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Polyneuropathies and chronic inflammatory demyelinating polyradiculoneuropathy in multiple sclerosis


Suanprasert, N and Taylor, BV and Klein, CJ and Roforth, MM and Karam, C and Keegan, BM and Dyck, PJB, Polyneuropathies and chronic inflammatory demyelinating polyradiculoneuropathy in multiple sclerosis, Multiple Sclerosis and Related Disorders, 30 pp. 284-290. ISSN 2211-0348 (2019) [Refereed Article]

Copyright Statement

2019 Elsevier B.V. All rights reserved.

DOI: doi:10.1016/j.msard.2019.02.026


Background: Polyneuropathies co-occurring with multiple sclerosis (MS) may be underdiagnosed while causing additional disability burden.

Objective: To determine polyneuropathy presence and type in MS and compare MS with chronic inflammatory demyelinating polyradiculoneuropathy (MS-CIDP) versus MS with other non-inflammatory polyneuropathies.

Methods: Retrospective chart review of Mayo Clinic cases diagnosed with MS and polyneuropathy. Serum from MS-CIDP for pan-IgG autoantibodies to neurofascin-155 were tested when available.

Results: From 1980-2013, 133 co-existing MS/ polyneuropathy cases were identified. Twenty-eight MS patients had inflammatory neuropathy (11 CIDP, 5 plexopathy, 2 vasculitis, 4 monoclonal gammopathy-associated, 6 other), 15 inherited neuropathy (8 axonal, 7 demyelinating), 32 diabetic sensorimotor polyneuropathy, and 58 other. 109 had neuropathy beginning simultaneous to or after MS diagnosis (82%). Compared to MS cases with other polyneuropathy subtypes, MS-CIDP cases had absent or reduced ankle reflexes (100 vs. 70%, p = 0.04), earlier age of neuropathy recognition (52 vs. 58 years, p = 0.048), worse impairment (NIS 27 vs. 22 points, p < 0.03), and more acquired demyelinating electrophysiology features (46% vs. 9%, p < 0.003). Of MS-CIDP cases with available serum, 1-in-3 had IgG4 autoantibodies to neurofascin-155.

Conclusion: (1) Polyneuropathies occurring in MS contribute to neurological disability. (2) Diagnosing polyneuropathies in people with MS is challenging and, likely, under-diagnosed. Recognition is important as some polyneuropathies (e.g., CIDP) are treatable. (3) The probable over-representation of inflammatory neuropathy (especially CIDP) in MS suggests a shared dysimmune pathogenesis, supported by autoantibodies to neurofascin-155.

Item Details

Item Type:Refereed Article
Keywords:chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), multiple sclerosis (MS), neurofascin-155, non-inflammatory polyneuropathy
Research Division:Biomedical and Clinical Sciences
Research Group:Neurosciences
Research Field:Central nervous system
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Taylor, BV (Professor Bruce Taylor)
ID Code:133985
Year Published:2019
Web of Science® Times Cited:6
Deposited By:Menzies Institute for Medical Research
Deposited On:2019-07-18
Last Modified:2022-08-23

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