Electrophysiology in Fisher syndrome.
Identifieur interne : 000554 ( Main/Exploration ); précédent : 000553; suivant : 000555Electrophysiology in Fisher syndrome.
Auteurs : Satoshi Kuwabara [Japon] ; Yukari Sekiguchi [Japon] ; Sonoko Misawa [Japon]Source :
- Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology [ 1872-8952 ] ; 2017.
Descripteurs français
- KwdFr :
- Ataxie (diagnostic), Ataxie (physiopathologie), Conduction nerveuse (physiologie), Humains (MeSH), Nerf oculomoteur (physiopathologie), Phénomènes électrophysiologiques (physiologie), Potentiels évoqués somatosensoriels (physiologie), Proprioception (physiologie), Réflexe H (physiologie), Réflexes anormaux (physiologie), Syndrome de Miller-Fisher (diagnostic), Syndrome de Miller-Fisher (physiopathologie).
- MESH :
- diagnostic : Ataxie, Syndrome de Miller-Fisher.
- physiologie : Conduction nerveuse, Phénomènes électrophysiologiques, Potentiels évoqués somatosensoriels, Proprioception, Réflexe H, Réflexes anormaux.
- physiopathologie : Ataxie, Nerf oculomoteur, Syndrome de Miller-Fisher.
- Humains.
English descriptors
- KwdEn :
- Ataxia (diagnosis), Ataxia (physiopathology), Electrophysiological Phenomena (physiology), Evoked Potentials, Somatosensory (physiology), H-Reflex (physiology), Humans (MeSH), Miller Fisher Syndrome (diagnosis), Miller Fisher Syndrome (physiopathology), Neural Conduction (physiology), Oculomotor Nerve (physiopathology), Proprioception (physiology), Reflex, Abnormal (physiology).
- MESH :
- diagnosis : Ataxia, Miller Fisher Syndrome.
- physiology : Electrophysiological Phenomena, Evoked Potentials, Somatosensory, H-Reflex, Neural Conduction, Proprioception, Reflex, Abnormal.
- physiopathology : Ataxia, Miller Fisher Syndrome, Oculomotor Nerve.
- Humans.
Abstract
Fisher syndrome (FS), a variant of Guillain-Barré syndrome (GBS), is characterized by the clinical triad of ophthalmoplegia, ataxia, and areflexia. The lesion sites for these unique clinical features include the oculomotor nerves and group 1a neurons in the dorsal root ganglion, and the presence of FS is determined by the expression of ganglioside GQ1b in the human nervous system. Neurophysiological findings suggest that ataxia and areflexia are due to an impaired proprioceptive afferent system. Typically, the soleus H-reflex is absent and a body-sway analysis using posturography shows a 1-Hz peak, which indicates proprioception dysfunction. Sensory nerve action potentials and somatosensory-evoked potentials are abnormal in approximately 30% of FS patients, indicating the occasional involvement of cutaneous (group 2) afferents. During the disease course, approximately 15% of FS patients suffer an overlap of axonal GBS with nerve conduction abnormalities that reflect axonal dysfunction. This review summarizes electrophysiological abnormalities and their clinical significance in FS.
DOI: 10.1016/j.clinph.2016.11.009
PubMed: 27923188
Affiliations:
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The lesion sites for these unique clinical features include the oculomotor nerves and group 1a neurons in the dorsal root ganglion, and the presence of FS is determined by the expression of ganglioside GQ1b in the human nervous system. Neurophysiological findings suggest that ataxia and areflexia are due to an impaired proprioceptive afferent system. Typically, the soleus H-reflex is absent and a body-sway analysis using posturography shows a 1-Hz peak, which indicates proprioception dysfunction. Sensory nerve action potentials and somatosensory-evoked potentials are abnormal in approximately 30% of FS patients, indicating the occasional involvement of cutaneous (group 2) afferents. During the disease course, approximately 15% of FS patients suffer an overlap of axonal GBS with nerve conduction abnormalities that reflect axonal dysfunction. This review summarizes electrophysiological abnormalities and their clinical significance in FS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27923188</PMID><DateCompleted><Year>2017</Year><Month>05</Month><Day>31</Day></DateCompleted><DateRevised><Year>2018</Year><Month>06</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8952</ISSN><JournalIssue CitedMedium="Internet"><Volume>128</Volume><Issue>1</Issue><PubDate><Year>2017</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology</Title><ISOAbbreviation>Clin Neurophysiol</ISOAbbreviation></Journal><ArticleTitle>Electrophysiology in Fisher syndrome.</ArticleTitle><Pagination><MedlinePgn>215-219</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S1388-2457(16)30665-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.clinph.2016.11.009</ELocationID><Abstract><AbstractText>Fisher syndrome (FS), a variant of Guillain-Barré syndrome (GBS), is characterized by the clinical triad of ophthalmoplegia, ataxia, and areflexia. The lesion sites for these unique clinical features include the oculomotor nerves and group 1a neurons in the dorsal root ganglion, and the presence of FS is determined by the expression of ganglioside GQ1b in the human nervous system. Neurophysiological findings suggest that ataxia and areflexia are due to an impaired proprioceptive afferent system. Typically, the soleus H-reflex is absent and a body-sway analysis using posturography shows a 1-Hz peak, which indicates proprioception dysfunction. Sensory nerve action potentials and somatosensory-evoked potentials are abnormal in approximately 30% of FS patients, indicating the occasional involvement of cutaneous (group 2) afferents. During the disease course, approximately 15% of FS patients suffer an overlap of axonal GBS with nerve conduction abnormalities that reflect axonal dysfunction. This review summarizes electrophysiological abnormalities and their clinical significance in FS.</AbstractText><CopyrightInformation>Copyright © 2016 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kuwabara</LastName><ForeName>Satoshi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. Electronic address: kuwabara-s@faculty.chiba-u.jp.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sekiguchi</LastName><ForeName>Yukari</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Misawa</LastName><ForeName>Sonoko</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>11</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Clin Neurophysiol</MedlineTA><NlmUniqueID>100883319</NlmUniqueID><ISSNLinking>1388-2457</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001259" MajorTopicYN="N">Ataxia</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055724" MajorTopicYN="N">Electrophysiological Phenomena</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005073" MajorTopicYN="N">Evoked Potentials, Somatosensory</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006181" MajorTopicYN="N">H-Reflex</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019846" MajorTopicYN="N">Miller Fisher Syndrome</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009431" MajorTopicYN="N">Neural Conduction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009802" MajorTopicYN="N">Oculomotor Nerve</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011434" MajorTopicYN="N">Proprioception</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012021" MajorTopicYN="N">Reflex, Abnormal</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Anti-GQ1b antibody</Keyword><Keyword MajorTopicYN="Y">Fisher syndrome</Keyword><Keyword MajorTopicYN="Y">Group 1a afferent</Keyword><Keyword MajorTopicYN="Y">H-reflex</Keyword><Keyword MajorTopicYN="Y">Sensory nerve conduction</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>07</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>10</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>11</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>12</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>12</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27923188</ArticleId><ArticleId IdType="pii">S1388-2457(16)30665-4</ArticleId><ArticleId IdType="doi">10.1016/j.clinph.2016.11.009</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Kuwabara, Satoshi" sort="Kuwabara, Satoshi" uniqKey="Kuwabara S" first="Satoshi" last="Kuwabara">Satoshi Kuwabara</name></noRegion><name sortKey="Misawa, Sonoko" sort="Misawa, Sonoko" uniqKey="Misawa S" first="Sonoko" last="Misawa">Sonoko Misawa</name><name sortKey="Sekiguchi, Yukari" sort="Sekiguchi, Yukari" uniqKey="Sekiguchi Y" first="Yukari" last="Sekiguchi">Yukari Sekiguchi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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