Amputation of a body part can result in several forms of disordered sensation. These can be characterized as phantom sensation (nonpainful sensation referred to the amputated limb or body part), stump pain (pain at the amputation site), and phantom pain (pain referred to the amputated limb or body part). Phantom pain is defined as "pain referred to a surgically removed limb or portion thereof" by the International Association for the Study of Pain Task Force on Taxonomy (Merskey & Bogduk, 1994). It is characterized by continuous cramping, aching, burning sensations and painful loss of sensation often described as "pins and needles." It is often associated with stump pain. Prevalence varies, with reports of pain experience in up to 80% of amputees (Warton, Hamann, Wedley, & McColl, 1997). Episodes may last seconds to days and recur from a few times per year to hourly. Further information on the topic can be obtained from a recent review (Nikolajsen & Jensen, 2001).
The mechanism for development of phantom pain is debated, but there is agreement that it is related to pain in the limb prior to amputation, often referred to as "pain memory" (Nikolajsen, Ilkajaer, Kroner, Christensen, & Jensen, 1997). It has been stated in several case reports that the pain may be similar to that experienced several years before the amputation. Indications from the Nikolajsen study are an increased incidence of phantom pain in the first six months following amputation in patients who experienced preoperative pain, compared to those who did not. This correlation no longer existed 2 years following amputation. The authors concluded that there may be a relationship between intensity of preamputation pain and presence of phantom pain, but presence of preamputation pain may not be related to duration or nature of phantom pain.
Painful conditions of a neurogenic nature often present with similar symptoms, but the diversity of etiology of the conditions is too great to permit them to be described in global terms. In an attempt to describe the development of phantom phenomena, Melzack described the concept of a "neuromatrix" (Melzack, 1990). This involves a network of neurons that link different areas of the brain, including the somatosensory cortex, the thalamocortical area, and the limbic system. Input from the periphery and the cortex itself is coprocessed by these areas and shared with other regions of the brain to develop an overall picture of the intact body. Melzack suggested that the neuromatrix may maintain a long-term representation of the amputated limb.
Cortical reorganization has been implicated in the etiology of phantom pain and may help to explain why some patients experience phantom pain while others do not (Bir-baumer et al., 1997). For many years it has been demonstrated in case reports that sensations in the phantom limb can be elicited by stimulating anatomically unrelated areas. For example, touching an area on the face may cause the patient to experience sensation in the phantom finger. This suggests that the cortex is receiving stimuli that, via neuronal reorganization, it perceives to originate in the phantom limb. Advanced neuromagnetic imaging techniques have permitted the demonstration of cortical reorganization in patients experiencing phantom pain. No corresponding cortical reorganization has been demonstrated in amputees not experiencing phantom pain. Cortical reorganization in patients with phantom pain was reversed following the administration of a regional anaesthetic block in those patients whose pain was resolved by the block (Birbaumer et al., 1997). This capacity to reverse cortical reorganization, even after prolonged periods of time, provides hope that effective treatments for phantom pain could be developed. Telescoping, described as the gradual shrinking and eventual disappearance of the phantom limb, has also been described. It is thought that this phenomenon may also be attributed to ongoing cortical reorganization over time.
Phantom limb pain is difficult to manage, with no individual treatment gaining universal acceptance. Treatment approaches for phantom pain include surgery, pharmacological management, physical therapies, and psychological interventions. Surgical procedures that attempt to cut or ablate the pain pathways have little if any benefit. However, surgical implantation of electrodes to stimulate the spinal cord and various parts of the brain may be of value in treating patients with phantom limb pain that is unresponsive to other treatments (Saitoh et al., 2000). Pharmacological management of phantom limb pain can involve drugs from many different classes, such as tricyclic antide-pressants, opioids, benzodiazepines, antiarrythmics, anticonvulsants, antipsychotics, peptides (e.g., calcitonin), and NMDA-receptor antagonists (e.g., ketamine). In all cases, successful management in small-scale studies has been reported. Drug combination therapies are also used. In addition, regional anaesthetic nerve blocks (Birbaumer et al., 1997) and epidural and intrathecal blocks (Omote, Ohmori, Kawamata, Matsumoto, & Namiki, 1995) have been used to manage phantom limb pain. In many cases the effect of regional, epidural, or intrathecal block significantly outlasts the duration of the block, suggesting a long-term modulatory influence on the pain mechanism. One of the most common physical therapy approaches has been use of transcutaneous electrical nerve stimulation (TENS) for symptomatic relief. Acupuncture has also been used. Recent studies have demonstrated that active use of a functional limb prosthesis is effective in reducing phantom limb pain, possibly due to reversal of cortical reorganization resulting from activity of the limb (Weiss, Miltner, Adler, Bruckner, & Taub, 1999). Psychological issues related to loss the of limb, such as grief, may increase pain. Development of effective coping strategies has been shown to reduce pain in small studies (Pucher, Kickinger, & Frischenschlager, 1999).
It is likely that a multifaceted approach to pain management will be most effective, but further research is required to better understand the pain-causing mechanisms and determine effective treatment protocols for this common and difficult clinical problem.
Birbaumer, N., Lutzenberger, W., Montoya, P., Larbig, W., Unertl, K., Topfner, S., et al. (1997). Effects of regional anaesthesia on phantom limb pain are mirrored in changes in cortical reorganisation. Journal of Neuroscience, 17, 5503-5508. Melzack, R. (1990). Phantom limbs and the concept of a neuromatrix. Trends in Neuroscience, 13, 88-92. Merskey, H., & Bogduk, N. (1994). Classification of chronic pain: Descriptions of chronic pain syndromes and definitions of pain terms (2nd ed.). Seattle: International Association for the Study of Pain.
Nikolajsen, L., Ilkajaer, S., Kroner, K., Christensen, J. H., & Jensen, T. S. (1997). The influence of preamputation pain on postamputation stump and phantom pain. Pain, 72, 393-405. Nikolajsen, L., & Jensen, T. S. (2001). Phantom limb pain. British
Journal of Anaesthesiology, 87, 107-116. Omote, K., Ohmori, H., Kawamata, M., Matsumoto, M., & Namiki, A. (1995). Intrathecal buprenorphine in the treatment of phantom limb pain. Anesthesia and Analgesia, 80, 1030-1032. Pucher, I., Kickinger, W., & Frischenschlager, O. (1999). Coping with amputation and phantom limb pain. Journal of Psychosomatic Research, 46, 379-383. Saitoh, Y., Shibata, M., Hirano, S., Hirata, M., Mashimo, T., & Yoshimine, T. (2000). Motor cortex stimulation for central and peripheral deafferentation pain: Report of eight cases. Journal of Neurosurgery, 92, 150-155. Warton, S. W., Hamann, W., Wedley, J. R., & McColl, I. (1997). Phantom pain and sensations among British veteran amputees. British Journal of Anaesthesiology, 78, 652-659. Weiss, T., Miltner, W. H., Adler, T., Bruckner, L., & Taub, E. (1999). Decrease in phantom limb pain associated with prosthesis-induced increased use of an amputation stump in humans. Neuroscience Letters, 272, 131-134.
Heather A. E. Benson
Curtin University of Technology
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