Narupat Suanprasert1, Bruce V Taylor2, Christopher J Klein3, Matthew M Roforth4, Chafic Karam5, B Mark Keegan6, P James B Dyck7. 1. Peripheral Neuropathy Research Laboratory, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; Department of Neurology, Prasat Neurological Institute, 312 Ratchawithi Rd, Khwaeng Thung Phaya Thai, Khet Ratchathewi, Bangkok 10400, Thailand. 2. Menzies Research Institute Tasmania, University of Tasmania, 17 Liverpool St, Hobart Tasmania 7000, Australia. Electronic address: bruce.taylor@utas.edu.au. 3. Peripheral Neuropathy Research Laboratory, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: klein.christopher@mayo.edu. 4. Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: Roforth.Matthew@mayo.edu. 5. Department of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA. 6. Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: Keegan.BMark@mayo.edu. 7. Peripheral Neuropathy Research Laboratory, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: dyck.pjames@mayo.edu.
Abstract
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.
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.
Authors: Shahar Shelly; Kamal Shouman; Pritikanta Paul; JaNean Engelstad; Kimberly K Amrami; Robert J Spinner; Divyanshu Dubey; Rocio Vazquez Do Campo; Peter J Dyck; Christopher J Klein; P James B Dyck Journal: Neurology Date: 2021-03-02 Impact factor: 9.910
Authors: Michael Auer; Harald Hegen; Anna Hotter; Wolfgang Löscher; Klaus Berek; Anne Zinganell; Elena Fava; Paul Rhomberg; Florian Deisenhammer; Franziska Di Pauli Journal: J Cent Nerv Syst Dis Date: 2022-03-28