Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Aug 3;11(8):1035. doi: 10.3390/brainsci11081035

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Pathophysiology of LEMS. In normal conditions, the depolarization of the presynaptic nerve terminal leads to calcium ions influx, acetylcholine (ACh) release, and binding to the ACh receptors (AChR) with a consequent influx of positively charged ions, mainly sodium, generation of an endplate potential (EPP) and muscle contraction. In LEMS, voltage gated calcium channel (VGCC) antibodies block calcium influx causing a reduction of the ACh released at the presynaptic terminal with consequent reduction of the EPP amplitude. High-frequency repetitive nerve stimulation however can increase the EPP amplitude through calcium accumulation in the presynaptic terminal and increased ACh release.