“Why don’t we take a look?” This question increasingly arises in modern-day neuromuscular clinics and electrodiagnostic laboratories, where neuromuscular ultrasound (NMUS) has become a valuable extension of the clinical examination. NMUS adds diagnostic value in neuromuscular disorders, ^{Reference Gasemaltayeb, Wannarong, Ticku and Preston1} particularly in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), where enlarged nerve cross-sectional area (CSA) is now a supportive diagnostic criterion per the 2021 European Academy of Neurology/Peripheral Nerve Society guideline. ^{Reference Van den Bergh, van Doorn and Hadden2} NMUS assists in distinguishing CIDP from hereditary demyelinating neuropathies and other immune-mediated polyneuropathies, including multifocal motor neuropathy (MMN), by evaluating characteristic nerve CSA patterns. ^{Reference Grimm, Vittore and Schubert3,Reference Kerasnoudis, Pitarokoili, Gold and Yoon4}

In this issue, Niu et al. present a large prospective study comparing NMUS and nerve conduction study (NCS) findings across typical CIDP (n = 117), motor CIDP (n = 15) and MMN (n = 19), ^{Reference Niu, Ding, Hu, Cui and Liu5} adding to the growing body of literature emphasizing ultrasonographic and electrodiagnostic features that aid differentiation. Consistent with prior studies, ^{Reference Grimm, Vittore and Schubert3,Reference Kerasnoudis, Pitarokoili, Gold and Yoon4} they demonstrate greater and more proximal nerve CSA enlargement in CIDP than in MMN, particularly at cervical roots and brachial plexus trunks. The authors also report higher Erb’s point-to-axilla CMAP amplitude ratios in MMN, supporting lesser proximal involvement and aligning with NMUS findings. ^{Reference Niu, Ding, Hu, Cui and Liu5} These findings reflect underlying pathophysiological differences: CIDP features inflammatory segmental demyelination with remyelination and hypertrophic onion bulb formation, as observed on nerve biopsy, ^{Reference Beecher, Howe and Shelly6} while MMN involves antibody-mediated nodal disruption, causing conduction block and multifocal axonal loss without segmental demyelination or hypertrophic onion-bulbs. ^{Reference Beecher, Howe and Shelly6} Interestingly, intranerve CSA variability did not differ between MMN and CIDP, contrasting with prior reports of predominantly focal enlargement in MMN. ^{Reference Grimm, Vittore and Schubert3,Reference Kerasnoudis, Pitarokoili, Gold and Yoon4} This discrepancy may reflect methodological or population differences or disease chronicity.

A notable strength of this study ^{Reference Niu, Ding, Hu, Cui and Liu5} is the inclusion of the motor CIDP subtype, for which NMUS data are limited. Although motor CIDP and MMN are often clinically distinct – typically symmetric proximal/distal weakness in motor CIDP versus asymmetric predominantly distal upper limb weakness in MMN – diagnostic overlap can occur due to shared electrophysiological features and intravenous immunoglobulin responsiveness. The observation of more pronounced proximal nerve enlargement in motor CIDP may aid differentiation in diagnostically ambiguous cases, especially where treatment implications differ (e.g., corticosteroids may worsen MMN).

Lastly, the authors highlight that CSA and motor conduction velocity values across MMN, motor CIDP and typical CIDP form a continuum, potentially reflecting gradations in pathology and immune mechanisms.

While overlapping CSA values preclude using NMUS in isolation for diagnosis, this study underscores the utility of combining NMUS with NCS in assessing immune-mediated neuropathies – tools best interpreted in a clinical context.