The vast amount of research over the past decades has significantly added to our knowledge of phantom limb pain. Multiple factors including site of amputation or presence of preamputation pain have been found to have a positive correlation with the development of phantom limb pain. The paradigms of proposed mechanisms have shifted over the past years from the psychogenic theory to peripheral and central neural changes involving cortical reorganization. More recently, the role of mirror neurons in the brain has been proposed in the generation of phantom pain. A wide variety of treatment approaches have been employed, but mechanism-based specific treatment guidelines are yet to evolve.
The usual pattern of afferent nerve input to the spinal cord is disrupted as a result of severe tissue and neuronal destruction. The proximal part of the severed nerve sprouts to create neuromas after this, a process known as deafferentation . In these neuromas, there is an elevated molecular buildup that promotes sodium channel development, leading to hype-excitability and spontaneous discharges . It is believed that the stump discomfort, including phantom pain, may have its origin in this aberrant peripheral activity . This notion is further supported by studies showing that medicines that block sodium channels reduce phantom pain