Phantom Limbs and Theories of Self

While accounts of both phantom limb awareness and pain have been reported for over 500 years (1), only in recent decades have patients reporting such sensations of missing limbs not been classified as pathological. In fact, recent studies report 60-80% incidence rate of PLP, whereas in the middle of the 20th century, reported PLP cases were as low as 4% (3). Rather, modernized technologies and advancements in the field of neuroscience have revealed evidence indicating that the mechanisms involved in such sensations are actually responsive and adaptive (2), perhaps accounting for the increased rate in cases reported. Such adjustments take place in the central nervous system in the form of cortical changes and reorganization.

Although the cause of phantom limb sensations is unknown, it has been suggested that the trauma of amputation surgery on the nerves could lead to unusual levels of ectopic discharge which could be translated in the brain as pain (1). Because it has also been established that after amputation, changes from abnormal input occur in the brainstem, thalamus, and cortex, it is reasonable to associate these changes with phantom limb pain (PLP), however such causations have not been verified. It is important to realize, as well, that PLP and phantom sensations also occur in people who are born without limbs, thereby indicating that these changes occur not only after surgical removal but possibly throughout one’s life.

Types of Phantom Sensations

It is necessary to recognize that phantom experiences vary greatly. There are different types of PLP, including stump pain and telescoping, and while many patients don’t feel pain in any way, almost all amputees have been shown to report phantom sensations (3). Guimmarra, Gibson, Georgiou-Karistianis, and Bradshaw (2007) discuss limb proprioception, and affirm that patients often report a posture or position of the limb, and even believe they feel movement, though with a limited range (4). Another phenomenon of PLP is telescoping, in which the limb that has been amputated exists within the stump that is still present. Telescoping is thought to occur because the terminal portion is the most represented part of a limb in the cortex, and cortical and perception changes may be the mechanism behind telescoping. Interestingly, then, it is reasonable to infer that “more weakly represented regions of the limb may ‘fade from consciousness’” (Guimmarra et al, 2007, p. 222). Overall, these sensations have been attributed to alterations and enhanced expansion of the “receptive fields” of spinal cord dorsal horn neurons (5).

Psychological Explanations

There are both psychological and physiological explanations behind the phenomenon of PLP. Research has been done indicating a link to personality type and PLP rates: high scores of “compulsive self reliance” and “rigid” correlate to persistent PLP. It was suggested that relying on others led to stress, thereby leading to pain (5). Other theories propose that a psychological defense mechanism is at play, and the patient is in denial of the loss of the limb.

One of the most prominent psychological theories regarding phantom sensations is that of Ronald Melzack, in which the concept of the self is broken down into the “body-self neuromatrix,” which analyzes sensory input and produces perceptual output, and the “neurosignature,” out of which arises one’s awareness of ownership of one’s body, phantom or not (6). Melzack believes the phantom limb is thus representing our normal body experience, “but without the input that normally modulates the central neural processes that produce that experience” (7). The neuromatrix is a network of neurons to which input is missing in phantom limb patients, but still exists in the brain. The neuromatrix is responsible for creating the pattern of self known as the neurosignature, which, in the case of phantom limb sensations, is still being generated even after the limb and its sensory inputs have been removed (8).

Physiological Explanations

After amputating a limb, nodules (also known as neuromas) form at the severed nerve endings and produce unusual impulses which may be the cause of PLP. Another possible explanation can be seen in the spinal cord itself, and the observed abnormal signaling of spinal cord neurons. A third theory, proposed by Melzack and Loeser, suggests that the reduction in input that results from decreased peripheral sensation following amputation leads to disinhibition at both the spinal level and the cortical level (5).

Further, more specific changes in the spinal cord have also been established. Central sensitization, the change in responsiveness to dorsal horn neurons in reaction to increased nociception, might also result from nerve injury. Secondly, spinal cord hyperexcitability might also be attributed to decrease in the number of opioid receptors, thus increases disinhibition processes. In addition, after nerve injury of the peripheral nervous system, deafferentation, the interruption of sensory input due to injury or annihilation of the sensory nerves, often occurs. Such denervation causes the projections of the dorsal roots to the spinal cord to cease. Finally, there is also evidence that PLP leads to reorganizational changes in the brainstem and thalamus, as well (2).

Cortical reorganization. An emergent theory is based on the recent work of Vilanyur Ramachandran and the idea of cortical reorganization. He proposes there is a hidden neural circuitry that appears after prolonged lack of activation of input from the amputated limb. Once the hidden circuit is activated, it links to other areas of the body that are nearby on the homunculus. The idea of the homunculus is based on the cortical mapping of the human body, indicating that each area of the body, when it receives sensory input, remits the perceptual message to the neural connections in the sensory cortex, or the homunculus (6). In other words, the cortical area responsible for processing input from one nearby area on the homunculus (ie. the face) invades the area that previously processed input from the now amputated limb.

Cortical reorganization has become a well-documented phenomenon. It has been shown that this remapping can change over time, thus is it completely malleable and not at all a static entity (2). Research shows that in adult monkeys, mouth and chin inputs reorganize to the cortices of arm and digit representation when such limbs lose usual incoming input. Interestingly, a direct relationship has also been established between level of pain and degree of organization among human PLP patients (3).

The adaptability and beneficial usage of cortical reorganization has been directly challenged. Because of the misperceptions, and the obvious pain, involved in the mechanism, many researchers wonder why such a phenomenon evolved. Kaas (1998) concluded that the reactivation of hidden, unactivated circuits indicates that there is “a subcortical locus for much of the reorganization that follows limb amputation” (333). Kaas also revealed that organization does not occur in all patients, indicating that reactivation of neurons of the phantom limb can reorganize either to the existent stump or the previously intact limb (10).

Treatments

Phantom limb pain has been shown to be not just a creation of the patient but has neural correlations to support its existence. Therefore, research has focused on how to treat such chronic pain, as to many patients it appears to be unbearable to live with in daily life. Tricyclic antidepressants and sodium channel blockers are currently the pharmacological treatment of choice, although their degree of efficacy is questionable (3). Surgical options include the lesioning of the dorsal root entry zone, but this is believed to have a limited effect as well. Various other non-invasive treatments have been recommended, including transcutaneous electrical nerve stimulation, acupuncture, and vibration therapy (3).

However, the most innovative and seemingly successful treatment (although a scientific experiment has not yet been conducted) is that of mirror therapy. By placing a mirror such that the visual system translates to the brain that the missing limb is actually present appears to significantly reduce pain in PLP patients (11). Ramachandran, the designer of this treatment, believes that it works by thwarting the normal misfiring that occurs with reorganization because the brain has been tricked into thinking the limb is still present.

Discussion Questions

Because the phenomenon of phantom limb pain was thought for so long to be a mere delusion of the patient, I was hoping to gear discussion towards other societal influences that may skew our perception of mental suffering today. In response to Melzack’s theory of phantom pain with regards to the self, I thought it might be interesting to discuss the personality testing done on PLP patients. First, it seemed to me that many of the conclusions drawn from that research were distorted by experimenter biases and the relationships between personality and PLP experience was ambiguous. This made me think of other personality testing and correlations that are often drawn up after the fact. In addition, I wanted to discuss a blog that I found regarding phantom limb pain and faith and the afterlife. The blog writer equated dualism with faith, and implied that if the amputated limb is still attached to the soul, then it would not be “uncontrollable” and PLP would not exist.

Finally, discussion with respect to PLP itself was meant to involve the topic of prosthetics and a possible explanation for the finding of enhanced phantom sensations with the use of such technology. Additionally, why might cortical reorganization have evolved if such a mechanisms appears to have more harmful and confounding effects than no sensation at all? Lastly, in discussing treatments for PLP, I was hoping to establish a conversation between the use of non-invasive treatments, and the apparent obsession of society with technology where we seem to overlook the creativity involved in the scientific process to begin with. Also, what might the success of non-invasive over medical or surgical treatments imply about the inner-workings of PLP?

Reflection:

Both the class conversation and the forum were greatly focused on the idea of psychosomatics, which was not part of my portion of the presentation. However, the comments made about PLP were intriguing and pertinent to my discussion topics. One student asked “why is phantom perceived as less important when it is an actual phenomenon?” This student continued to offer discussion about the dangers of diagnosing based solely on self-report. Moreover, the subjective nature of pain is an important aspect to realize, as researchers, students, and society members, and we cannot judge or doubt another’s perceptions.

Another student suggested that the mechanism of cortical reorganization evolved in order for the brain to use all available resources. “There is no reason to reserve brain areas for […] arm stimulation when there is no arm.” In addition, this student mentioned the memory of pain, a topic which I did not cover. However, memory of pain is a large part of PLP research, and so the student’s understanding of this, in relation to the treatments discussed during the presentation, seems to imply that PLP occurs because of the imprinted memory in the brain that exists after the limb is gone. This student asks, “what if the noxious stimulus is the brain?” I found these to be captivating and well thought out points.

Finally, many students also mentioned Body Dysmorphic Disorder (BDD), which was mostly discussed in the psychosomatic portion of the presentation. However, this disorder can be thought of in terms of the self, as noted in Melzack’s theory, and the analogous idea of ownership of one’s body. In Melzack’s theory, the neurosignature is what leads to phantom sensations because amputees do not have the corresponding input to the neuromatrix. To think of this theory in terms of BDD is an interesting one. Perhaps patients with BDD have an abnormal neurosignature, and thus, reject the ownership of their body, their self.

Future Directions

It seems evident that future research on this topic should be focused on the pain experienced by phantom limb patients. Although the mirror therapy appears to be the most cost efficient and effective, the reasoning for its efficiency remains unclear. Much research has been dedicated to virtual reality tactics that seemingly accomplish the same thing as the mirrors, but the underlying mechanisms are unknown. While conceptual theories, such as Melzack’s, are important for understanding brain processes, in establishing a more concrete understanding of how, when, and why cortical reorganization occurs, perhaps a design for more successful treatments can be devised from those results.

Perhaps other directions this research can lead to is that regarding the importance but also the reliability of self report. We briefly discussed in one class the idea of measuring perception without relying on self report, but the problem arises when such measures don’t correspond with the patient’s reported perception. Further discussion on how much doctors and scientists should take another’s perception (whether it be true or not) into their own hands is difficult, yet essential to the future of sciene.
References

(1) King, Steven (2005). Exploring Phantom Limb Pain. Psychiatric Times, 23. <http://www.psychiatrictimes.com/display/article/10168/49106>

(2) Flor, Herta; Nikolajsen, Lone; and Staehelin, Troels (2006). Phantom limb pain: a case of maladaptive CNS plasticity? Nature Reviews Neuroscience, 7, 873-881

<http://www.nature.com/nrn/journal/v7/n11/full/nrn1991.html>

(3) Nikolajsen, Lone and Jensen, T. S. (2001). Phantom limb pain. British Journal of Anesthesia, 87, 107-116.

<http://bja.oxfordjournals.org/cgi/content/full/87/1/107>

(4) Giummarra, Melita J.; Gibson, Stephen J.; Georgiou-Karistianis, Nellie; and Bradshaw, John L. (2007). Central mechanisms in phantom limb perception: The past, present and future. Brain Research Reviews, 54, 219-232.

<http://www.bcs.rochester.edu/people/bfaber/CSP502/6-Giummarra-2007.pdf>

(5) Hill, Anne (1999). Phantom Limb Pain A Review of the Literature on Attributes and Potential Mechanisms. Journal of Pain and Symptom Management, 17, 125-142.

<http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T8R-3VTHPX4-8&_user=423519&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000020258&_version=1&_urlVersion=0&_userid=423519&md5=9f35cb0916de1467902ae060f706e483>

(6) Department of Psychology at Macalester College Website

<http://www.macalester.edu/psychology/whathap/UBNRP/Phantom/phantompain.html>

(7) Melzack, Ronald (1989). Phantom limbs, the self and the brain. Canadian Psychology, 30.

<http://www.psych.mcgill.ca/perpg/fac/melzack/phantom_limbs.pdf>

(8) Melzack, Ronald (1992). Phantom Limbs. Scientific American, 266, 120-126.

(9) Kaas, John (1998). Neurobiology: Phantoms of the brain. Nature, 391, 331-333.

<http://www.nature.com/nature/journal/v391/n6665/full/391331a0.html>

(10) Miles, Donna (2008) Mirror therapy shows promise in amputee treatment. American Forces Press Service

<http://www.af.mil/news/story.asp?id=123082546>