60th Annual Meeting of the Japanese Society of Neurology

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Symposium

[S-17] Mechanisms of novel pathogenic autoantibodies in chronic immune-mediated neuropathies

Thu. May 23, 2019 3:35 PM - 5:35 PM Room 10 (Osaka International Convention Center 12F Grande Toque)

Chair:Jun-ichi Kira(Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Japan), Masahiro Sonoo(Department of Neurology, Teikyo University School of Medicine, Japan)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.

[S-17-1] Ultrastructure of CIDP: A role of autoantibodies to nodal or paranodal proteins in the pathogenesis

Haruki Koike (Department of Neurology, Nagoya University Graduate School of Medicine, Japan)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.

[S-17-2] Autoantibodies against nodes of Ranvier and paranodes in CIDP

Hidenori Ogata1, Ryo Yamasaki2, Jun-ichi Kira2 (1.Department of neurology, Kyushu University Hospital, Japan, 2.Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.

[S-17-3] The ganglionic AChR antibodies in autoimmune autonomic ganglionopathy

Shunya Nakane1,2, Yukio Ando1 (1.Department of Neurology, Kumamoto University Hospital, Japan, 2.Department of Molecular Neurology and Therapeutics, Kumamoto University Hospital, Japan)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.

[S-17-4] Anti-plexinD1 antibody and painful neuropathy

Takayuki Fujii, Ryo Yamasaki, Jun-ichi Kira (Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Japan)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.