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  • Updated 08.23.2021
  • Released 10.23.1997
  • Expires For CME 08.23.2024

Lambert-Eaton myasthenic syndrome

Introduction

Overview

Lambert-Eaton myasthenic syndrome is an autoimmune neurologic disorder characterized by dysfunction at the level of the neuromuscular junction. The unique constellation of symptoms distinctive among paraneoplastic disorders include proximal muscle weakness, autonomic dysfunction with xerostomia, and postexertional facilitation primarily in the context of small cell lung cancer, in 50% of cases. The authors review the clinical features, autoimmune etiology, and management of Lambert-Eaton myasthenic syndrome.

Key points

Lambert-Eaton myasthenic syndrome is a disorder of decreased release of acetylcholine from the presynaptic nerve terminals and is believed to be due to autoantibodies against voltage-gated calcium channels.

Lambert-Eaton myasthenic syndrome typically presents with a myopathy-like picture with proximal limb weakness, occasional ptosis, and diminished muscle stretch reflexes but is uniquely characterized by postexertion or postactivation facilitation and a transient improvement in deep tendon reflexes as a result.

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, in conjunction with Eaton, was the first to clearly delineate a syndrome of weakness in patients with bronchiogenic carcinoma and its characteristic electrophysiologic abnormalities.

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