Experimental pain is known to affect neuroplasticity of the motor cortex as well as motor performance, but less is known about neuroplasticity of somatosensory processing in the presence of pain. Early somatosensory evoked potentials (SEPs) provide a mechanism for investigating alterations in sensory processing and sensorimotor integration (SMI). The overall aim of this study was to investigate the interactive effects of acute pain, motor training, and sensorimotor processing. Two groups of twelve participants (N = 24) were randomly assigned to either an intervention (capsaicin cream) or placebo (inert lotion) group. SEP amplitudes were collected by stimulation of the median nerve at baseline, post-application and post-motor training. Participants performed a motor sequence task while reaction time and accuracy data were recorded. The amplitude of the P22-N24 complex was significantly increased following motor training for both groups F(2,23) = 3.533, p < 0.05, while Friedman's test for the P22-N30 complex showed a significant increase in the intervention group [χ(2) (df = 2, p = 0.016) = 8.2], with no significant change in the placebo group. Following motor training, reaction time was significantly decreased for both groups F(1,23) = 59.575, p < 0.01 and overall accuracy differed by group [χ(2) (df = 3, p < 0.001) = 19.86], with post hoc testing indicating that the intervention group improved in accuracy following motor training [χ(2) (df = 1, p = 0.001) = 11.77] while the placebo group had worse accuracy [χ(2) (df = 1, p = 0.006) = 7.67]. The improved performance in the presence of capsaicin provides support for the enhancement of knowledge acquisition with the presence of nontarget stimuli. In addition, the increase in SEP peak amplitudes suggests that early SEP changes are markers of SMI changes accompanying motor training and acute pain.

Recent work demonstrated that capsaicin-induced acute pain improved motor learning performance; however, baseline accuracy was very high, making it impossible to discern the impact of acute pain on motor learning and retention. In addition, the effects of the spatial location of capsaicin application were not explored. Two experiments were conducted to determine the interactive effects of acute pain vs control (experiment 1) and local vs remote acute pain (experiment 2) on motor learning and sensorimotor processing. For both experiments, somatosensory evoked potential (SEP) amplitudes and motor learning acquisition and retention (accuracy and response time) data were collected at baseline, after application, and after motor learning. Experiment 1: N11 (P < 0.05), N13 (P < 0.05), and N30 (P < 0.05) SEP peak amplitudes increased after motor learning in both groups, whereas the N20 SEP peak increased in the control group (P < 0.05). At baseline, the intervention group outperformed the control group in accuracy (P < 0.001). Response time improved after motor learning (P < 0.001) and at retention (P < 0.001). Experiment 2: The P25 SEP peak decreased in the local group after application of capsaicin cream (P < 0.01), whereas the N30 SEP peaks increased after motor learning in both groups (P < 0.05). Accuracy improved in the local group at retention (P < 0.005), and response time improved after motor learning (P < 0.005) and at retention (P < 0.001). This study suggests that acute pain may increase focal attention to the body part used in motor learning, contributing to our understanding of how the location of pain impacts somatosensory processing and the associated motor learning.

Previous work has demonstrated differential changes in early somatosensory evoked potentials (SEPs) when motor learning acquisition occurred in the presence of acute pain; however, the learning task was insufficiently complex to determine how these underlying neurophysiological differences impacted learning acquisition and retention. To address this limitation, we have utilized a complex motor task in conjunction with SEPs. Two groups of 12 participants (n = 24) were randomly assigned to either a capsaicin (capsaicin cream) or a control (inert lotion) group. SEP amplitudes were collected at baseline, after application, and after motor learning acquisition. Participants performed a motor acquisition task followed by a pain-free retention task within 24-48 h. After motor learning acquisition, the amplitude of the N20 SEP peak significantly increased (P < 0.05) and the N24 SEP peak significantly decreased (P < 0.001) for the control group while the N18 SEP peak significantly decreased (P < 0.01) for the capsaicin group. The N30 SEP peak was significantly increased (P < 0.001) after motor learning acquisition for both groups. The P25 SEP peak decreased significantly (P < 0.05) after the application of capsaicin cream. Both groups improved in accuracy after motor learning acquisition (P < 0.001). The capsaicin group outperformed the control group before motor learning acquisition (P < 0.05) and after motor learning acquisition (P < 0.05) and approached significance at retention (P = 0.06). Improved motor learning in the presence of capsaicin provides support for the enhancement of motor learning while in acute pain. In addition, the changes in SEP peak amplitudes suggest that early SEP changes reflect neurophysiological alterations accompanying both motor learning and mild acute pain.

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Prior work showed differential alterations in early somatosensory evoked potentials (SEPs) and improved motor learning while in acute tonic pain. The aim of the current study was to determine the interactive effect of acute tonic pain and early motor learning on corticospinal excitability as measured by transcranial magnetic stimulation (TMS). Two groups of twelve participants (n = 24) were randomly assigned to a control (inert lotion) or capsaicin (capsaicin cream) group. TMS input–output (IO) curves were performed at baseline, post-application, and following motor learning acquisition. Following the application of the creams, participants in both groups completed a motor tracing task (pre-test and an acquisition test) followed by a retention test (completed without capsaicin) within 24–48 h. Following an acquisition phase, there was a significant increase in the slope of the TMS IO curves for the control group (p < 0.05), and no significant change for the capsaicin group (p = 0.57). Both groups improved in accuracy following an acquisition phase (p < 0.001). The capsaicin group outperformed the control group at pre-test (p < 0.005), following an acquisition phase (p < 0.005), and following a retention test (p < 0.005). When data was normalized to the pre-test values, the learning effects were similar for both groups post-acquisition and at retention (p < 0.005), with no interactive effect of group. The acute tonic pain in this study was shown to negate the increase in IO slope observed for the control group despite the fact that motor performance improved similarly to the control group following acquisition and retention. This study highlights the need to better understand the implications of neural changes accompanying early motor learning, particularly while in pain.