Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8690625 | Pratique Neurologique - FMC | 2018 | 5 Pages |
Abstract
Chronic inflammatory demyelinating polyneuropathies are rare but the most frequent immune-mediated neuropathies. Studies in the five past years led to a better understanding of underlying CIDP pathophysiological mechanisms by showing the existence of autoantibodies directed against cell adhesion molecules in the nodal region: Neurofascin 155, 140 and 186, Contactin 1 and Caspr-1. These molecules are potential targets of autoantibodies leading to the dysfunction of the node of Ranvier. Hence, the concept of nodoparanodopathy has been proposed. These antibodies have to be looked for in a special context of CIDP patients, mainly with a severe and subacute neuropathy refractory to intravenous immunoglobulins.
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Authors
C. Rosier, J.P. Camdessanché,