I think I understand that MG responds to mestinon because mestinon provides what our body has destroyed but needs for nerves and muscles to talk but I havent yet been able to understand what the other drugs are for. I have done a lot of reading about MG but havent found anything that goes beyond the basic of that.

Why prednisone, imuran, etc? Are they for side effects, secondary symptons?

Does anyone have link to more in depth info that might give me more insight/understanding of this illness? It is my nature to try to understand things - obviously within the narrow scope of my ability as I am lawyer/accountant by training and sciences were never my strong point, otherwise I would have followed my true love and been veterinarian :-)

Thanks in advance for being such a great helpful (and truly lifesaving) group!

Mestinon does not provide what our body destroys. It delays the acetocholene mop up at the neuro-muscular junction. Prednisone and other steroids are taken because they supress the immune system - this reduces the amount of damage done at the neuro-muscular junction. IVIG and Plasmapheresis are ways to reduce the bad anti-bodies in your system.

This site should give you a good high-level start on what's going on:
http://www.medicinenet.com/myastheni...is/article.htm

The sample pdf from the book you, me an myasthenia gravis has a great explanation of what it is:

http://www.youmeandmg.com/YouMeAndMG-Chapter-1.pdf


Cheers,

Brian

Recently I saw an mg specialist at a local Muscular Dystrophy Association clinic, and he said "Over the next few months if we notice that the mestinon isn't helping enough, we could talk about immunosuppresants". That would be the other group of medications you mentioned.

Btw, the MDA web site has a section on MG, and a great descriptive file as a download there.

Our body actually destroys the junction that connects the nerve to the muscle. Sorry if I get too technical, but the neuron releases neurotransmitters which cause an electrical reaction in the muscle when they reach a certain level (action potential). Our body is missing the junction where these neurotransmitters would latch on and the body mops the excess up pretty quickly. As Brennan said, the Mestinon inhibits the chemical that mops up the excess transmitter. This leaves extra transmitter to connect to the few junctions we have left.

This looks very helpful and as if the information is more practical than clinical

Thanks

My car wouldn't start. It had a good battery. The wires were good. The engine was good. But there was something in the connection. Gunk.

Myesthenia gravis is a disorder in which the receptors for the neurotransmitter are blocked.

So we have the battery -- the nervous impulse and the release of the acetylcholine.

We have the engine -- the muscles.

The acetylcholine just can't attach to the receptor sites on the muscle.

So we lack a connection. There is gunk in the connection. (antibody)

Mestinon causes the acetycholine that is released to stay around longer. This allows the receptor sites that aren't blocked to have a better chance at getting a signal.

Excellent explanation, thanks. I used to have a wave runner I had to maintain myself (once battery problem caused me to stat floating away in the ocean) so I think I understand but now I have to ask wouldnt it make more sense to clean the gunk (can't we attack the antibody?) or is that what the other drugs (prednisone) do?

As a Slashdot user I love car analogies. You just made my day.