The motor output is amplified due to the missing limb; therefore, the patient may experience the overflow of information as pain. The patient contains repressed memories from previous motor commands of clenching the hand and sensory information from digging their nails into their palm. These memories remain due to previous neural connections in the brain. Phantom limb syndrome
The term "phantom limb" was coined by physician Silas Weir Mitchell in 1871. For many years, the dominant hypothesis for the cause of phantom limbs was irritation in the peripheral nervous system at the amputation site (neuroma). By the late 1980s, Ronald Melzack had recognized that the peripheral neuroma account could not be correct, because many people born without limbs also experienced phantom limbs. According to Melzack the experience of the body is created by a wide network of interconnecting neural structures, which he called the "neuromatrix".Pons and colleagues (1991) at the National Institutes of Health (NIH) showed that the primary somatosensory cortex in macaque monkeys undergoes substantial reorganization after the loss of sensory input.Hearing about these results, Vilayanur S. Ramachandran hypothesized that phantom limb sensations in humans could be due to reorganization in the human brains somatosensory cortex. Ramachandran and colleagues illustrated this hypothesis by showing that stroking different parts of the face led to perceptions of being touched on different parts of the missing limb. Later brain scans of amputees showed the same kind of cortical reorganization that Pons had observed in monkeys.Maladaptive changes in the cortex may account for some but not all phantom limb pain.
Pain researchers such as Tamar Makin (Oxford) and Marshall Devor (Hebrew University, Jerusalem) argue that phantom limb pain is primarily the result of "junk" inputs from the peripheral nervous system.Despite a great deal of research on the underlying neural mechanisms of phantom limb pain there is still no clear consensus as to its cause. Both the brain and the peripheral nervous system may be involved.Research continues into more precise mechanisms and explanations. Neural mechanisms
Pain, temperature, touch, and pressure information are carried to the central nervous system via the anterolateral system (spinothalamic tracts, spinoreticular tract, spinomesencefalic tract), with pain and temperature information transferred via lateral spinothalamic tracts to the primary sensory cortex, located in the postcentral gyrus in the parietal lobe, where sensory information is represented somatotropically, forming the sensory homunculus.In phantom limb syndrome, there is sensory input indicating pain from a part of the body that is no longer existent. This phenomenon is still not fully understood, but it is hypothesized that it is caused by activation of the somatosensory cortex. Treatment
Most approaches to treatment over the past two decades have not shown consistent symptom improvement. Treatment approaches have included medication such as antidepressants, spinal cord stimulation, vibration therapy, acupuncture, hypnosis, and biofeedback. Reliable evidence is lacking on whether any treatment is more effective than the others. Most treatments are not very effective. Ketamine or morphine may be useful around the time of surgery. Morphine may be helpful for longer periods of time. Evidence for gabapentin is mixed.