Autonomic dysfunction in Lambert-Eaton myasthenic syndrome.
Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder characterized by muscle weakness and autonomic dysfunction. Recent ex vivo and in vitro studies demonstrate that autoantibodies to the P/Q-subtype of voltage-gated calcium channel inhibit transmitter release from parasympathetic, sympathetic, and enteric neurons, a mechanism likely to underlie the widespread autonomic dysfunction in LEMS. This review summarizes clinical studies characterizing the autonomic symptoms and signs in LEMS and the effectiveness of treatment in alleviating these symptoms. Serological assays and in vitro pharmacologic and electrophysiologic studies are also discussed.
Waterman
S A
SA
Department of Immunology, Allergy and Arthritis, Flinders Medical Centre, Bedford Park, South Australia, Australia. Sally.Waterman@flinders.edu.au
D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D015220:Calcium Channels / Q000502:physiology; D002986:Clinical Trials as Topic; D006801:Humans; D015624:Lambert-Eaton Myasthenic Syndrome / Q000378:metabolism / Q000503:physiopathology*
D015220:Calcium Channels