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Anti‐GM 1 antibodies and impaired blood–nerve barrier may interfere with remyelination in multifocal motor neuropathy
Author(s) -
Kaji Ryuji,
Hirota Nobuyuki,
Oka Nobuyuki,
Kohara Nobuo,
Watanabe Tetsuya,
Nishio Takeshi,
Kimura Jun
Publication year - 1994
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880170117
Subject(s) - remyelination , antibody , medicine , motor nerve , multifocal motor neuropathy , lesion , neuroscience , pathology , immunology , anatomy , central nervous system , myelin , biology , mismatch negativity , electroencephalography , psychiatry
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–nerve 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–nerve 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. © 1994 John Wiley & Sons, Inc.