Proprioceptive Feedback from AMI Amputation Modulates Cortical and Subcortical Reorganization

Abstract

Maladaptive cerebral neuroplasticity is a well-established consequence of limb amputation. However, little is known about the potentially causal role of neuromuscular feedback in preserving the cortical and subcortical structures essential for sensation and motor planning, or modulating phantom limb sensation and pain. In this investigation, we study the impact of the agonist-antagonist myoneural interface (AMI) amputation procedure, which preserves proprioceptive neuromuscular feedback, on subcortical and cortical reorganization. We perform neuroimaging on subjects with AMI amputation (AA, n = 10), traditional amputation (TA, n = 10) and no amputation (NA, controls, n = 10). While TAs demonstrate diminished subcortical gray matter volume in the pallidum, accumbens and thalamus (p < 0.05) as compared to NAs, AAs had no significant changes when compared to NAs (p < 0.05). Cortical thickness of Broadmann area 3a and 3b were also significantly increased in TAs, but remained unchanged in AAs, as compared to NAs (p < 0.05). Further, we find phantom limb sensation to be significantly correlated with the reorganization of the accumbens, thalamus, Broadmann area 3a and 3b, suggesting a potential mechanistic linkage to sensorimotor reorganization. The AMI amputation, by preserving afferent proprioceptive feedback, may minimize reorganization and promote conventional sensorimotor neurophysiological pathways.