Lambert‐Eaton Myasthenic Syndrome: A Review

Abstract

Lambert‐Eaton myasthenic syndrome (LEMS) is an auto‐immune disorder caused by neuromuscular transmission failure, and is a representative pre‐neuromuscular junctional disorder. The auto‐immune antibody is anti‐P/Q‐type voltage‐gated calcium channel (P/Q‐type VGCC) antibody detected in approximately 80 to 90% of LEMS patients. Approximately 60% of LEMS patients have small cell lung cancer (SCLC), approximately 10% of patients have other malignant tumors, and the remaining 30% have no malignancy. Thus, the therapeutic strategy for LEMS depends on the presence of a malignant tumor. LEMS with a malignant tumor is also considered to be a representative paraneoplastic neurological syndrome. Recently, new chemotherapeutic drugs for malignant tumors including SCLC have been developed. In cases with no malignancy, several new immune‐mediated therapies have become available. Therefore, we can expect improved therapeutic responses for this disorder.