Eric H Denys1, Vanda A Lennon. 1. Department of Neurosciences, California Pacific Medical Center, San Francisco, California, USA.
Abstract
INTRODUCTION: All descriptions of the Lambert-Eaton syndrome are based on symptomatic patients. We incidentally encountered electromyographic evidence of this syndrome in a patient being studied for another reason. The patient had controlled hypothyroidism and smoked for 9 pack-years but never had symptoms of weakness or had evidence of cancer. METHODS: Detailed electrophysiological and serological evaluations were undertaken in this study. RESULTS: Neuromuscular transmission tests were consistent with a presynaptic disorder. Autoantibodies specific for P/Q-type voltage-gated calcium channels (VGCC) were detected in the serum and persisted throughout 7 years of follow-up. Multiple IgG markers of thyrogastric autoimmunity also were detected. CONCLUSIONS: This demonstration of asymptomatic Lambert-Eaton syndrome persisting for 8 years provided novel insight into the natural history of the disorder. It is plausible that patients with a subclinical syndrome would have abrupt neuromuscular decompensation when challenged with medications that compromise the safety factor for synaptic transmission.
INTRODUCTION: All descriptions of the Lambert-Eaton syndrome are based on symptomatic patients. We incidentally encountered electromyographic evidence of this syndrome in a patient being studied for another reason. The patient had controlled hypothyroidism and smoked for 9 pack-years but never had symptoms of weakness or had evidence of cancer. METHODS: Detailed electrophysiological and serological evaluations were undertaken in this study. RESULTS: Neuromuscular transmission tests were consistent with a presynaptic disorder. Autoantibodies specific for P/Q-type voltage-gated calcium channels (VGCC) were detected in the serum and persisted throughout 7 years of follow-up. Multiple IgG markers of thyrogastric autoimmunity also were detected. CONCLUSIONS: This demonstration of asymptomatic Lambert-Eaton syndrome persisting for 8 years provided novel insight into the natural history of the disorder. It is plausible that patients with a subclinical syndrome would have abrupt neuromuscular decompensation when challenged with medications that compromise the safety factor for synaptic transmission.