The neurological basis and mechanisms for<unk>  limb pain are all derived from experimental theories and observations. Little is known about the true mechanism causing<unk> s, and many theories highly overlap. Historically,<unk> s were thought to originate from neuromas located at the stump tip. Traumatic neuromas, or non-tumor nerve injuries, often arise from surgeries and result from the abnormal growth of injured nerve fibers. Although stump neuromas contribute to<unk> s, they are not the sole cause. This is because patients with congenital limb deficiency can sometimes, although rarely, experience<unk> s. This suggests that there is a central representation of the limb responsible for painful sensations. Currently, theories are based on altered neurological pathways and cortical reorganization. Peripheral mechanisms Neuromas formed from injured nerve endings at the stump site are able to fire abnormal action potentials, and were historically thought to be the main cause of<unk>  limb pain. Although neuromas are able to contribute to<unk> , pain is not completely eliminated when peripheral nerves are treated with conduction blocking agents. Physical stimulation of neuromas can increase C fiber activity, thus increasing<unk> , but pain still persists once the neuromas have ceased firing action potentials. The peripheral nervous system is thought to have at most a modulation effect on<unk>  limb pain. Spinal mechanisms In addition to peripheral mechanisms, spinal mechanisms are thought to have an influencing role in<unk> s. Peripheral nerve injury can lead to the degeneration of C fibers in the dorsal horn of the spinal cord, and terminating A fibers may subsequently branch into the same lamina. If this occurs, A fiber inputs could be reported as noxious stimuli. Substance P, involved in the transmission of pain signals, is usually expressed by Aδ and C fibers, but following peripheral nerve damage, substance P is expressed by Aβ fibers. This leads to hyperexcitability of the spinal cord, which usually occurs only in the presence of noxious stimuli. Because patients with complete spinal cord injury have experienced<unk> s, there must be an underlying central mechanism responsible for the generation of<unk> s. Central mechanisms Under ordinary circumstances, the genetically determined circuitry in the brain remains largely stable throughout life. For much of the twentieth century, it was believed that no new neural circuits could be formed in the adult mammalian brain, but experiments from the 1980s onward cast this into doubt. For instance, functional MRI studies in amputees have shown that almost all patients have experienced motor cortical remapping. The majority of motor reorganization has occurred as a downward shift of the hand area of the cortex onto the area of face representation, especially the lips. Sometimes there is a side shift of the hand motor cortex to the ipsilateral cortex. In patients with<unk>  limb pain, the reorganization was great enough to cause a change in cortical lip representation into the hand areas only during lip movements. It has also been found that there is a high correlation between the magnitude of<unk>  limb pain and the extent to which the shift of the cortical representation of the mouth into the hand area in motor and somatosensory cortical reorganization has occurred. Additionally, as<unk> s in upper extremity amputees increased, there was a higher degree of medial shift of the facial motor representation. There are multiple theories that try to explain how cortical remapping occurs in amputees, but none have been supported to a great extent. The neuromatrix The neuromatrix theory proposes that there is an extensive network connecting the thalamus and the cortex, and the cortex and the limbic system. It is a theory that extends beyond body schema theory and incorporates the conscious awareness of oneself. This theory proposes that conscious awareness and the perception of self are generated in the brain via patterns of input that can be modified by different perceptual inputs. The network is genetically predetermined, and is modified throughout one’s lifetime by various sensory inputs to create a neurosignature. It is the neurosignature of a specific body part that determines how it is consciously perceived. The input systems contributing to the neurosignature are primarily the somatosensory, limbic, and thalamocortical systems. The neuromatrix theory aims to explain how certain activities associated with pain lead to the conscious perception of<unk> . The persistence of the neurosignature, even after limb amputation, may be the cause of<unk>  sensations and pain.<unk>  may arise from abnormal reorganization in the neuromatrix to a pre-existing pain state. Opposition to the neuromatrix theory exists largely because it fails to explain why relief from<unk>  sensations rarely eliminates<unk> s. It also does not address how sensations can spontaneously end and how some amputees do not experience<unk>  sensations at all. In addition, a major limitation of the neuromatrix theory is that it too broadly accounts for various aspects of<unk>  limb perception. It is also likely that it is too difficult to be tested empirically, especially when testing painless<unk>  sensations.
Phantom pain
Neuropathic pain
Allodynia
Visceral pain
Tenderness 
Psychogenic pain
Pain
Radicular pain