Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1999-5-27
pubmed:abstractText
A Fisher syndrome (FS) patient with antibody to tetrasyaloganglioside GQ1b (GQ1b) developed late limb weakness. Serial motor conduction velocities (MCVs) showed a marked reduction of distal compound muscle action potential (CMAP) amplitudes, worse at 2-3 weeks, followed by a dramatic increase in week 5. Motor conduction velocities were always in the normal range, distal motor latencies changed only slightly, and conduction block in intermediate nerve segments was absent. These electrophysiological data might suggest an axonal neuropathy or a distal demyelinating conduction block. However, the dramatic increase of distal CMAP amplitudes over a short time without significant changes of distal motor latencies, CMAP duration, and morphology indicate that weakness in this FS patient might be due to a block of acetylcholine release from motor terminals, possibly mediated by anti-GQ1b antibodies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0148-639X
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
640-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Fisher syndrome with tetraparesis and antibody to GQ1b: evidence for motor nerve terminal block.
pubmed:affiliation
Center for Neuromuscular Diseases, University G. d'Annunzio, Clinica Neurologica Ospedale Clinicizzato SS Annunziata, Chieti, Italy.
pubmed:publicationType
Journal Article, Case Reports, Research Support, Non-U.S. Gov't