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. 2019 Dec 28;77(13):2497–2506. doi: 10.1007/s00018-019-03431-8

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© The Author(s) 2019

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Clinical implication of inflammatory demyelinating Schwann cells (iDSC) with special references to paranodal and segmental demyelination. Segmental demyelination, which shows slowed conduction velocity and temporal spreading in electrophysiology, depends on the cooperative interaction of macrophage-associated demyelination (MAD) and iDSC. Specific antibodies to nodal/paranodal proteins are associated with paranodal demyelination (nodo/paranodopathy), and it is characterized by reversible conduction failure (RCF) in electrophysiology without MAD-iDSC interaction in pathomechanism. Even though paranodal demyelination is not sufficient for eliciting segmental demyelination, iDSC may provide a turning point of paranodal demyelination becoming segmental demyelination