Knowing the basics of neuromuscular transmission and stimulation of muscle movement enables a better understanding of LEMS.



Nerve impulses in the body are electrical and currents that travel down a nerve fibre. When they reach the end of that nerve fibre, they trigger the release of a chemical neurotransmitter such as acetylcholine.
Acetylcholine must cross a tiny gap called the synapse in order to stimulate the muscle to contract. The nerves leading to the synapse or synaptic junction are called the presynaptic nerve.
In LEMS, antibodies stop the nerve releasing enough acetylcholine to get a strong nerve impulse from the nerve to the muscle – there is not enough acetylcholine released.



Treatment options therefore rely on either:
- Reducing the antibodies and therefore get more of the acetylcholine released
- Ensuring that the acetylcholine that is released is used most effectively (stop it being broken down)
- Releasing more acetylcholine into the neuromuscular junction despite the antibodies.

The figure to the right illustrates how this flow of chemicals works at the neuromuscular junction.
In Lambert-Eaton Myasthenic Syndrome, the body's immune system accidentally treats part of the presynaptic nerve as if it was foreign.

The antibodies attach to the Voltage Gated Calcium Channels. This means that the release of acetylcholine into the synapse is compromised, resulting in less acetylcholine being available to stimulate the muscle.

 


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LEMS is estimated to affect 4 to 10 cases per million people, or approximately 2,000 to 4,000 patients in Europe and 1,200 to 3,100 patients in the United States. This is a rare condition.



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