At the end of the axon, the impulse must be transmitted across the synapse at the myoneural junction. To do this, the electrical impulse stimulates the release of a chemical neurotransmitter, acetylcholine (ACh), which is stored in "presynaptic vesicles" in the terminal end of the axon.
Several theories have been proposed to explain what interferes with the myoneural junction nerve transmission in MG (Barker, 1994; Hickey, 1992; Maehling, 1990).
The symptoms of MG result from the impaired neurotransmission at the myoneural junction and the resulting weakness which may range from mild to severe "paralysis." The symptoms tend to be worse in the evening or after strenuous activity and improve significantly with rest.
ACh is the primary neurotransmitter in this system and since anticholinergic medications are not receptor specific, they "jumpstart" the ACh in the parasympathetic system as a whole as well as at the myoneural junction. Oral atropine may be used to manage these side effects if they become particularly problematic.
The first line of treatment is anti-cholinesterase therapy, which involves administering medications that block the breakdown of acetylcholine in the synapse in the myoneural junctions
. Mestinon (pyridostigmine bromide), Prostigmin (neostigmine), or Mytelase (ambenonium chloride) is commonly given.