@article{oai:nagasaki-u.repo.nii.ac.jp:00002046,
 author = {Motomura, Masakatsu and Nakata, Ruka and Shiraishi, Hirokazu},
 issue = {3},
 journal = {Clinical and Experimental Neuroimmunology},
 month = {Aug},
 note = {Lambert?Eaton myasthenic syndrome (LEMS) is an autoimmune disease of the neuromuscular junction and approximately 60% of LEMS patients have a tumor, mostly small cell lung cancer, as a paraneoplastic neurological syndrome. LEMS patients develop a unique set of clinical characteristics, which include proximal muscle weakness, depressed tendon reflexes with post-tetanic potentiation and autonomic symptoms. Interestingly, slightly <10% of LEMS patients have cerebellar ataxia (LEMS with paraneoplastic cerebellar degeneration). Considering its pathomechanism, LEMS is a presynaptic disorder of neuromuscular transmission in which quantal release of acetylcholine is impaired by autoantibodies for P/Q-type voltage-gated calcium channels at active zones, although an animal model by immunizing purified P/Q-type voltage-gated calcium channels has not yet been successful., Clinical and Experimental Neuroimmunology, 7(3), pp.238-245; 2016},
 pages = {238--245},
 title = {Lambert?Eaton myasthenic syndrome: Clinical review},
 volume = {7},
 year = {2016}
}