Induction of cortical plasticity reveals the mechanism of the phantom limb pain and develops novel treatment

Objectives. Phantom limb pain is neuropathic pain after amputation of a limb and partial or complete deafferentation such as brachial plexus root avulsion. The underlying cause of this pain has been attributed to maladaptive plasticity of the sensorimotor cortex. It has been suggested that experimental reorganization would affect pain. Here, we tested the hypothesis that a training to use brain–machine interface (BMI) based on magnetoencephalographic (MEG) signals will induce some cortical plasticity in the sensorimotor cortex and modulate the phantom limb pain. Methods. This study included 10 phantom limb patients (9 brachial plexus root avulsion and 1 amputee). MEG signals during movements of the phantom hand or intact hand were used to train the decoder inferring movements of each hand. The robotic hand was controlled by the decoder. Patients controlled the robotic hand by moving the phantom hand. The training effects were compared among trainings with the phantom decoder, real hand decoder, and random decoder in a randomized cross– over trial. Results. BMI training with the phantom decoder increased the decoding accuracy of phantom hand movements and pain. In contrast, BMI training with the intact hand decoder reduced accuracy and pain. Discussion. It was suggested that BMI training to modulate the motor representation of phantom hand controlled pain. The sensorimotor cortical plasticity might induce pain. Symposium 4 : The 39th Annual Meeting of JASP