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Effect of 3,4‐diaminopyridine on the time course of decay of compound muscle action potential augmentation in the Lambert–Eaton myasthenic syndrome
Author(s) -
Maddison Paul,
NewsomDavis John,
Mills Kerry R.
Publication year - 1998
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199809)21:9<1196::aid-mus11>3.0.co;2-q
Subject(s) - lambert eaton myasthenic syndrome , compound muscle action potential , neuromuscular junction , myasthenia gravis , anesthesia , medicine , electrophysiology , chemistry , neuroscience , psychology
3,4‐Diaminopyridine (3,4‐DAP) is known to be beneficial in the symptomatic treatment of the Lambert–Eaton myasthenic syndrome (LEMS). The effects of 3,4‐DAP on the decay of postexercise augmentation were observed in 6 patients with LEMS. After 10 s maximal voluntary contraction, the amplitude of the compound muscle action potential (CMAP) recorded from abductor digiti minimi decayed exponentially after an initial rise. The rate of decay in CMAP amplitude was increased after treatment with 3,4‐DAP, suggesting that this drug has an effect on the efflux of calcium ions from the presynaptic nerve terminal. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:1196–1198, 1998.