Lambert-Eaton myasthenic syndrome

Edward J Dropcho MD (Dr. Dropcho of Indiana University Medical Center has no relevant financial relationships to disclose.)
Originally released October 23, 1997; last updated May 18, 2017; expires May 18, 2020

This article includes discussion of Lambert-Eaton myasthenic syndrome, Lambert-Eaton syndrome, and Eaton-Lambert syndrome. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Lambert-Eaton myasthenic syndrome is distinctive among paraneoplastic disorders in several respects: (1) It is the most common neurologic paraneoplastic disorder in adults, (2) it frequently occurs in patients without a tumor, (3) its autoimmune pathogenesis is solidly established, and (4) most patients show definite neurologic improvement with some combination of tumor treatment, immunosuppression, and agents that facilitate neuromuscular transmission. The author reviews the clinical features, autoimmune etiology, and management of Lambert-Eaton syndrome.

Key points


• Lambert-Eaton myasthenic syndrome is caused by autoantibodies against voltage-gated calcium channels, which inhibit release of acetylcholine at the neuromuscular junction.


• Lambert-Eaton myasthenic syndrome typically presents with fatigue, proximal limb weakness, and diminished muscle stretch reflexes. In some patients the clinical presentation is more complicated.


• At least one half of cases of Lambert-Eaton myasthenic syndrome occur as a paraneoplastic syndrome, almost always in association with small cell lung carcinoma.


• Most patients with Lambert-Eaton myasthenic syndrome show improved strength with successful tumor treatment, agents that facilitate neuromuscular transmission, and immunosuppressive therapy.

Historical note and terminology

Lambert and colleagues were the first to clearly delineate a syndrome of weakness in patients with bronchial carcinoma and its characteristic electrophysiologic abnormalities (Lambert et al 1956).

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