Centrocentral Short Circuiting for Management of Stump Neuroma Pain in Amputees

Abstract

ostamputation pain (PAP) is a common cause of morbidity among amputees and poses challenging management for P the treating physician. Most amputees will suffer some degree of PAP, which often causes further disability owing to inability using the prosthesis. PAP can be categorized according to the basic mechanism and contributing level in the neuraxis with cortical and spinal cord reorganization or peripheral nervous system involvement. Understanding the pathophysiologic basis and appreciating the main etiology responsible for pain is vital to offer the appropriate treatment specifically tailored for each individual. Supratentorial mechanism involves reorganization of the somatosensory cortex of the deafferentated limb, resulting in phantom sensation and phantom limb pain. Reorganization also occurs in the spinal cord where decreased inhibitory impulses from brainstem reticular areas cause increased autonomous activity of the dorsal horn neurons. Peripheral nerve injury and regenerative sprouting result in increased sensory input, which is thought by many investigators to be the predominant mechanism involved in stump neuroma pain, also known as residual limb pain. The biomolecular bases comprise of altered expression of transduction molecules, voltage-sensitive sodium channels up-regulation, potassium channels down-regulation, and misdirected axons, which ultimately increase the afferent input into the central nervous system.