Anti‐GM1 antibodies and impaired blood–nerve barrier may interfere with remyelination in multifocal motor neuropathy
- 1 January 1994
- journal article
- review article
- Published by Wiley in Muscle & Nerve
- Vol. 17 (1), 108-110
- https://doi.org/10.1002/mus.880170117
Abstract
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.This publication has 10 references indexed in Scilit:
- Pathological findings at the site of conduction block in multifocal motor neuropathyAnnals of Neurology, 1993
- Patterns of reactivity of human anti‐GM1 antibodies with spinal cord and motor neuronsAnnals of Neurology, 1992
- Multifocal demyelinating motor neuropathyNeurology, 1992
- Inhibition of Schwann cell myelination in vitro by antibody to the L1 adhesion moleculeJournal of Neuroscience, 1990
- A syndrome of asymmetric limb weakness with motor conduction blockNeurology, 1990
- A treatable multifocal motor neuropathy with antibodies to GM1 gangliosideAnnals of Neurology, 1988
- Multifocal acquired demyelinating neuropathy masqurading as motor neuron diseaseMuscle & Nerve, 1988
- Gangliosides of the neuronTrends in Neurosciences, 1985
- Multifocal demyelinating neuropathy with persistent conduction blockNeurology, 1982
- Antiserum‐mediated demyelination: Relationship between remyelination and functional recoveryAnnals of Neurology, 1980