{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T14:49:20Z","timestamp":1791902960379,"version":"4.3.4"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"887","license":[{"start":{"date-parts":[[1999,9,1]],"date-time":"1999-09-01T00:00:00Z","timestamp":936144000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1999,9,1]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The Lambert-Eaton myasthenic syndrome is a neuromuscular disorder characterised by defective neurotransmitter release at autonomic neurones and presynaptic terminals of the neuromuscular junction. It is caused by an IgG autoantibody formed against especially the P\/Q type of voltage-gated calcium channels (VGCC) which is an essential component of the mechanism of neurotransmitter release. Many patients have an associated small cell carcinoma of the lung which appears to provide the antigenic stimulus for antibody production, although there is another group with no underlying malignancy. Both groups show an association with immunological disorders. Assay of VGCC antibody titres and electrophysiological tests help to differentiate Lambert-Eaton myasthenic syndrome from other disorders of the neuromuscular junction. Several drugs and therapeutic interventions capable of producing significant clinical improvement are currently available. Patients should also be investigated for underlying tumours, the specific treatment of which can result in remission or amelioration of symptoms.<\/jats:p>","DOI":"10.1136\/pgmj.75.887.516","type":"journal-article","created":{"date-parts":[[2015,2,18]],"date-time":"2015-02-18T00:04:10Z","timestamp":1424217850000},"page":"516-520","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":24,"title":["Lambert-Eaton myasthenic syndrome"],"prefix":"10.1093","volume":"75","author":[{"given":"Udaya","family":"Seneviratne","sequence":"first","affiliation":[{"name":"Department of Neurology, Institute of Neurological Sciences, Southern General Hospital , Glasgow G51 4TF, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajith","family":"de Silva","sequence":"additional","affiliation":[{"name":"Department of Neurology, Essex Centre for Neurological Sciences, Oldchurch Hospital , Romford, Essex RM7 0BE, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[1999,9,1]]},"reference":[{"key":"2023042617064059800_B1","doi-asserted-by":"crossref","first-page":"1291","DOI":"10.1016\/S0140-6736(53)91358-0","article-title":"Bronchial neoplasm with myasthenia: prolonged apnoea after administration of succinylcholine","volume":"2","author":"Anderson","year":"1953","journal-title":"Lancet"},{"key":"2023042617064059800_B2","first-page":"612","article-title":"Defect of neuromuscular conduction associated with malignant neoplasms","volume":"187","author":"Lambert","year":"1956","journal-title":"Am J Physiol"},{"key":"2023042617064059800_B3","doi-asserted-by":"crossref","first-page":"1117","DOI":"10.1001\/jama.1957.02970480021005","article-title":"Electromyography and electrical stimulation of nerves in diseases of the motor unit: observations on a myasthenic syndrome associated with malignant tumours","volume":"163","author":"Eaton","year":"1957","journal-title":"JAMA"},{"key":"2023042617064059800_B4","doi-asserted-by":"crossref","first-page":"577","DOI":"10.1093\/brain\/111.3.577","article-title":"The Lambert-Eaton myasthenic syndrome. 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