Stimulation of a motor neuron causes it to release acetylcholine, which is stored up in vesicles at the axon terminal. The acetylcholine binds to nicotinic receptors on the muscle fiber, which open sodium channels and depolarizes the muscle cell. As nerve stimulation is rapidly repeated, the acetylcholine stored in the nerve terminal is gradually depleted, and there is a slight weakening of the acetylcholine signal sent to the muscle fiber, resulting in smaller endplate potentials (EPPs). In normal muscle, although the EPPs become smaller with<unk>  stimulation, they remain above the threshold needed to trigger muscle contraction. In myasthenia gravis, where many of the acetylcholine receptors are blocked, the EPP may exceed the threshold initially, but quickly falls below threshold with<unk>  stimulation, resulting in the muscle fiber failing to contract. As one by one the muscle fibers fail to contract, the overall CMAP measured grows smaller and smaller, leading to the pathologic decremental response.
Repetitive nerve stimulation
Electrical muscle stimulation
Transcutaneous electrical nerve stimulation
Cortical stimulation mapping
Electromyography
Electroneuronography
Nerve block
Percutaneous tibial nerve stimulation