Early high‑frequency spinal cord stimulation modulates the ROS/p38 MAPK/NF‑κB and CXCL10/CXCR3 pathways to alleviate neuropathic pain and promote spinal cord injury repair.

A preclinical study published in the International Journal of Molecular Medicine found that early application of high-frequency spinal cord stimulation (SCS) reduced neuropathic pain and supported spinal cord injury repair in animal models. The mechanism appears to involve suppression of the ROS/p38 MAPK/NF-κB inflammatory signaling cascade alongside modulation of the CXCL10/CXCR3 chemokine pathway. These findings suggest a molecular rationale for the therapeutic timing and frequency parameters of SCS in neurorehabilitation contexts.

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