Annie,
At least from my experience (regarding myself and other patients) when neurologists have to pull their patients out of crisis, it is either because they or the patient (or many times both) neglected to recognize earlier signs of it.
I agree that when you don't know much about the illness (in the early days) and have a neurologist with a similar level of knowledge the risk of this happening is quite significant. ( I can sadly attest to that from my own experience).
Like you yourself say
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I had gotten weak so slowly that I didn't notice the degree of weakness.
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. You only recognized it when you reached dangerous levels which could not properly sustain the basic needs of life.
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Alice, I have to disagree about having "signs" before any MG crisis.
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Mestinon works on the AchE not only in the NMJ (nicotinic recpetors) but also in the autonomic nervous system (muscarinic receptors). Activation of the muscarinic receptors leads to GI symptoms, hpersalivation etc. Those would be evident long before you have reached levels that can lead to muscle paralysis.
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I'm confused by what you're saying here. Mestinon keeps AChE away and from mopping up ACh so that we can use what we have longer. Since our antibodies destroy our muscle receptors, how could Mestinon recruit more of them? I just want to clarify what you mean by that.
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I will try and explain. In normal muscle function we use only a small portion of the muscle's ability. We have a lot of AchR which are not activated. (this I believe is called "the safety margin"). Even with normal maximal activity we don't use all our muscle's potential. That's why normal people can do the same action many times without overt fatigue of their muscles.
If we have say half of the amount of AchR we have less "safety margin" but we still use the same proportion of the muscle's ability. Taking mestinon, leads to recruiting a larger proportion of those recpetors which leads to better muscle force at the price of decreasing the "safety margin" even further.
The picture becomes even more complicated if the problem is not with the AchR itself, but a further step in muscle contraction. In that case recruiting more AchR and more muscle fibers can lead to a rapid depletion of the ability of that downstream protein.
That is a possible reason why some patients with MuSK MG/seronegative MG have worsening of their symptoms with mestinon instead of doing better.
This is also why ( I believe) they can have significant improvement followed by rapid deterioration. (or what Osserman called "brittle myasthenia" in which the patient would rapidly go from "myasthenic crisis" to "cholinergic crisis").
Regardless of the possible explanations, I fully agree with you that patients with MG (and even more so in the early days of their illness, when they have not yet learned to recognize the pattern of their specific illness) should err on the side of caution.