Abstract

MYASTHENIA GRAVIS: CURRENT INSIGHTS INTO PATHOPHYSIOLOGY, DIAGNOSIS, AND TREATMENT APPROACHES

Rupali Pawar*, Prem Pokale, Yash Chavhan, Shailesh Pawar, Anand Kamble, Dr.

Abstract

Skeletal muscle weakness and fatigability fluctuate in myasthenia gravis (MG), an acquired autoimmune neuromuscular condition. The condition is mostly caused by autoantibodies that impede neuromuscular transmission; these antibodies are typically directed against muscle-specific kinase (MuSK) and the acetylcholine receptor (AChR). Clinically, MG manifests as involvement of the eyes, brain, limbs, and respiratory system; the degree of involvement depends on the antibody subtype and immunogenetic background. In terms of pathophysiology, MG is a model autoimmune illness that exhibits postsynaptic membrane injury at the neuromuscular junction, complement activation, and antigenic modulation. Improved serological testing for AChR, MuSK, and LRP4 antibodies, as well as clinical assessment scales and electrophysiological methods like repetitive nerve stimulation and single-fiber electromyography, have all contributed to increased precision in diagnosis. Imaging is essential for identifying thymic disease, especially CT/MRI of the mediastinum. Pulmonary involvement, with immunogenetic background and antibody subtype influencing severity. Beyond traditional immunosuppression and symptomatic cholinesterase inhibitors, therapeutic approaches now include targeted biological medicines such neonatal Fc-receptor (FcRn) blockers and complement inhibitors (eculizumab). For certain people, thymectomy is still a recognized treatment option. Unmet needs still exist despite significant advancements, particularly in the areas of seronegative MG, therapy response variability, biologics access, and long-term illness monitoring. Personalized immunotherapy, biomarker-guided stratification, and enhanced outcome prediction are key areas for future research. All things considered, MG research keeps moving in the direction of safer, more individualized, and more focused management approaches.

Keywords: Myasthenia Gravis (MG), Autoimmune disorder, Neuromuscular junction, Immunotherapy, Complement inhibitors.