Myasthenia Gravis (gMG)

MG is complex. A neuromuscular specialist or academic MG center will have experience with the full treatment range. The MGFA (myasthenia.org) maintains a provider directory.

Test for both AChR and MuSK antibodies. If both are negative and MG is still suspected, get LRP4 antibody testing. Your antibody status determines which treatments are most appropriate.

Go to the ER immediately if you have worsening shortness of breath, inability to clear secretions, or rapidly worsening weakness — this is a medical emergency.

Myasthenia gravis (MG) is an autoimmune disease where the immune system attacks the neuromuscular junction — the connection between nerve cells and muscles. The most common antibodies target acetylcholine receptors (AChR), disrupting nerve-to-muscle signal transmission and causing fluctuating muscle weakness.

Hallmark symptoms include: ptosis (drooping eyelids), diplopia (double vision), dysarthria (slurred speech), dysphagia (difficulty swallowing), proximal limb weakness, and breathing difficulties in severe cases. Symptoms worsen with activity and improve with rest — this fluctuating pattern is distinctive of MG.

FcRn inhibitors (Vyvgart, Rystiggo) block the receptor that recycles IgG antibodies, accelerating degradation of pathogenic antibodies causing MG. Complement inhibitors (Ultomiris) block complement cascade activation at the neuromuscular junction. FcRn inhibitors work faster and are useful across multiple antibody subtypes.