The pathogenesis of multiple sclerosis
Identifieur interne : 001A84 ( Main/Exploration ); précédent : 001A83; suivant : 001A85The pathogenesis of multiple sclerosis
Auteurs : Charles M. Poser [États-Unis]Source :
- 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
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 000690
- to stream Istex, to step Curation: 000657
- to stream Istex, to step Checkpoint: 000483
- to stream Main, to step Merge: 001B00
- to stream Main, to step Curation: 001A84
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>The pathogenesis of multiple sclerosis</title><author><name sortKey="Poser, Charles M" sort="Poser, Charles M" uniqKey="Poser C" first="Charles M." last="Poser">Charles M. Poser</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:51A24426A511CBC197A5CA23DE968EA6A7D49E92</idno><date when="1993" year="1993">1993</date><idno type="doi">10.1016/0022-510X(93)90203-B</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-V3F6SPRX-M/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000690</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000690</idno><idno type="wicri:Area/Istex/Curation">000657</idno><idno type="wicri:Area/Istex/Checkpoint">000483</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000483</idno><idno type="wicri:doubleKey">0022-510X:1993:Poser C:the:pathogenesis:of</idno><idno type="wicri:Area/Main/Merge">001B00</idno><idno type="wicri:Area/Main/Curation">001A84</idno><idno type="wicri:Area/Main/Exploration">001A84</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">The pathogenesis of multiple sclerosis</title><author><name sortKey="Poser, Charles M" sort="Poser, Charles M" uniqKey="Poser C" first="Charles M." last="Poser">Charles M. Poser</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Harvard Medical School and Neurological Unit, Beth Israel Hospital, Boston, MA</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">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><idno type="ISSN">0022-510X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acta</term><term>Acta neurol</term><term>Acta neuropathol</term><term>Acute lesions</term><term>Beth israel hospital</term><term>Blood vessel wall</term><term>Blood vessels</term><term>Brain inflammation</term><term>Brain injury</term><term>Brain lesions</term><term>Bystander demyelination</term><term>Cell membrane</term><term>Cerebrospinal fluid</term><term>Cervical cord</term><term>Cervical spondylosis</term><term>Churchill livingstone</term><term>Clinical manifestations</term><term>Compston</term><term>Concussion</term><term>Concussional trauma</term><term>Convincing evidence</term><term>Crucial role</term><term>Demyelinating</term><term>Demyelination</term><term>Disease process</term><term>Edema</term><term>Electrolytic lesion</term><term>Encephalomyelitis</term><term>Endothelial cells</term><term>Entire life</term><term>Esiri</term><term>Exact mechanism</term><term>Experimental evidence</term><term>Familial subclinical</term><term>Gadolinium enhancement</term><term>Genetic susceptibility</term><term>Head injury</term><term>Hickey</term><term>Humoral</term><term>Humoral mediators</term><term>Hyperactive immunocompetent responsiveness</term><term>Imaging</term><term>Immune</term><term>Immune complexes</term><term>Immune reaction</term><term>Immune response</term><term>Immune system</term><term>Immunocompetent cells</term><term>Immunological</term><term>Impermeability</term><term>Important role</term><term>Inflammation</term><term>Inflammatory</term><term>Inflammatory cells</term><term>Inflammatory changes</term><term>Inflammatory reaction</term><term>Influenza</term><term>Lesion</term><term>Lesion development</term><term>Local breakdown</term><term>Lymphocyte</term><term>Magnetic resonance imaging</term><term>Magnetization transfer imaging</term><term>Many investigators</term><term>Many studies</term><term>Many years</term><term>Mediator</term><term>Mimicry</term><term>Molecular mimicry</term><term>Multiple sclerosis</term><term>Myelin</term><term>Myelin components</term><term>Myelin proteolipid protein</term><term>Myelin sheath</term><term>Nervous system</term><term>Neurol</term><term>Neurology</term><term>Neuropathol</term><term>Neurosurg</term><term>Obligatory step</term><term>Oligoclonal bands</term><term>Other hand</term><term>Other words</term><term>Pathogenesis</term><term>Peripheral blood</term><term>Perivascular spaces</term><term>Permeability</term><term>Personal communication</term><term>Personal communications</term><term>Pivotal role</term><term>Plaque</term><term>Poser</term><term>Possible importance</term><term>Primary event</term><term>Primary target</term><term>Progression</term><term>Psychiat</term><term>Safety margin</term><term>Same patient</term><term>Sclerosis</term><term>Several mechanisms</term><term>Single event</term><term>Systemic condition</term><term>Target organ</term><term>Trait</term><term>Trauma</term><term>Unaffected siblings</term><term>Unanswered questions</term><term>Vaccination</term><term>Vaccine</term><term>Viral</term><term>Viral antibodies</term><term>Viral infection</term><term>Viral proteins</term><term>White matter</term><term>White matter lesions</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region></list><tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Poser, Charles M" sort="Poser, Charles M" uniqKey="Poser C" first="Charles M." last="Poser">Charles M. Poser</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/CovidV2/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001A84 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001A84 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= CovidV2
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:51A24426A511CBC197A5CA23DE968EA6A7D49E92
|texte= The pathogenesis of multiple sclerosis
}}
| This area was generated with Dilib version V0.6.33. |  |