Lambert-eaton syndrome

R. M. Pascuzzi, Y. I. Kim

Research output: Contribution to journalReview article

9 Scopus citations

Abstract

LES is an autoimmune disorder of the neuromuscular junction in which autoantibodies directed against voltage-dependent Ca2+ channels block nerve-evoked Ca2+ entry at the motor nerve terminal. The pathogenic IgG is likely to produce a similar inhibitory effect on the Ca2+ channel function in other cholinergic synapses of the autonomic nervous system. This pathophysiology is sufficient to account for the distinctive clinical, immunologic, and electrophysiologic manifestations in patients with LES. Etiology of this disease is uncertain but in view of its frequent association with small cell lung cancer, this specific type of neoplasm may be implicated in the initiation of auto-immune response. Recent studies indeed support the possibility that the antigenic stimulus in the neoplastic form of LES may arise from voltage-dependent Ca2+ channels found in the lung cancer cells.

Original languageEnglish (US)
Pages (from-to)35-41
Number of pages7
JournalSeminars in Neurology
Volume10
Issue number1
DOIs
StatePublished - Jan 1 1990

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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