The moral of the story

Now if you think that Jo/Bo=nerve cell
Magic paper=Acetyl-choline
Longer lasting magic paper=using mestinon etc.
Ao=acetyl-choline-receptor (AchR)
Co=Calcium signaling
Mo=myosin and the machinery of muscle contraction.
Abducting aliens=anti AchR antibodies
Police investigation=Single Fiber EMG.
Ao. receiving orders= transmission of the electrical signal from the nerve to the muscle at the NMJ.
Sophisticated aliens=anti MuSK (and possibly other not yet recognized Abs.)
Private detective investigations= direct measurement of muscle contraction and fatigability. (not done routinely)
Po=adrenergic receptor.
Bloops=salbutamol etc.

You can ( I hope) understand better the different types of MG.
Why even with severe disease there is normal SFEMG in certain types.
Why mestinon works in an ackward manner in certain types.
And what is the role of salbutamol etc.

The AchR antibodies indeed "abduct" the AchR. They lead to their destruction by an inflammatory process. Those antibodies belong to a sub-type called IgG1 which promote the inflammatory response.

The anti-MuSK antibodies belong to a different sub-type called IgG4. They do not lead to destruction but impair function. That is why there is a very small decrease in the number of AchR, many times they are able to receive the electric stimulation properly (hence a completely normal SFEMG) but they are severely impaired (the exact mechanism is not clear yet) in their ability to transmit this signal in a way that will create a normal muscle contraction.
Giving them more Acetyl-choline may sometimes help, but can also cause them to give signals at the wrong time. Making small parts of the muscle contract in a very inefficient way. This is called "fasiculations".

As opposed to "classical" MG in which the severity of the illness is in direct correlation to the number of preserved AchR, this is not so in MuSK MG, therefore the disease tends to be much less predictable and stable. It also (for the above reasons) has a much less predictable response to medications like mestinon. The same dose can lead to improvement, worsening or do nothing. This (in my opinion) led to the wrong notion of "cholinergic crisis" which many neurologists think doesn't exist. And also to the term "brittle myasthenia" in which patients can go from having too little to having too much mestinon within minutes. (those phenomena were described in the 60s and refuted by many modern neurologists, who gladly attributed this instability to "emotional problems").