Phantom-Limb Pain: Causes and Treatment Options
2014, Vol. 6 No. 11 | pg. 1/2 | »
IN THIS ARTICLE
Phantom-limb pain (PLP) is a frequent consequence of amputation which has been reported to affect up to 80% of patients who have suffered an extremity loss (Flor 2002: 182; Nikolajsen and Jensen 2001: 107). Cases of phantom-limb pain have also been found and studied among patients with congenital limb deficiency (Melzack et al. 1997).
Knowledge of phantom-limb sensations has been developing for centuries, but medical practitioners, for obvious reasons, have mostly been interested in investigating the issue of painful sensory experiences connected with phantom limbs with the aim of finding optimal treatment solutions to the problem. The term itself was coined by Silas Weir Mitchell in 1872 (Flor 2002: 182; Subedi and Grossberg 2011: 1) and early studies of phantom-limb pain focused on the psychological aspects of the problem, since it was believed that such experiences must have their origin in a patient’s mind.Relatively recent advancements in medical technology, including the development of advanced neuroimaging techniques, have contributed to an improved understanding of the phenomenon (Knotkova et al. 2012: 40). Now it is known that practically every patient who has suffered an extremity loss experiences some sort of phantom sensation (Nikolajsen and Jensen 2001: 107).
Wounded Warriors participate in the 2012 Army Ten Miler, Oct. 21, 2012 in Washington, D.C. Photo: U.S. Army photo by Staff Sgt. Teddy Wade CC-2
Historically, research into phantom-limb pain gained momentum after the tragic experience of World War I, which left many veterans disabled by a limb loss. Unfortunately, traumatic amputation rates remained high due to later military actions during World War II, the Vietnam War, and the recent conflicts in Iraq and Afghanistan. Fortunately, the intense investigation of phantom-limb-related phenomena has resulted in a good understanding of the causes and has led to the development of a wealth of possible treatment methods.
Practically every patient who has suffered an extremity loss experiences some sort of phantom sensation.
Recent research has focused on the central and peripheral nervous systems as primary venues responsible for the sensory experience of pain in phantom limbs. The aspect that has received much attention concerns the changes that affect the brain’s somatosensory cortex following limb amputation. It has been found that the magnitude of perceived phantom-limb pain and the amount of cortical reorganization are positively correlated (Flor et al. 1995: 482).
In the case of the peripheral nerves, the formation of abnormally active neuromas in the proximity of the area where a nerve has been severed is the likely contributor to the sensation of phantom-limb pain. The multiplicity of potential factors influencing the experience of phantom-limb pain is also reflected in a great number of treatment methods. Steps that can be taken in order to treat patients with phantom-limb pain can be grouped into three categories that include pharmacological treatment, non-invasive non-pharmacological treatment and invasive treatment (Knotkova et al. 2012: 40).
1: Major Causes of Phantom-Limb Pain
Since the beginning of systematic research into phantom phenomena, with a particular emphasis on phantom-limb pain, scholars and practitioners have been trying to identify the primary agents of painful sensations in phantom extremities. Here, it is significant not to confuse phantom-limb pain with other phenomena related to amputation, which may include both painful and non-painful experiences such as stump pain or telescoping (i.e. an impression of the phantom limb retracting towards the stump) (Knotkova et al. 2012: 39).
Phantom-limb pain is usually described as burning, stabbing, throbbing, cramping or squeezing (Flor 2002: 182; Nikolajsen and Jensen 2001: 108). Researchers have identified a number of factors having a modulatory effect on the probability of the occurrence of phantom-limb pain. Among the best documented variables which can contribute to the development of phantom-limb pain sensations are the amputation site, pre-amputation pain, residual limb pain, time after amputation, sex, as well as conditions of psychological nature like stress and depression (Knotkova et al. 2012: 39; Subedi and Grossberg 2011: 1).
However, it is extremely important to emphasize that the above factors cannot be regarded as direct causes of phantom-limb pain, but rather as variables correlated with the presence of phantom-limb pain. In search of the direct causes of painful sensations related to phantom limbs, most researchers seem to focus on three aspects. According to Flor (2002: 182), “[c]entral changes seem to be a major determinant of phantom-limb pain; however, peripheral and psychological factors may contribute to it.” This implies that the most likely source of phantom-limb pain is the central nervous system, i.e., the brain. Subedi and Grossberg (2011: 1) observed that “[t]he paradigms of proposed mechanisms have shifted over the past years from the psychogenic theory to peripheral and central neural changes (…).” Converging with the latter approach, this section describes two major causes of phantom-limb pain based on changes in peripheral and central nervous systems.
1.1. Formation of Neuromas in Proximal Portions of Severed Nerves (Peripheral Neural Changes)
Amputation of a limb means also cutting a peripheral nerve. In the face of damage, various systems of our body try to regenerate; this is also the case with nerves. However, with respect to this particular system, the process of reconstruction is relatively ineffective. The physical impossibility of regeneration (i.e. lack of a limb, in which the severed nerve could be recreated) complicates it further. After a peripheral nerve is cut during amputation, the portion of the nerve proximal to the cut site sprouts and the formation of neuromas is observed. This could be seen as a failed attempt to regenerate.
Such neuromas are characterized by abnormal firing patterns, which can be both spontaneous and mechanically or chemically evoked. This translates to increased activity in sodium channels (Flor 2002: 184-185; Nikolajsen and Jensen 2001: 110; Subedi and Grossberg 2011: 2). Flor (2002: 184-185) claims that such abnormalities have been viewed as a significant source of phantom-limb pain. The support for this idea comes from “the moderately high correlation between residual-limb and Phantom-limb pain” (Flor 2002: 184-185). However, this explanation cannot account for all cases of phantom-limb pain experiences by amputees. Flor (2002: 185) makes a further notice that many patients have phantom-limb pain sensations immediately following the operation, i.e. long before neuromas could have formed.
An even more obvious observation is made by Ramachandran and Hirstein (1998: 1604), who say phantom-limb pain in patients with congenital limb deficiency cannot be due to neuromas. Nevertheless, a great number of phantom-limb pain cases can be attributed to the process described above, and for this reason, it should be approached as one of the most significant determinants of Phantom-limb pain.
1.2. Post-Amputation Cortical Reorganization (Central Neural Changes)
Research into the central nervous system (not only human) has shown that changes in the peripheral nerves stimulate alternations in the central cortical networks. As has been shown in adult monkeys, the somatosensory cortex exhibits considerable plasticity following amputation. This finding has suggested that cortical reorganization might have an adaptive function and phantom phenomena could be a side effect of the process (Flor et al. 1995: 482).
The cortical reorganization, which is manifested in the “remodelling of the functional architecture of the cortex in response to nervous-system damage,” can be seen as an adaptive mechanism in that it is meant to compensate for the loss of afferent input, thus preparing the ground for potential restoration of function. However, this process in patients with phantom-limb pain seems to be maladaptive (Flor et al. 1995: 483-484). The cortical reorganization causes the areas adjacent to the one which was responsible for the amputated limb to take it over. This applies to both the motor and the primary somatosensory cortex (Subedi and Grossberg 2011: 2).
Further research found a positive correlation between chronic back pain and the magnitude of cortical reorganization. It has been hypothesized that changes in the cortical architecture after amputation can also account for the occurrence of phantom-limb pain (Flor et al. 1995: 482). And in fact, empirical investigation of the idea showed that there is a clear link. Flor et al. (1995: 482) “report a very strong direct relationship (r = 0.93) between the amount of cortical reorganization and the magnitude of phantom limb pain (but not non-painful phantom phenomena) experienced after arm amputation.” Subedi and Grossberg (2011: 2) report that the size of the region which lost the afferent input also matters as far as the degree of pain is concerned.
These findings suggest that changes in both the peripheral and the central nervous systems might be inter-related and could account for the majority of phantom-limb pain cases. However, the two major causes of phantom-limb pain outlined in this section concern two different and distal sites, and therefore, provide two regions for treatment. The next section describes some of the known treatment methods.Continued on Next Page »
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