Comparative Clinical and Electrophysiological Profiles of Chronic Inflammatory Demyelinating Polyneuropathy in Patients with and without Diabetes Mellitus: An Observational Study

Background: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an immune-mediated, treatable neuropathy with clinical and electrophysiological features that overlap with diabetic polyneuropathy, complicating diagnosis and delaying immunotherapy. This study compared the clinical and electrophysiological characteristics of CIDP in patients with and without diabetes mellitus (DM) to determine whether diabetes modifies disease presentation or severity. Methods: This cross-sectional comparative study was conducted at the National Institute of Neurosciences and Hospital, Dhaka, Bangladesh, from January 2018 to December 2023. Consecutive patients aged ≥ 15 years with CIDP diagnosed per EFNS/PNS 2010 criteria and reclassified using 2021 EAN/PNS guidelines were enrolled and stratified into CIDP+DM and CIDP−DM groups. Clinical data, disability scores (MRCSS, I-RODS, INCAT), and electrophysiological parameters were compared using Mann–Whitney U and chi-square tests. Results: Of 143 patients (21 CIDP+DM; 122 CIDP−DM), those with diabetes were older at symptom onset (median 55 vs 45 years, p = 0.034) and demonstrated significantly greater distal muscle weakness (p = 0.045), though overall disability scores were comparable. Electrophysiological assessment confirmed demyelination in both groups; however, CIDP+DM patients exhibited more pronounced axonal involvement, evidenced by reduced median and ulnar compound muscle action potential amplitudes (p = 0.034– 0.046) and increased tibial F-wave abnormalities (p = 0.042). In age- and sex-adjusted multivariable analyses, diabetes independently modified CIDP by reducing distal muscle power (β = − 1.13; p < 0.001), median CMAP at elbow (β = − 1.32 mV; p = 0.0006), ulnar CMAP at wrist (β = − 1.97 mV; p = 0.0004) and elbow (β = − 1.55 mV; p < 0.001), tibial F-wave presence (β = − 0.46; p = 0.0002), and overall function with lower MRCSS (β = − 3.20; p = 0.04) and higher INCAT scores (β = 1.81; p = 0.004). Conclusion: Diabetes modifies CIDP, producing a mixed demyelinating–axonal phenotype with greater distal motor impairment. Keywords: chronic inflammatory demyelinating polyradiculoneuropathy, diabetes mellitus, electrophysiology, demyelination, axonal neuropathy