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bioRxiv · 10.1101/2025.05.09.653032

Pain and touch differentially modulate corticospinal excitability, independent of afferent inhibition

Abstract

Pain can profoundly impact motor functioning to support self-preservation but is also associated with motor and somatosensory disturbances. Despite considerable research exploring the influence of pain and touch on motor and sensorimotor processes, the nature of this relationship remains elusive. Specifically, it is uncertain whether pain and touch modulate motor processes independently of each other or are interconnected. Across two experiments, an afferent inhibition (AI) paradigm was tested to probe the effects of tactile and nociceptive inputs on corticospinal processes and sensorimotor interactions. In Experiment 1 (N=20), the effect of electrocutaneous stimulation duration (0.2 vs. 0.4 ms) on transcranial magnetic stimulation (TMS)-induced corticospinal excitability (CSE) was assessed using a short and long-latency AI paradigm. A single electrocutanous stimulus was delivered to the left index finger before single pulse-TMS over the right-first dorsal interosseous (FDI) motor hotspot at one of five delays (15, 25, 35, 45, 60 or 160 ms). In Experiment 2 (N=20), the same paradigm was used to examine if this effect of sensorimotor interaction is changed when moderate tonic heat pain is delivered to the forearm. Significant AI was observed in both experiments at delays of 25, 35 and 160 ms, with afferent facilitation at 60 ms. This effect was not influenced by the duration of afferent stimulation (Experiment 1) nor by the presence of heat pain (Experiment 2). However, we found a significant reduction in CSE in painful compared to painless conditions, indicating that while tonic pain modulates CSE, tactile afferent inhibition remains unaffected. This supports the notion that pain has a direct (inhibitory) effect on motor output; however, in this context, tactile sensorimotor interactions remain unaltered.

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BibTeXRIS

Gwynne, L., Tame, L.. 2025-05-14. Pain and touch differentially modulate corticospinal excitability, independent of afferent inhibition. https://doi.org/10.1101/2025.05.09.653032

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