Electrophysiology in Fisher syndrome.
Identifieur interne : 000589 ( Main/Corpus ); précédent : 000588; suivant : 000590Electrophysiology in Fisher syndrome.
Auteurs : Satoshi Kuwabara ; Yukari Sekiguchi ; Sonoko MisawaSource :
- Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology [ 1872-8952 ] ; 2017.
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
Links to Exploration step
pubmed:27923188Le document en format XML
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<author><name sortKey="Kuwabara, Satoshi" sort="Kuwabara, Satoshi" uniqKey="Kuwabara S" first="Satoshi" last="Kuwabara">Satoshi Kuwabara</name>
<affiliation><nlm: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.</nlm:affiliation>
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<author><name sortKey="Sekiguchi, Yukari" sort="Sekiguchi, Yukari" uniqKey="Sekiguchi Y" first="Yukari" last="Sekiguchi">Yukari Sekiguchi</name>
<affiliation><nlm:affiliation>Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.</nlm:affiliation>
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<author><name sortKey="Misawa, Sonoko" sort="Misawa, Sonoko" uniqKey="Misawa S" first="Sonoko" last="Misawa">Sonoko Misawa</name>
<affiliation><nlm:affiliation>Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.</nlm:affiliation>
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<affiliation><nlm: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.</nlm:affiliation>
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<author><name sortKey="Sekiguchi, Yukari" sort="Sekiguchi, Yukari" uniqKey="Sekiguchi Y" first="Yukari" last="Sekiguchi">Yukari Sekiguchi</name>
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<series><title level="j">Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Ataxia (diagnosis)</term>
<term>Ataxia (physiopathology)</term>
<term>Electrophysiological Phenomena (physiology)</term>
<term>Evoked Potentials, Somatosensory (physiology)</term>
<term>H-Reflex (physiology)</term>
<term>Humans (MeSH)</term>
<term>Miller Fisher Syndrome (diagnosis)</term>
<term>Miller Fisher Syndrome (physiopathology)</term>
<term>Neural Conduction (physiology)</term>
<term>Oculomotor Nerve (physiopathology)</term>
<term>Proprioception (physiology)</term>
<term>Reflex, Abnormal (physiology)</term>
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<keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Ataxia</term>
<term>Miller Fisher Syndrome</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Electrophysiological Phenomena</term>
<term>Evoked Potentials, Somatosensory</term>
<term>H-Reflex</term>
<term>Neural Conduction</term>
<term>Proprioception</term>
<term>Reflex, Abnormal</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Ataxia</term>
<term>Miller Fisher Syndrome</term>
<term>Oculomotor Nerve</term>
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<front><div type="abstract" xml:lang="en">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.</div>
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<Title>Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology</Title>
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<ArticleTitle>Electrophysiology in Fisher syndrome.</ArticleTitle>
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<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>
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<Author ValidYN="Y"><LastName>Misawa</LastName>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D001259" MajorTopicYN="N">Ataxia</DescriptorName>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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<MeshHeading><DescriptorName UI="D019846" MajorTopicYN="N">Miller Fisher Syndrome</DescriptorName>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Anti-GQ1b antibody</Keyword>
<Keyword MajorTopicYN="Y">Fisher syndrome</Keyword>
<Keyword MajorTopicYN="Y">Group 1a afferent</Keyword>
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