Abstract
Myasthenia gravis (MG) with antibodies to muscle-specific tyrosine kinase (MuSK) receptors is characterized by prominent weakness of facial and bulbar muscles. MuSK MG often requires aggressive immunosuppression, and inadequate treatment may leave patients with permanent, fixed weakness due to structural changes in the neuromuscular junction. Even with appropriate therapy, only 50% of patients reach minimal manifestations of disease or remission.1
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