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Nodopathy: chronic inflammatory demyelinating polyneuropathy with anti-neurofascin 155 antibodies
  1. Satoshi Kuwabara,
  2. Sonoko Misawa,
  3. Masahiro Mori
  1. Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan
  1. Correspondence to Dr Satoshi Kuwabara, Department of Neurology, Graduate School of Medicine, Chiba University 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan; kuwabara-s{at}

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Anti-neurofascin 155 antibodies cause myelin detachment and ‘nodopathy’ in a subgroup of patients diagnosed with chronic inflammatory demyelinating polyneuropathy

While peripheral neuropathies have conventionally been classified into demyelinating or axonal, recent studies have proposed a novel concept, namely a ‘nodopathy’, whereby microstructural changes restricted to the nodal and paranodal regions may induce significant nerve dysfunction.1 The nodes of Ranvier are the sites where sodium channels are clustered at their highest density and therefore remain the critically important region for the generation of action potentials. At the paranodes, the terminal myelin loops are tightly connected to the axolemma by adhesion molecules, such as contactin-1, contactin-associated protein (Caspr) and neurofascin-155. Detachment of the myelin terminal loops may lead to massive leaks of driving current, with resultant substantial reduction of the safety factor for impulse transmission, and consequent conduction failure.1

The term nodopathy focuses attention to the site of primary nerve damage, and …

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  • Contributors SK and SM wrote the manuscript and MM revised it.

  • Funding This work was supported in part by the Health and Labour Sciences Research Grant on Intractable Diseases (Neuroimmunological Diseases) from the Ministry of Health, Labour and Welfare of Japan.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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