Nicole E. Acerra(a,b) and G. Lorimer Moseley(b)
(a) Division of Physiotherapy, The University of Queensland and Department of Physiotherapy, Royal Brisbane and Women’s Hospital, Brisbane
(b) School of Physiotherapy, The University of Sydney, Australia
People with complex regional pain syndrome type 1 (CRPS1) watched a reflected image of their unaffected limb being touched and felt pain or paresthesia at the corresponding site on the affected limb. The authors suggest that allodynia and paresthesia can be mediated by the brain and that dysynchiria has implications for the understanding and management of CRPS1.
From the discussion
…This work has clinical implications for CRPS1 and potentially for other conditions characterized by brain changes. The observation of dysynchiria suggests that allodynia and paresthesia can be mediated
by the brain, which is in contrast to conventional notions that allodynia and paresthesia must reflect state-dependent changes, or breakdown, in peripheral or second-order spinal neurons. That said, the mechanisms by which this might occur are unclear. Possible mechanisms include bilateral projections to sensory cortices, or activation of the “mirror neuron system.” Alternatively, it seems feasible that the same sensitivity changes that are known to occur at, for example, the dorsal horn, also occur in the brain. In that situation, perhaps activity of bimodal visual–somatosensory cells is sufficient to activate pain systems. Further research should elucidate these mechanisms. Finally, the effect of “training the brain” both on the affected limb and on dysynchiria and synchiria suggest that the brain could be a viable target for treatment in other groups characterized by reorganization, pain, and paresthesia, e.g., spinal cord injury and stroke.
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