Structure-function correlations in myasthenia gravis and a new myasthenic syndrome.

Andrew G Engel, E. H. Lambert

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The physiologic hallmark of MG is the small amplitude of the mepp. This can be correlated with a deficiency of postsynaptic AChR. The AChR deficiency is caused by antiAChR antibodies. Antibody dependent, complement mediated lysis of the postsynaptic membrane contributes significantly to the AChR deficiency. The abundance of immune complexes localized at the end-plate correlates with the amount of AChR remaining at the end-plate and with the mepp amplitude. The physiologic hallmarks of the new myasthenic syndrome are a small quantum content of the end-plate potential due to a decreased store of immediately releasable quanta, repetitive response of the muscle to a single nerve stimulus and refractoriness to anticholinesterase drugs. The findings are explained by a marked decrease of the size of the nerve terminal and by the total absence of AChE from the end-plate.

Original languageEnglish (US)
Pages (from-to)469-477
Number of pages9
JournalElectroencephalography and clinical neurophysiology. Supplement
Issue number34
StatePublished - 1978

Fingerprint

Myasthenia Gravis
Muscle Weakness
Antibodies
Excitatory Postsynaptic Potentials
Cholinesterase Inhibitors
Antigen-Antibody Complex
Muscles
Membranes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{acabfdffbbbb427f968e8c799b28afe8,
title = "Structure-function correlations in myasthenia gravis and a new myasthenic syndrome.",
abstract = "The physiologic hallmark of MG is the small amplitude of the mepp. This can be correlated with a deficiency of postsynaptic AChR. The AChR deficiency is caused by antiAChR antibodies. Antibody dependent, complement mediated lysis of the postsynaptic membrane contributes significantly to the AChR deficiency. The abundance of immune complexes localized at the end-plate correlates with the amount of AChR remaining at the end-plate and with the mepp amplitude. The physiologic hallmarks of the new myasthenic syndrome are a small quantum content of the end-plate potential due to a decreased store of immediately releasable quanta, repetitive response of the muscle to a single nerve stimulus and refractoriness to anticholinesterase drugs. The findings are explained by a marked decrease of the size of the nerve terminal and by the total absence of AChE from the end-plate.",
author = "Engel, {Andrew G} and Lambert, {E. H.}",
year = "1978",
language = "English (US)",
pages = "469--477",
journal = "Electroencephalography and clinical neurophysiology. Supplement",
issn = "0424-8155",
publisher = "Elsevier BV",
number = "34",

}

TY - JOUR

T1 - Structure-function correlations in myasthenia gravis and a new myasthenic syndrome.

AU - Engel, Andrew G

AU - Lambert, E. H.

PY - 1978

Y1 - 1978

N2 - The physiologic hallmark of MG is the small amplitude of the mepp. This can be correlated with a deficiency of postsynaptic AChR. The AChR deficiency is caused by antiAChR antibodies. Antibody dependent, complement mediated lysis of the postsynaptic membrane contributes significantly to the AChR deficiency. The abundance of immune complexes localized at the end-plate correlates with the amount of AChR remaining at the end-plate and with the mepp amplitude. The physiologic hallmarks of the new myasthenic syndrome are a small quantum content of the end-plate potential due to a decreased store of immediately releasable quanta, repetitive response of the muscle to a single nerve stimulus and refractoriness to anticholinesterase drugs. The findings are explained by a marked decrease of the size of the nerve terminal and by the total absence of AChE from the end-plate.

AB - The physiologic hallmark of MG is the small amplitude of the mepp. This can be correlated with a deficiency of postsynaptic AChR. The AChR deficiency is caused by antiAChR antibodies. Antibody dependent, complement mediated lysis of the postsynaptic membrane contributes significantly to the AChR deficiency. The abundance of immune complexes localized at the end-plate correlates with the amount of AChR remaining at the end-plate and with the mepp amplitude. The physiologic hallmarks of the new myasthenic syndrome are a small quantum content of the end-plate potential due to a decreased store of immediately releasable quanta, repetitive response of the muscle to a single nerve stimulus and refractoriness to anticholinesterase drugs. The findings are explained by a marked decrease of the size of the nerve terminal and by the total absence of AChE from the end-plate.

UR - http://www.scopus.com/inward/record.url?scp=0018244376&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018244376&partnerID=8YFLogxK

M3 - Article

C2 - 220007

AN - SCOPUS:0018244376

SP - 469

EP - 477

JO - Electroencephalography and clinical neurophysiology. Supplement

JF - Electroencephalography and clinical neurophysiology. Supplement

SN - 0424-8155

IS - 34

ER -