Pain suppresses corticospinal excitability, independent of tactile afferent inhibition

Pain can profoundly impact motor functioning to support self-preservation, yet its influence on the interaction between tactile input and corticospinal excitability (CSE) remains unclear. Across two experiments, a short- and long-latency afferent inhibition (AI) paradigm examined (i) whether tactile AI is modulated in the presence of tonic pain and (ii) the effect of pain on CSE in the presence of tactile afferent stimulation. In experiment 1, a single electrotactile stimulus (0.2- or 0.4-ms duration) was delivered to the index finger at one of six intervals (15 to 160 ms) before transcranial magnetic stimulation (TMS) over the ipsilateral first dorsal interosseous (FDI) hotspot. In experiment 2, the same procedure was tested during moderate, tonic forearm heat pain. Both experiments showed significant AI at 25, 35, and 160 ms delays, with facilitation at 60 ms. This effect was not influenced by the duration of afferent stimulation (experiment 1) nor by tonic heat pain (experiment 2). However, CSE was significantly reduced in painful compared to painless conditions (P = 0.021, η2p = 0.132), indicating that while tonic pain modulates CSE, tactile afferent inhibition is unaffected. These findings show an inhibitory effect of pain on motor output that, in this context, occurs alongside preserved tactile-motor interactions.