Neurophysiological models of phantom limb pain: what can be learnt.

摘要: Phantom Limb Pain (PLP) is a dysesthesic painful sensations perceived in the lost limb, resulting from complex interactions between structural and functional nervous systems changes. We analyze its main pathogenetic models speculate on candidate therapeutic targets. The neuroma model considers PLP to arise spontaneous activity of residual limb injured axons. Other peripheral-origin attribute damage somatosensory receptors or vascular According cortical remapping model, loss bidirectional flow need enhance alternative functions trigger reorganization arm face skin afferents "invade" hand territory. On contrary, persistent representation suggests that continued inputs preserve that, instead shrinkage, associated with larger stronger activity. In neuromatrix mismatch body representation, which remains intact despite amputation, real appearance generates pain. Another hypothesis proprioceptive memories associate specific positions pre-amputation pain may be recalled by those positions. Finally, stochastic entanglement offers direct relationship sensorimotor neural Amputation disrupts motor circuits, allowing for maladaptive wiring circuits causing without nociception. Relief depends solely circuitry engagement, making anthropomorphic visual feedback dispensable. Existing apparently contradicting theories might not mutually exclusive. All them involve several intertwined potential mechanisms replacing amputated an artificial one could counteract PLP.