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Altogether, these results are consistent with our prior hypothesis66,67 that long-term BMI use is capable of changing the cortical body representation by including either new artificial actuators (robotic limbs or avatar bodies) or even by inducing a reactivation of the representation for paralyzed limbs, in the present case, legs. Therefore, based on these EEG findings, we propose that our long-term BMI-based training triggered a significant process of functional plasticity in S1/M1. Such functional cortical plasticity may have accounted for the re-emergence of lower limb representations in these cortical areas, as documented by the EEG analysis described above and in another study with the same patients50. Such a functional cortical plasticity likely led to the reactivation of upper motor cortical neurons that normally project to the spinal cord, via the corticospinal tract. Given that a small fraction of spinothalamic, vestibulospinal and rubrospinal tract axons may have survived the initial SCI event and remained silent for many years, even in our ASIA A patients, the peculiar motor recovery observed in our study, involving primarily hip extensor and flexor muscles, could be explained by the functional reactivation of these residual axons as a byproduct of plasticity induced by long-term, intensive BMI training (Fig. 5).
Based on our clinical findings, we propose that long-term gait training with a BWS that employs BMI-based robotic actuators, combined with rich tactile feedback, could recruit the activation of CPGs in SCI patients81. Likely, BMI-based training and tactile feedback in a virtual reality environment could also enhance CPG activity by recruiting cortical afferents to influence locomotion control. If some corticospinal or vestibulospinal axons are still intact in a fraction of SCI patients, these locomotion-related signals could reach lower alpha-motor neurons below the level of the SCI. Moreover, by making patients walk routinely upright and against load, peripheral tactile and proprioceptive feedback would be generated and transmitted back to the spinal cord, contributing to the process of spinal cord functional reorganization (Fig. 6B). 2ff7e9595c
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