Differential cortical responses to neuromuscular electrical vs. peripheral magnetic stimulation: a multimodal TMS-fNIRS study.

OBJECTIVE

To investigate cortical modulatory effects of neuromuscular electrical stimulation (NMES) and peripheral magnetic stimulation (PMS) applied to the wrist extensors of healthy adults, using fNIRS as the primary assessment modality.

METHODS

In a randomized crossover design, 15 right-handed adults received NMES and PMS sessions (separated by ≥48 h). Stimulation intensity was functionally calibrated to elicit a matched, maximal painless wrist dorsiflexion. Corticospinal excitability was assessed via motor evoked potentials (MEPs) before and after each intervention. Real-time cortical hemodynamics were monitored with functional near-infrared spectroscopy (fNIRS) during stimulation, quantifying changes in oxygenated ([HbO]) and deoxygenated ([HbR]) hemoglobin concentrations across the sensorimotor (SMC), prefrontal (PFC), and occipital (OC) cortices.

RESULTS

Neither NMES nor PMS induced significant changes in MEP amplitude (NMES: p = 0.674; PMS: p = 0.794). However, fNIRS revealed fundamentally distinct cortical activation patterns during stimulation. NMES was associated with widespread decreases in [HbO] within the PFC, ipsilateral SMC, and OC (p < 0.05). In contrast, PMS elicited focal activation in the contralateral SMC, characterized by a significant increase in [HbO] (ch23: p = 0.005; ch35: p = 0.022) and a concurrent decrease in [HbR] (p < 0.05) compared to the NMES condition. General linear model analysis confirmed more robust contralateral SMC activation during PMS. No significant differences in task-based functional connectivity were observed between the two modalities.

CONCLUSIONS

A single session of NMES and PMS differentially modulates real-time cortical hemodynamics without altering corticospinal excitability. PMS induces focal, excitatory-dominant activation of the contralateral SMC, while NMES evokes a pattern of widespread cortical modulation, reflecting their distinct afferent mechanisms.