A study recently published in Multiple Sclerosis and Related Disorders has found that neurological disability in multiple sclerosis (MS) is affected by polyneuropathies, which are difficult to diagnosis and are likely underdiagnosed. However, certain polyneuropathies such as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are treatable. CIDP and other inflammatory neuropathies are likely overrepresented in MS, suggesting a shared dysimmune disease development.

This retrospective chart review included 133 cases of comorbid MS and polyneuropathy from the Mayo Clinic between 1980 and 2013. Serum from 3 cases with MS-CIDP and 3 healthy controls was tested for pan immunoglobulin G autoantibodies to neurofascin-155.

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Disease duration, clinical course, treatment and response to treatment, investigation, polyneuropathy and MS type and severity, and demographic characteristics were included in the data recorded from medical records. The Wilcoxon rank sum test or Fisher’s exact test were used to compare CIDP with the immune-mediated or noninflammatory neuropathies groups.

Among the study population, inflammatory neuropathy was present in 21% (n=28) of those with MS (CIDP, n=11; plexopathy, n=5; vasculitis, n=2; monoclonal gammopathy-associated, n=4; other, n=6), diabetic sensorimotor polyneuropathy in 32, inherited neuropathy in 15 (axonal, n=8; demyelinating, n=7), and other diagnosis in 58. Neuropathy presented simultaneously with or after diagnosis of MS in the majority (n=109, 82%) of cases.

Those with MS-CIDP showed decreased or absent ankle reflexes compared with cases of MS and other polyneuropathies (100% vs 70%; P =.04), as well as earlier age of neuropathy identification (52 vs 58 years, P =.048), greater impairment scores on the Neuropathy Impairment Score (22 vs 27 points; P <.003), and greater number of acquired demyelinating electrophysiology features (46% vs 9%; P <.003).

Those with MS-CIDP also presented with more demyelinating features (45.5% vs 7.5%; P <.003), slower conduction velocity (36% vs 11%; P =.04), and longer distal latency (36% vs 10%; P =.03). Among those with MS-CIDP who had available serum, immunoglobulin-G4 autoantibodies to neurofascin-155 were present in one out of three.

Limitations to this study include a retrospective design, a small sample of individuals with MS-CIDP, performance of the study before the McDonald criteria 2017, a lack of population data on polyneuropathy in MS, and underdocumentation of certain individuals with MS with polyneuropathy.

The study researchers conclude that “over-representation of inflammatory neuropathy and CIDP in MS compared to the expected numbers raises the question of a possible shared dysimmune pathogenesis.”

Reference

Suanprasert N, Taylor BV, Klein CJ, et al. Polyneuropathies and chronic inflammatory demyelinating polyradiculoneuropathy in multiple sclerosis [published online February 27, 2019]. Mult Scler Relat Disord. doi: 10.1016/j.msard.2019.02.026