Experimental tonic hand pain modulates the corticospinal plasticity induced by a subsequent hand deafferentation

- Hand pain condition the increase in corticospinal excitability induced in forearm muscles by hand deafferentation.
- Pain can modulate the plasticity induced by another event, such as a peripheral lesion.
- This phenomenon could contribute to explain the sensorimotor reorganization often reported in chronic pain populations.

Sensorimotor reorganization is believed to play an important role in the development and maintenance of phantom limb pain, but pain itself might modulate sensorimotor plasticity induced by deafferentation. Clinical and basic research support this idea, as pain prior to amputation increases the risk of developing post-amputation pain. The aim of this study was to examine the influence of experimental tonic cutaneous hand pain on the plasticity induced by temporary ischemic hand deafferentation. Sixteen healthy subjects participated in two experimental sessions (Pain, No Pain) in which transcranial magnetic stimulation was used to assess corticospinal excitability in two forearm muscles (flexor carpi radialis and flexor digitorum superficialis) before (T0, T10, T20, and T40) and after (T60 and T75) inflation of a cuff around the wrist. The cuff was inflated at T45 in both sessions and in the Pain session capsaicin cream was applied on the dorsum of the hand at T5. Corticospinal excitability was significantly greater during the Post-inflation phase (p = 0.002) and increased similarly in both muscles (p = 0.861). Importantly, the excitability increase in the Post-inflation phase was greater for the Pain than the No-Pain condition (p = 0.006). Post-hoc analyses revealed a significant difference between the two conditions during the Post-inflation phase (p = 0.030) but no difference during the Pre-inflation phase (p = 0.601). In other words, the corticospinal facilitation was greater when pain was present prior to cuff inflation. These results indicate that pain can modulate the plasticity induced by another event, and could partially explain the sensorimotor reorganization often reported in chronic pain populations.