Introduction/Aims: The biological changes in motor neurons and motor axons that correlate with the clinical benefits of nusinersen, an antisense oligonucleotide, in spinal muscular atrophy (SMA) remain poorly understood. This study aimed to investigate changes in axonal excitability and motor unit number estimation (MUNE) parameters following a four‐dose loading regimen of nusinersen in adult SMA patients.Methods: Adult patients with SMA were assessed using the Hammersmith Functional Motor Scale Expanded (HFMSE) and the Medical Research Council (MRC) scale at baseline and after nusinersen treatment. Axonal excitability studies and MScanFit MUNE were conducted in SMA patients before and after treatment. Baseline axonal excitability and MScanFit MUNE parameters in SMA patients were compared with those of a healthy control (HC) group.Results: Compared to the HC group (n = 10), SMA patients (n = 12) exhibited a significantly prolonged strength‐duration time constant (SDTC), a higher resting current/voltage (I/V) slope, and prolonged refractoriness at 2.5 ms. However, no significant changes in axonal excitability parameters were observed following nusinersen treatment. Similarly, there were no significant changes in MUNE or in other parameters, including D50, compound muscle action potentials, and steps%. In contrast, a significant increase in HFMSE and MRC scores was observed after treatment (p < 0.01 and p = 0.01, respectively).Discussion: A prolongation of SDTC, likely due to its effect on sodium channel function, was observed in this study, consistent with existing literature. Despite improvements in motor function, no significant electrophysiological changes were detected in adult SMA patients.

Background: High-resolution ultrasound is increasingly used as a complementary tool in carpal tunnel syndrome (CTS), but the value of median nerve cross-sectional area (CSA) for severity stratification remains uncertain. This study evaluated whether median nerve CSA measured at the pisiform level can distinguish severe from moderate CTS classified according to the Bland grading scale. Methods: This prospective cross-sectional study included 72 participants: moderate CTS (n = 34), severe CTS (n = 24), and healthy controls (n = 14). Nerve conduction studies, abductor pollicis brevis needle electromyography, and ultrasound examinations were performed on the same day. CSA was measured three times by a blinded examiner, and the mean value was used for analysis. Correlation, age-adjusted linear regression, and receiver operating characteristic curve analyses were performed. Results: Median nerve CSA increased progressively from controls to moderate and severe CTS groups (8.0 ± 1.1, 16.5 ± 4.6, and 19.8 ± 3.4 mm², respectively; p < 0.001), with significant pairwise differences. Intraobserver and interobserver reliability were excellent (ICC = 0.95 and 0.91, respectively). CSA correlated positively with distal motor and sensory latencies and inversely with compound muscle action potential and sensory nerve action potential amplitudes. CSA also showed a weak positive association with neurogenic motor unit action potentials. In age-adjusted regression analysis, distal motor latency remained independently associated with CSA (B = 0.873, p = 0.002). A CSA cut-off of 18.5 mm² distinguished severe from moderate CTS with an area under the curve (AUC) of 0.728, sensitivity of 66.67%, and specificity of 79.41%. Conclusions: Median nerve CSA measured at the pisiform level may provide useful adjunctive structural information for CTS severity assessment and may show moderate discriminatory performance for differentiating severe from moderate CTS. CSA should be interpreted in conjunction with clinical and electrodiagnostic findings rather than as a stand-alone severity marker.