I don't know if anyone has asked this before, or if anyone knows the answer. But I am wondering, MG is caused when the message does not reach the receptors on the muscles.

Some descriptions state that the receptors stop working. If this is the case, is it possible to regenerate those receptors? If not then we are never going to get back to where we were strength wise. I would just like to know, if anyone has any information about this.

It is my understanding that it just blocks the receptors. If you get rid of the antibody, things should go back to normal. I don't know for sure if this is right or if anybody even knows. Good question for sure.

Annie?

My understanding is that the receptors on the muscles that receive the chemical message from the nerves are attacked by T-cells that have been instructed by our immune systems that the receptors are foreign bodies and they must get rid of them. Some of our receptors are destroyed but many more are damaged, but not destroyed. Our bodies cannot regrow new receptors, but they can heal the damaged ones.

This Is exactly the question I asked when, about 5 years into my journey with mg, I realized that my left eyelid which had drooped so badly when I was first diagnosed was doing just fine, but now my right eyelid was drooping badly. How could this be? My internist did some research for me and explained it to me in plain English. My neuro tried, but I just didn't understand his medical mumbo-jumbo. Actually, I think my internist called my neuro (they're friends) and translated it for me.

Hope this helps!

Juanita

Yes, permanent—if there is destruction.

In MG, antibodies attack the muscle receptors. They can block, damage, or destroy them.

http://emedicine.medscape.com/articl...ew#aw2aab6b2b3

http://163.178.103.176/AIBC/Document...ogiadelaMG.pdf

As to whether or not damaged receptors can heal, I have not as yet found a study which confirms that. I'm still looking.

Think of a thousand airline passengers trying to make it through one security checkpoint. That's what our acetylcholine is up against.

Mestinon helps us use the acetylcholine (ACh) longer by blocking the enzyme (acetylcholinesterase) that mops ACh up when it's done making muscle strong. But it does absolutely nothing about the antibody attack.

This is a complex topic, also involving calcium release, muscle fiber size, and so many other details of the neuromuscular junction and muscles.

Scientists can't know for certain how many of our neuromuscular junction muscle receptors are damaged or destroyed. They do guess, though. It might be that those who have more "brittle MG" have more destruction, but, again, only a guessing game.

That's why the clinical presentation is so important in MG. They can't see what our NMJ is up to, but they can see the effects of the antibody attack on our muscles.

What is certain, however, is that the longer you go undiagnosed and untreated, the higher the chance that more of that destruction that can occur.

So the bottom line about your question is that, if you have MG, you need someone to get a grip and help you figure this out!

Hello . . . are there any physicians in the Netherlands who know how to diagnose a patient? Quickly.

Do you know that your country is listed as the fourth happiest in the world? Did they consider healthcare in that equation?


Annie

Annie, thanks as always. Clear answers, if only doctors could learn to do that.

That is what I was understanding from my research.

Yes of course there are, it is just a question of finding them. Well no, it takes time to find them. I am trying to short circuit the Dutch system as much as I can, but it is tough.

I do now have an appointment with a Neuro-ophthalmologist, but it is not until 17 Sept!

So does this permanent damage cause visible atrophy then? I have diffuse mild atrophy.. but it's hard to know if its from the disease process itself, or if it's due to me being unable to condition my muscles and work out like i used to

Hi Bny, that is/was part of my reason for asking the question. Because of the nature of this disease, it is impossible to be be sure. I was wondering whether doing exercises, when possible, would help, but I have already lost so much condition, even if the disease was taken away today, I would be considerably weaker than I was 7 months ago. It would take some time to recover that lost strength. But since it is clear that at least some of that loss is permanent, no matter what, we have to accept that.

But further, I think this point should be made clearer to Doctors, because it does add a small level of urgency to the diagnosis process, since as Annie said, "the longer you go undiagnosed and untreated, the higher the chance that more of that destruction that can occur."

very true!! There was definitely a lack of urgency with my case in the beginning.. it wasn't until it affected my respiratory muscles pretty badly that the sense of urgency on their part happened.. not fun!

Yes, I'm WAY weaker than I was before this all started over 3 years ago, but WAY stronger than I was 2.75 years ago! I used to work out, run, was toned.. haha now... I have to save my muscle strength for the essentials of work, kids and everyday "chores"..not sure I"ll ever get back to being able to work out again.. I can hope!

All we can do is do what we can do.

This Catch-22 disease is a pain. I try to exercise when I can and be as physical as I can, but then MG kicks you a day or two later as well as right afterwards. It's so hard to tell when that will happen. I don't even keep a "schedule."

Atrophy is not good. If you can, be evaluated by a physical therapist to determine how bad it is and what could be done about it.

JJ, doctors should at least be able to communicate ideas to patients. I think they spend so many years sucking in information that they aren't taught how to regurgitate it—in a nice way.

Annie