We retrospectively reviewed 10 patients with treatment-resistant, relapsing, or atypical immune-mediated neuropathy who underwent nodal/paranodal antibody analysis. Clinical phenotype, cerebrospinal fluid, neuro-imaging, nerve conduction studies, antibody profiles, and treatment response were analysed. Antibody testing included NF140, NF155, NF186, CASPR2, sulfatide IgM, GAD65, and unclassified neuronal antibodies using ELISA.

Immune-mediated neuropathies extend beyond the classical spectrum of GBS and CIDP. Recently, antibodies targeting nodal and paranodal proteins have been recognized as a distinct group of disorders termed autoimmune nodopathies.

We retrospectively reviewed 10 patients with treatment-resistant, relapsing, or atypical immune-mediated neuropathy who underwent nodal/paranodal antibody testing. Clinical phenotype, cerebrospinal fluid, neuro-imaging, serial nerve conduction studies, antibody profiles, and treatment response were analyed. Antibody testing included NF140, NF155, NF186, CASPR2, sulfatide IgM, GAD65, and unclassified neuronal antibodies using ELISA.

Ten patients (mean age 50.4 years; range 29-81 years) with immune-mediated neuropathy were identified. Clinical presentations included acute GBS (n=3), CIDP (n=3), motor-predominant neuropathy mimicking motor neuron disease (n=1), painful small-fiber-predominant neuropathy (n=1), immune-mediated brachial plexopathy (n=1), and GBS-CIDP overlap phenotype (n=1). Nodal/paranodal antibodies were detected in the majority of patients, including neurofascin-155 (n=2), neurofascin-140 (n=2), neurofascin-186 (n=2), and sulfatide IgM (n=2), while two patients demonstrated unclassified neuronal antibodies.

Autoimmune nodopathies can masquerade as peripheral neuropathy. Integrating clinical phenotype, serial electrophysiology, antibody testing, especially in a resistant and atypical presentation may improve diagnostic accuracy.