The effect of pain on training-induced plasticity of the corticomotor system

Pain is thought to interfere with training-induced plasticity of corticomotor pathways. Although this implies direct interference with plastic processes, it may be explained by compromised performance in the training task during pain. Repeated finger movements can induce plasticity and change the amplitude/direction of acceleration of finger movement evoked by transcranial magnetic stimulation (TMS). We hypothesized that if pain interferes with plasticity, acceleration of finger movement would not change when the training task was painful, despite control of training task performance. TMS was applied over the optimal scalp site to evoked index finger abduction movements in nine participants. Participants then trained finger adduction with feedback of finger acceleration for three 8-min sessions, in three conditions on separate days.

Conditions: first dorsal interosseus (FDI) pain and control (no-pain), with injection of 5% and 0.9% hypertonic saline, respectively, into FDI; and remote pain (5% saline injection into infrapatellar fat pad). Peak acceleration of TMS-evoked finger movement and amplitude of motor evoked potentials (MEPs) in FDI were measured at baseline, between training sessions, and at three 5-min intervals after training ceased. Plastic change was observed (reduced TMS evoked peak finger acceleration in the abduction direction) after motor training during control and FDI pain, but not during the remote pain. There was no change in FDI MEPs in any conditions. These data do not support direct effects of nociceptive input (pain) on training-induced plasticity of corticomotor pathways. Remote pain may compromise learning due to distraction from the training task or other complex central pain processes.