Neural Plasticity on Body Representations: Advancing Translational Rehabilitation

Copyright © 2016 Naoyuki Takeuchi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Various physical/mental disorders lead to changes in body representation in the brain that could significantly impact the daily life and function. Advances in noninvasive brain imaging technologies have increased our understanding of neural plasticity that induces functional and structural changes in the central nervous system. Although some neural plasticity aids in the acquisition of new skills and compensates for a loss of function in the body, it has been reported that injury and excessive training drive neural plasticity to maladap-tive directions. This neural plasticity is called " maladaptive plasticity " that inhibits complete recovery after injury [1]. This phenomenon is well investigated in body representations after amputation. Maladaptive plasticity after amputation is associated with increased local reorganization within and/or beyond the deafferented sensorimotor cortex [2]. One remote effect of this phenomenon is the reduction of hemispheric asymmetry after amputation, which may reflect the inter-hemispheric imbalance induced by such reorganization of the deafferented sensorimotor cortex and/or use-dependent changes in the overused intact limb representation. Investigating neural plasticity after amputation will help facilitate appropriate selection of brain-targeted interventions and reveal cortical reorganization. As a brain-targeted intervention, noninvasive brain stimulation (NIBS) technique alters human cortex excitability, which might lead to adaptive plasticity after amputation. Previous studies revealed that using excitatory NIBS over the deprived sensorimotor cortex improved the phantom pain that was thought to result from maladaptive plasticity [3]. The underlying mechanism for this improvement involves the antalgic effects of the motor cortex stimulation that follow the restoration of the defective intracortical inhibitory processes that appear to be impaired following amputation. Moreover, it is speculated that the analgesic action of the exitatory NIBS to the deafferented motor cortex may be based on the reinforcement of the phantom limb motor representation. On the other hand, the use of inhibitory NIBS over the contralateral deaffer-ented sensorimotor cortex might be effective in decreasing maladaptive plasticity after amputation since the cortical excitability of this cortex might be high due to the excessive nonamputated limb use. Aside from direct brain stimulation, brain activation feedback might also be effective in correcting maladaptive plasticity and in inducing adaptive plasticity after amputation. Brain-computer interface (BCI) systems record, decode, and translate brain signals for control …