{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T15:29:09Z","timestamp":1787239749547,"version":"build-2736575974"},"reference-count":20,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,10,7]],"date-time":"2004-10-07T00:00:00Z","timestamp":1097107200000},"content-version":"vor","delay-in-days":7403,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1984,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>A term infant required intubation for respiratory depression. Examination revealed hypotonia and areflexia with intact extraocular movements. Electrodiagnostic studies demonstrated defective neuromuscular transmission characterized by borderline low motor evoked amplitudes, profound decremental responses at all stimulation rates, and moderate facilitation (50 to 740%) 15 seconds after 5 seconds of 50 Hz stimulation. Repetitive muscle action potential responses were not recorded following stimulation of nerves by single shocks. Sensory evoked responses and needle electromyographic findings were normal, as were acetylcholine receptor antibody levels. Results of muscle histochemical analyses, including acetylcholinesterase stains, were normal. End\u2010plate histometric analyses demonstrated only a slight reduction in mean synaptic vesicle diameter compared with that in an adult control subject. In vitro muscle contractile properties, stimulating the muscle directly, were normal. Anticholinesterase medications were ineffective. Guanidine produced clinical deterioration. The amplitude of motor evoked responses progressively declined, whereas the percentage of decrement and amount of post\u2010tetanic facilitation increased. Although the nature of the transmission defect was not identified, the data are consistent with abnormal acetylcholine resynthesis, mobilization, or storage without abnormality of release or receptors.<\/jats:p>","DOI":"10.1002\/ana.410160107","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T12:10:45Z","timestamp":1104581445000},"page":"28-34","source":"Crossref","is-referenced-by-count":27,"title":["Abnormal neuromuscular transmission in an infantile myasthenic syndrome"],"prefix":"10.1002","volume":"16","author":[{"given":"James W.","family":"Albers","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John A.","family":"Faulkner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katerina","family":"Dorovini\u2010Zis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kate F.","family":"Barald","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachel E.","family":"Must","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard D.","family":"Ball","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2004,10,7]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3476(75)80651-2"},{"key":"e_1_2_1_3_2","first-page":"222","article-title":"Antiacetylcholine receptor antibodies in neonatal myasthenia gravis","volume":"135","author":"Donaldson JO","year":"1981","journal-title":"Am J Dis Child"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1968.215.3.535"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1965.sp007639"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410010403"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410110603"},{"key":"e_1_2_1_8_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1982.243.1.C66"},{"key":"e_1_2_1_9_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1978.00500260035009"},{"key":"e_1_2_1_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/0014-4886(77)90065-6"},{"key":"e_1_2_1_11_2","first-page":"556","article-title":"A congenital, familial myasthenic syndrome caused by a presynaptic defect of transmitter resynthesis or mobilization","volume":"29","author":"Hart ZH","year":"1979","journal-title":"Neurology (NY)"},{"key":"e_1_2_1_12_2","first-page":"125","article-title":"Studies in neuromuscular function. 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