In this study, Vaso et al performed spinal and intraforaminal blocks with local anesthetic lidocaine in amputees who suffered from PLP3. Immediately after the injection, the ectopic impulse discharge generated from periphery neurons were prevented from feeding upwards3. With no access of those signals in cortex, patients reported reduced or even extinguished painful and nonpainful sensation of the phantom limb3. These results were highly consistent with the hypothesis that instead of brain maladaptation due to loss of sensory input, PLP was primarily driven by abnormal neural activities within DRGs, and thus highlighted PLP as a bottom-up …show more content…
A further examination of these two articles indicated that each study design had its own relative strengths and limitations. Yanagisawa and his colleagues adopted an innovating approach, inducing changes in sensorimotor cortex and altering the cortical presentation of phantom limb with BMI training, which established pathways between brain and external device2. This novel method shed light on future investigation on impacts of neuroplasticity. However, it should be noted that while the effect of cortical plasticity on PLP was carefully studied, the authors failed to take periphery nervous system activity as possible reason of cortical maladaptation, into account. A controversial conclusion might be drawn due to the lack of comprehensiveness. On the other hand, Vaso and his colleagues interpreted the results not only based on their study, but also referred to a thorough comparison between these two alternative hypotheses, which enhanced the reliability of their conclusion3. Nevertheless, in this study, the observations for blacebo controlled trials did not meet the accepted criteria due to practical reasons, which left the effect duration of spinal and intraforaminal blocks an open question awaiting further