MYASTHENIA: ISSUES OF PATHOGENESIS AND TREATMENT

Abstract

Myasthenia is a chronic autoimmune neuromuscular disease that manifests primarily as muscle weakness and fatigue. The disorder is caused by impaired transmission at the neuromuscular junction, most often due to antibodies directed against acetylcholine receptors (AChR) or muscle-specific kinase (MuSK). The pathogenesis of myasthenia involves complex immune mechanisms, including dysfunction of T-cells, B-cells, and altered cytokine profiles. Treatment has evolved significantly over the past decades, moving from symptomatic relief through acetylcholinesterase inhibitors to immunosuppressive drugs, plasmapheresis, intravenous immunoglobulins (IVIG), and novel biological therapies like monoclonal antibodies. This paper discusses key pathogenetic mechanisms of myasthenia and evaluates current treatment approaches with a focus on their efficacy, safety, and long-term outcomes.