA</affiliation></author><idno type="istex">51A24426A511CBC197A5CA23DE968EA6A7D49E92</idno><idno type="ark">ark:/67375/6H6-V3F6SPRX-M</idno><idno type="DOI">10.1016/0022-510X(93)90203-B</idno><idno type="PII">0022-510X(93)90203-B</idno></analytic><monogr><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="pISSN">0022-510X</idno><idno type="PII">S0022-510X(00)X0304-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993"></date><biblScope unit="volume">115</biblScope><biblScope unit="supplement">S</biblScope><biblScope unit="page" from="S3">S3</biblScope><biblScope unit="page" to="S15">S15</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Multiple sclerosis (MS) is acquired as a systemic “trait” by individuals who are genetically susceptible. This condition does not involve the central nervous system (CNS) and is characterized by a state of hyperactive immunocompetent responsiveness. It develops as the result of an antigenic challenge by a viral protein, either from a viral infection or a vaccination. In order for MS to become a disease affecting the CNS, it is necessary for the blood-brain barrier's (BBB) impermeability to be altered. This is now a fully recognized fact. As a result of this change, the MS lesion, which consists of edema and inflammation occurs. It may but need not lead to demyelination. Several mechanisms can cause this increased permeability of the BBB. The role of the immune system, and in particular of T lymphocytes in initiating and continuing the process of lesion formation remains extremely controversial. In fact, there are unanswered questions regarding the actual target of MS: is it the myelin sheath itself or its forming cell, the oligodendrocyte, or is it the BBB itself leading to bystander demyelination? The role of mild, concussional trauma to the CNS in producing the alteration of the BBB and therefore acting as a trigger or facilitator in the development or enlargement of MS lesions in the CNS, is based on considerable clinical, neuropathological and experimental evidence. Along with another viral infection, it must be one of the commonest causes of progression of MS, and quite often leads to the onset of the clinical manifestations of an hitherto asymptomatic condition.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Multiple sclerosis</term></item><item><term>Pathogenesis</term></item><item><term>Blood-brain barrier</term></item><item><term>Trauma</term></item><item><term>Disease progression</term></item><item><term>Multiple sclerosis trait</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-V3F6SPRX-M/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JNS</jid><aid>9390203B</aid><ce:pii>0022-510X(93)90203-B</ce:pii><ce:doi>10.1016/0022-510X(93)90203-B</ce:doi><ce:copyright type="unknown" year="1993"></ce:copyright></item-info><head><ce:title>The pathogenesis of multiple sclerosis</ce:title><ce:subtitle>Additional considerations</ce:subtitle><ce:author-group><ce:author><ce:given-name>Charles M.</ce:given-name><ce:surname>Poser</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Department of Neurology, Harvard Medical School and Neurological Unit, Beth Israel Hospital, Boston, MA, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>Correspondence to: Charles M. Poser, MD, Neurological Unit, Harvard Medical School, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215, USA. Fax: (617) 735-5216.</ce:text></ce:correspondence></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Multiple sclerosis (MS) is acquired as a systemic “trait” by individuals who are genetically susceptible. This condition does not involve the central nervous system (CNS) and is characterized by a state of hyperactive immunocompetent responsiveness. It develops as the result of an antigenic challenge by a viral protein, either from a viral infection or a vaccination. In order for MS to become a disease affecting the CNS, it is necessary for the blood-brain barrier's (BBB) impermeability to be altered. This is now a fully recognized fact. As a result of this change, the MS lesion, which consists of edema and inflammation occurs. It may but need not lead to demyelination. Several mechanisms can cause this increased permeability of the BBB. The role of the immune system, and in particular of T lymphocytes in initiating and continuing the process of lesion formation remains extremely controversial. In fact, there are unanswered questions regarding the actual target of MS: is it the myelin sheath itself or its forming cell, the oligodendrocyte, or is it the BBB itself leading to bystander demyelination? The role of mild, concussional trauma to the CNS in producing the alteration of the BBB and therefore acting as a trigger or facilitator in the development or enlargement of MS lesions in the CNS, is based on considerable clinical, neuropathological and experimental evidence. Along with another viral infection, it must be one of the commonest causes of progression of MS, and quite often leads to the onset of the clinical manifestations of an hitherto asymptomatic condition.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Multiple sclerosis</ce:text></ce:keyword><ce:keyword><ce:text>Pathogenesis</ce:text></ce:keyword><ce:keyword><ce:text>Blood-brain barrier</ce:text></ce:keyword><ce:keyword><ce:text>Trauma</ce:text></ce:keyword><ce:keyword><ce:text>Disease progression</ce:text></ce:keyword><ce:keyword><ce:text>Multiple sclerosis trait</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>The pathogenesis of multiple sclerosis</title><subTitle>Additional considerations</subTitle></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>The pathogenesis of multiple sclerosis</title><subTitle>Additional considerations</subTitle></titleInfo><name type="personal"><namePart type="given">Charles M.</namePart><namePart type="family">Poser</namePart><affiliation>Department of Neurology, Harvard Medical School and Neurological Unit, Beth Israel Hospital, Boston, MA, USA</affiliation><description>Correspondence to: Charles M. Poser, MD, Neurological Unit, Harvard Medical School, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215, USA. Fax: (617) 735-5216.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1993</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Multiple sclerosis (MS) is acquired as a systemic “trait” by individuals who are genetically susceptible. This condition does not involve the central nervous system (CNS) and is characterized by a state of hyperactive immunocompetent responsiveness. It develops as the result of an antigenic challenge by a viral protein, either from a viral infection or a vaccination. In order for MS to become a disease affecting the CNS, it is necessary for the blood-brain barrier's (BBB) impermeability to be altered. This is now a fully recognized fact. As a result of this change, the MS lesion, which consists of edema and inflammation occurs. It may but need not lead to demyelination. Several mechanisms can cause this increased permeability of the BBB. The role of the immune system, and in particular of T lymphocytes in initiating and continuing the process of lesion formation remains extremely controversial. In fact, there are unanswered questions regarding the actual target of MS: is it the myelin sheath itself or its forming cell, the oligodendrocyte, or is it the BBB itself leading to bystander demyelination? The role of mild, concussional trauma to the CNS in producing the alteration of the BBB and therefore acting as a trigger or facilitator in the development or enlargement of MS lesions in the CNS, is based on considerable clinical, neuropathological and experimental evidence. Along with another viral infection, it must be one of the commonest causes of progression of MS, and quite often leads to the onset of the clinical manifestations of an hitherto asymptomatic condition.</abstract><subject><genre>Keywords</genre><topic>Multiple sclerosis</topic><topic>Pathogenesis</topic><topic>Blood-brain barrier</topic><topic>Trauma</topic><topic>Disease progression</topic><topic>Multiple sclerosis trait</topic></subject><relatedItem type="host"><titleInfo><title>Journal of the Neurological Sciences</title></titleInfo><titleInfo type="abbreviated"><title>JNS</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1993</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0304-8</identifier><part><date>1993</date><detail type="volume"><number>115</number><caption>vol.</caption></detail><detail type="supplement"><number>S</number><caption>Suppl.</caption></detail><extent unit="issue-pages"><start>S1</start><end>S74</end></extent><extent unit="pages"><start>S3</start><end>S15</end></extent></part></relatedItem><identifier type="istex">51A24426A511CBC197A5CA23DE968EA6A7D49E92</identifier><identifier type="ark">ark:/67375/6H6-V3F6SPRX-M</identifier><identifier type="DOI">10.1016/0022-510X(93)90203-B</identifier><identifier type="PII">0022-510X(93)90203-B</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-V3F6SPRX-M/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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