Advances in the Treatment of Myasthenia Gravis

Nils Erik Gilhus


Future Neurology. 2012;7(6):701-708. 

In This Article

Symptomatic Treatment

Acetylcholine esterase inhibition increases the availability of acetylcholine in the neuromuscular synapse and increases the chance of activating AChRs as a response to acetylcholine presynaptic release in MG patients. Thus, acetylcholine esterase inhibitors have a distinct symptomatic effect in most MG patients. The effect tends to be better in AChR antibody-positive patients than in those with MuSK antibodies.[7,20] Pyrodostigmine is the favored drug by most patients.[7] Ambenonium chloride is an alternative, but is not available everywhere. The optimal treatment should balance effect and dose-related side effects, these mainly being caused by cholinergic stimulation in the autonomic nervous system. No long-term negative effect of this cholinergic treatment has been demonstrated.

Drugs increasing acetylcholine release from the presynaptic nerve terminal, such as 3,4-diaminopyridine, are usually much less effective, and they are normally not used for autoimmune MG. They are, however, preferred as symptomatic treatment for Lambert Eaton myasthenic syndrome.[21] Most MG patients use an acetylcholine esterase inhibitor daily, in an individually tailored dose, and with possibilities for dose adjustment and variation according to their physical needs. For the majority, symptomatic treatment alone is not sufficient and should be combined with immunosuppressive therapy.