The neurological basis and mechanisms for phantom limb pain are all derived from experimental theories and observations. Little is known about the true mechanism causing phantom pains, and many theories highly overlap. Historically, phantom pains 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 phantom pains, they are not the sole cause. This is because patients with congenital limb deficiency can sometimes, although rarely, experience phantom pains. 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. Although they are highly intertwined, mechanisms are often separated into peripheral, spinal, and central mechanisms.
Various methods have been used to treat phantom limb pain. Some antidepressants or antiepileptics have been shown to have a beneficial effect on reducing phantom limb pain. Tricyclic antidepressants, such as amitriptyline, and sodium channel blockers, mainly carbamazepine, are often used to relieve chronic pain, and recently have been used in an attempt to reduce phantom pains. Pain relief may also be achieved through use of opioids, ketamine, calcitonin, and lidocaine. Often physical methods such as light massage, electrical stimulation, and hot and cold therapy have been used with variable results. Most treatments do not take into account the mechanisms underlying phantom pains, and are therefore ineffective. However, there are a few treatment options that have been shown to alleviate pain in some patients, but these treatment options usually have a success rate less than 30%.
Many researches such as “Factors associated with phantom limb pain: a 31/2-year prospective study.” are in progress and different organizations along with government are encouraging such projects.
The prevalence of phantom pain was 51%, of phantom sensations 76% and of stump pain 49%; 48% of the subjects experienced phantom pain a few times per day or more; 64% experienced moderate to very much suffering from the phantom pain. A significant association was found between phantom pain and phantom sensations (relative risk 11.3) and between phantom pain and stump pain (relative risk 1.9). No other factors associated with phantom pain or phantom sensations could be determined. Only 27% of all potential patients were referred during the first year of the prospective study.