A review of the histopathological findings in myasthenia gravis: clues to the pathogenesis of treatment-resistance in extraocular muscles

Pathogenic autoantibodies in myasthenia gravis (MG) target the nicotinic acetylcholine receptor (AChR) or other muscle endplate proteins such as muscle-specific kinase (MuSK) resulting in AChR loss or reduced clustering of AChRs at the endplate, respectively [1]. The first clinical manifestation of MG is often fatigable weakness of the extraocular muscles (EOMs) and /or levator palpebrae superioris resulting in fatigable diplopia and/or ptosis [2]. The disease may progress to involve the limb, bulbar and respiratory muscles resulting in variable weakness, which usually responds to cholinesterase inhibitors (CHEI) and/or immune therapies in cases where patients remain symptomatic on CHEIs.
Source: Neuromuscular Disorders - Category: Neurology Authors: Tags: Review Source Type: research