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  • Updated 05.18.2017
  • Released 10.23.1997
  • Expires For CME 05.18.2020

Lambert-Eaton myasthenic syndrome

Introduction

Overview

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 (35).

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