A Closer Look At Evolving Treatments For Phantom Limb Pain

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A Primer On The Early Research Into Phantom Limb Pain

Ambroise Paré was a 16th-century French barber, a surgeon who served in the military. Paré documented the pain experienced by amputees who perceived sensation in the “phantom” amputated limb.51 Paré believed that phantom pains occur in the brain and not in the remnants of the limbs.

In 1872, American neurologist S. Weir Mitchell, MD, described a bizarre symptom complex resulting from wounds to peripheral nerves in his book, Injuries of Nerves and Their Consequences. Mitchell saw a large number of patients who had been wounded in the Civil War and suffered from a chronic affliction he called causalgia and coined the term “phantom limb pain,” recording an incidence as high as 90 percent.8,52 The common treatment for causalgia associated with peripheral nerve injury was amputation.

In 1937, Leriche wrote his classic work La Chirurgie de la Douleur, in which he detailed his work on causalgia and phantom limbs.53,54 He acknowledged Mitchell's contribution and looked for ways to solve the problem of pain. Leriche's opportunity to study phantom limb pain came during World War I when he saw many soldiers with peripheral nerve damage.54 He observed vasomotor changes, which suggested to him an abnormality of vascular stimulation. In 1916, he attempted to alleviate the pain through periarterial sympathectomy.54 Leriche also saw patients with painful stumps and phantom limb pain.

W.K. Livingston, MD, had learned at Harvard that pain was a specific response to an unpleasant stimulus, a warning of tissue damage. One of the problems that puzzled him early in his career was visceral pain. Patients might experience no apparent pain from tissue damage to certain internal organs but would report "referred pain" in another part of the body.54 He studied other pain phenomena, such as causalgia and phantom limb pain, which presented similar enigmas.54 During World War II, Livingston was assigned to the Oakland Naval Hospital, where he assumed responsibility for patients with peripheral nerve injury and other difficult pain problems, including causalgia cases.54 Livingston used periarterial sympathectomies, ganglionectomies and novocaine blocks to treat his patients, but he recorded several cases in which the relief was only temporary and the pain returned.54

Robert G. Smith, DPM, MSc, RPh, C.Ped

Given the prevalence of phantom limb pain following amputation, this author explores the pathophysiology of such pain as well as pharmacologic and alternative treatments.

Congenital limb deficiency, cancer, vascular problems and trauma are among the common causes of limb loss. In the United States, an estimated 1.7 million patients have experienced limb amputation and 60 to 80 percent of these patients develop phantom limb pain.1,2

   It is likely that post-amputation pain or phantom limb pain has plagued humans for countless millennia. However, our understanding of post-amputation pain has significantly evolved over the centuries with the full impact beginning to unravel only recently. The risk factors for this condition are unknown but an accurate diagnosis of phantom limb pain is important for appropriate management.3

   Phantom limb pain is a sensation of pain in an absent limb, which patients often describe as burning, throbbing or lancinating. Also, phantom limb sensations are non-painful feelings occurring in absent limbs. In residual limb pain, also known as stump pain, the pain is limited to the remaining stump.3 Since the onset of combat activity in Iraq and Afghanistan, there have been over 1,100 major limb amputations among United States servicemen.4,5 With a sustained military presence in the Middle East, continued severe lower extremity trauma is inevitable.5

   Further, there is a commonly held belief that patients with diabetic amputations experience less phantom limb pain than amputees without diabetes because of the effects of diabetic peripheral neuropathy.6 Clark and colleagues suggest there is no large difference in the prevalence, characteristics or intensity of phantom limb pain when comparing amputation patients with and without diabetes.6 Finally, the prevalence of limb loss is estimated to increase from 1.6 million in 2005 to 3.6 million by 2050.1,7

   For these reason, the podiatric physician would benefit with an understanding of both the pathophysiology of phantom limb pain as well as the treatments to facilitate functional outcomes for these patients.

A Closer Look At The Pathophysiology And Mechanisms Of Phantom Limb Pain

Physicians once thought phantom limb pain to primarily be a psychiatric illness.8 The accumulation of clinical evidence has revealed the etiology of phantom limb pain is actually multifactorial and includes central, peripheral and psychological components.8,9

   We can broadly categorize the pathophysiology underlying phantom phenomena in terms of supraspinal, spinal and peripheral mechanisms.9 However, according to Subedi and Grossberg, none of these proposed theories appear to be able to explain the phenomenon of phantom limb pain independently.8 Further, these investigators assert that many experts believe that multiple mechanisms are likely responsible for phantom limb pain.8 Central neural mechanisms and peripheral mechanisms are among the hypotheses that have gained consensus as proposed mechanisms over recent years.8

   Supraspinal mechanisms related to phantom limb phenomena primarily involve reorganization of the somatosensory cortex surrounding the area representing the differentiated limb. Ramachandran and coworkers demonstrated that brushing the face of upper limb amputees could elicit phantom sensations.10 Additional, they hypothesized that somatosensory cortical reorganization could explain why afferent nociceptive stimulation of a body part whose cortical representation is adjacent to that of the phantom limb can produce sensations in the phantom limb.8,10 Finally, specifically, tactile, proprioceptive and nociceptive input from the face and tissues near the residual limb take over regions of the brain that no longer receive afferent input.8,10

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Bob Smithsays: October 5, 2013 at 10:59 pm

My deep gratitude to Podiatry Today and its staff for publishing this manuscript while I am away.

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DrDpmsays: October 30, 2013 at 1:13 pm

This is an excellent article on the topic of peripheral neuropathy! Phantom limb pain syndrome and residual limb pain syndrome are both variant examples of peripheral neuropathy in the distal lower extremities.

I disagree with this article that stated that people with peripheral neuropathy cannot feel the pain sensations from phantom or residual pain syndromes. Let me elaborate. There are two types of pain: nociceptive pain and neuropathic pain. A patient with diabetic neuropathy and residual pain syndrome (from an amputated toe) will not feel nociceptive pain but will feel neuropathic pain emanating from that amputated toe. Although the patient may feel "numbness," neuropathic pain is still present because the nerve is damaged from resection due to amputation.

I had a patient with diabetic neuropathy in the feet who experiences debilitating lancinating pain from an amputated toe. That agonizing pain flareup is the neuropathic pain, not nociceptive pain.

When it comes to the medical topic of peripheral neuropathy, all physicians, including podiatrists, must distinguish nociceptive pain mechanisms from neuropathic pain mechanisms. This can help improve diagnosis and treatment management.

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