Abstract
Lambert-Eaton myasthenic syndrome (LEMS) is a rare presynaptic disorder of neuromuscular transmission in which quantal release of acetylcholine (ACh) is impaired, causing a unique set of clinical characteristics, which include proximal muscle weakness, depressed tendon reflexes, posttetanic potentiation, and autonomic changes. [1] The initial presentation can be similar to that of myasthenia gravis (MG), but the progressions of the 2 diseases have some important differences. LEMS disrupts the normally reliable neurotransmission at the neuromuscular junction (NMJ). This disruption is thought to result from an autoantibody-mediated removal of a subset of the P/Q-type Ca2+ channels involved with neurotransmitter release.
Highlights
Lambert-Eaton Myasthenic Syndrome (LEMS) is characterized by weakness and fatigue, especially in the muscles of the legs and arms
LEMS syndrome is an autoimmune disorder of the neuromuscular junction
This is a false connection between the nerve cell and the muscle that leads to the gradual onset of muscle weakness
Summary
LEMS is characterized by weakness and fatigue, especially in the muscles of the legs and arms. 60% of patients with LEMS have SCLC, and the onset of LEMS symptoms often precedes the diagnosis of cancer. LEMS may affect the quality of life of patients, depending on the severity of the symptoms [1].
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