{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T20:28:05Z","timestamp":1761596885997},"reference-count":16,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,10,13]],"date-time":"2004-10-13T00:00:00Z","timestamp":1097625600000},"content-version":"vor","delay-in-days":3938,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[1994,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Multifocal motor neuropathy has pure motor manifestation and nonremittent clinical courses. Antiganglioside antibodies, though variable in titers, are characteristically elevated in the majority of these patient. In our cases, pathological findings at the site of conduction block suggested impaired remyelination and disruption of blood\u2013nerve barrier. These findings lead us to postulate that antibodies toward gangliosides or toward unknown antigens containing gangliosides initiate motorspecific demyelination. The lesion, once produced, may persist as a result of impaired remyelination caused by disrupted blood\u2013nerve barrier. The antibodies bound to denuded axons may also interfere with a remyelinative process. If so, antibodies may not always be circulating, thus accounting for variable levels of titers. \u00a9 1994 John Wiley &amp; Sons, Inc.<\/jats:p>","DOI":"10.1002\/mus.880170117","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T08:23:10Z","timestamp":1104567790000},"page":"108-110","source":"Crossref","is-referenced-by-count":34,"title":["Anti\u2010GM<sub>1<\/sub> antibodies and impaired blood\u2013nerve barrier may interfere with remyelination in multifocal motor neuropathy"],"prefix":"10.1002","volume":"17","author":[{"given":"Ryuji","family":"Kaji","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nobuyuki","family":"Hirota","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nobuyuki","family":"Oka","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nobuo","family":"Kohara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuya","family":"Watanabe","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takeshi","family":"Nishio","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jun","family":"Kimura","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2004,10,13]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410320402"},{"key":"e_1_2_1_3_2","first-page":"139","volume-title":"Anatomy","author":"Gardner E","year":"1969"},{"key":"e_1_2_1_4_2","first-page":"1042","volume-title":"Textbook of Neuropathology","author":"Johnson PC","year":"1991"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410330204"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.42.3.506"},{"key":"e_1_2_1_7_2","unstructured":"KornbergAJ PestronkA:The clinical and diagnostic role of anti\u2010GM1antibody testing. 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