Abstract
Lyme disease, caused by Borrelia burgdorferi, is a multisystem infection that rarely produces neuromuscular complications beyond classic neuroborreliosis. Myasthenia gravis (MG) is an autoimmune disorder characterized by fatigable weakness due to acetylcholine receptor (AChR) antibodies. We describe a 74-year-old man with coronary artery disease, chronic kidney disease, and prostate cancer who developed progressive dysphagia, dysphonia, ptosis, and neck weakness. Initial attribution to medication-related angioedema delayed recognition. Neurological examination revealed bulbar weakness and fatigable ptosis. Electrodiagnostic testing confirmed post-synaptic neuromuscular junction dysfunction, and AChR antibody assays were strongly positive across binding, blocking, and modulating subtypes. Concurrent Lyme serologies were positive for immunoglobulin G and immunoglobulin M. The patient required intensive care monitoring and was treated with plasma exchange, intravenous ceftriaxone, prednisone, and pyridostigmine, with marked improvement. This case illustrates a rare coexistence of neuroborreliosis and seropositive MG, highlighting potential molecular mimicry between Borrelia antigens and AChR epitopes.