Open Access Articles- Top Results for Phantom limb

Phantom limb

For other uses, see Phantom limb (disambiguation).
Phantom limb
Classification and external resources
ICD-10 G54.6-G54.7
ICD-9 353.6
DiseasesDB 29431
NCI Phantom limb
Patient UK Phantom limb
MeSH D010591
File:Cat with phantom forelimb.webmhd.webm
A cat attempting to use its left forearm to scoop litter several months after it has been amputated

A phantom limb is the sensation that an amputated or missing limb (even an organ, like the appendix) is still attached to the body and is moving appropriately with other body parts.[1][2][3] Approximately 60 to 80% of individuals with an amputation experience phantom sensations in their amputated limb, and the majority of the sensations are painful.[4] Phantom sensations may also occur after the removal of body parts other than the limbs, e.g. after amputation of the breast, extraction of a tooth (phantom tooth pain) or removal of an eye (phantom eye syndrome). It has even been reported for broken bones years after the injury. [5] The missing limb often feels shorter and may feel as if it is in a distorted and painful position. Occasionally, the pain can be made worse by stress, anxiety, and weather changes. Phantom limb pain is usually intermittent. The frequency and intensity of attacks usually declines with time.[6]

Although not all phantom limbs are painful, patients will sometimes feel as if they are gesturing, feel itches, twitch, or even try to pick things up. For example, Ramachandran and Blakeslee describe that some people's representations of their limbs do not actually match what they should be, for example, one patient reported that her phantom arm was about "6 inches too short".[7]

A slightly different sensation known as phantom pain can also occur in people who are born without limbs, and people who are paralyzed.[8] Phantom pains occur when nerves that would normally innervate the missing limb cause pain. It is often described as a burning or similarly strange sensation and can be extremely agonizing for some people, but the exact sensation differs widely for individuals. Other induced sensations include warmth, cold, itching, squeezing, tightness, and tingling.[3][7]

Neurological basis

File:Sensory Homunculus.png
The fact that the representation of the face lies adjacent to the representation of the hand and arm in the cortical homunculus is crucial to explaining the origin of phantom limbs.

Until recently, the dominant theory for cause of phantom limbs was irritation in the severed nerve endings (called "neuromas"). When a limb is amputated, many severed nerve endings are terminated at the residual limb. These nerve endings can become inflamed, and were thought to send anomalous signals to the brain. These signals, being functionally nonsense, were thought to be interpreted by the brain as pain. Treatments based on this theory were generally failures. In extreme cases, surgeons would perform a second amputation, shortening the stump, with the hope of removing the inflamed nerve endings and causing temporary relief from the phantom pain. But instead, the patients' phantom pains increased, and many were left with the sensation of both the original phantom limb, as well as a new phantom stump, with a pain all its own.[7] In some cases, surgeons even cut the sensory nerves leading into the spinal cord or in extreme cases, even removed the part of the thalamus that receives sensory signals from the body.[3]

By the late 1980s, Ronald Melzack had recognized that the peripheral neuroma account could not be correct. In his 1989 paper, "Phantom Limbs, The Self And The Brain"[9] Melzack proposed the theory of the "neuromatrix." According to Melzack the experience of the body is created by a wide network of interconnecting neural structures. In 1991, Tim Pons and colleagues at the National Institutes of Health (NIH) showed that the primary somatosensory cortex undergoes substantial reorganization after the loss of sensory input.[10] Hearing about these results, Vilayanur S. Ramachandran theorized that phantom limb sensations could be due to this reorganization in the somatosensory cortex, which is located in the postcentral gyrus, and which receives input from the limbs and body.[3][7] Ramachandran and colleagues illustrated this theory by showing that stroking different parts of the face led to perceptions of being touched on different parts of the missing limb.[11]

Ramachandran argued that the perception of being touched in different parts of the phantom limb was the perceptual correlate of cortical reorganization in the brain. However, research published in 1995 by Flor et al. demonstrated that pain (rather than referred sensations) was the perceptual correlate of cortical reorganization.[12] In 1996 Knecht et al. published an analysis of Ramachandran's theory that concluded that there was no topographic relationship between referred sensations and cortical reorganization in the primary cortical areas[13] Recent research by Flor et al. suggests that non-painful referred sensations are correlated with a wide neural network outside the primary cortical areas.[14]

Not all scientists support the theory that phantom limb pain is the result of maladaptive changes in the cortex. Pain researchers such as Tamar Makin (Oxford) and Marshall Devor (Hebrew University, Jerusalem) argue that phantom limb pain is primarily the result of "junk" inputs from the peripheral nervous system.[15] In 2013, Marshall Devor and researchers in Israel and Albania conducted experiments in which they were able to reduce or eliminate phantom limb pain for leg amputees by precisely injecting a local anesthetic into the lower back of 31 subjects. This result supports the theory that phantom limb pain is generated primarily in the peripheral nervous system.[16]

Recent research

In 2009 Lorimer Moseley and Peter Brugger carried out an experiment in which they encouraged seven arm-amputees to use visual imagery to contort their phantom limbs into impossible configurations. Four of the seven subjects succeeded in performing impossible movements of the phantom limb. This experiment suggests that the subjects had modified the neural representation of their phantom limbs and generated the motor commands needed to execute impossible movements in the absence of feedback from the body.[17] The authors stated that: "In fact, this finding extends our understanding of the brain's plasticity because it is evidence that profound changes in the mental representation of the body can be induced purely by internal brain mechanisms--the brain truly does change itself."

In 2012 V.S. Ramachandran and Paul McGeoch reported the case of a 57-year-old woman (known as R.N.) who was born with a deformed right hand consisting of only three fingers and a rudimentary thumb. After a car crash at the age of 18, the woman's deformed hand was amputated, which gave rise to feelings of a phantom hand. The phantom hand was experienced, however, as having all five fingers (although some of the digits were foreshortened). 35 years after her accident, the woman was referred for treatment after her phantom hand had become unbearably painful. McGeoch and Ramachandran trained R.N. using mirror box visual feedback, for 30 minutes a day, in which the reflection of her healthy left-hand was seen as superimposed onto where she felt her phantom right hand to be. After two weeks she was able to move her phantom fingers and was relieved of pain. Crucially, she also experienced that all five of her phantom fingers were now normal length. Ramachandran and McGeoch stated that this case provides evidence that the brain has an innate (hard-wired) template of a fully formed hand.[18]

In 2012 an experiment was conducted in which it was demonstrated that the movement of phantom limbs are "real" movements that involve the execution of a motor command. Amputees can also carry out imaginary movements of their phantom limbs, however these movements do not lead to a feeling that the phantom limb has changed position. This research indicates that clinicians using motor training for pain relief need to distinguish between imagined movements and real movements of phantom limbs.[19]

In 2013, experiments involving eight subjects were reported by Nadia Bolognini (University of Milano-Bicocca) in which transcranial direct current stimulation (tDCS) was used to temporarily reduce phantom limb pain. The researchers found that this type of stimulation could produce short-term (under 90 minutes) reduction of pain without affecting other amputation-related phenomena.[20]

Phantom limb pain

File:Virtually Painless. Science Museum Painless Exhibition Series.webm
A patient discusses the experience of phantom limb pain and two researchers explore a treatment using an Xbox Kinect.

Phantom limb pain (PLP) is a complex phenomenon that includes a wide variety of symptoms ranging from tingling and itching to burning and aching.[21][22] During the past twenty years researchers have advanced a number of theories to explain phantom limb pain. Three of the most prominent are: 1) maladaptive changes in the primary sensory cortex after amputation (maladaptive plasticity), 2) a conflict between the signals received from the amputated limb (proprioception) and the information provided by vision that serves to send motor commands to the missing limb, 3) vivid limb position memories that emerge after amputation.[23]

In 2013 Tamar Makin (Oxford University) published the results of an experiment which challenges the theory of maladaptive plasticity (first advanced by Herta Flor). Makin's research indicates that the cortical representation of the missing limb is actually stronger after amputation. That is, there is no cortical remapping after amputation. Peter Brugger (University of Zurich) stated that “This is truly significant work, which challenges previous views—close to axiomatic—that phantom limb pain is a marker of cortical reorganization." [24]

In 2013, a team of scientists led by Marshall Devor (Hebrew University) carried out research that strongly suggests that phantom limb pain originates in the nervous system rather than in the brain, as a result of cortical reorganization.[16] "Guided by medical imaging, the researchers injected 31 leg amputees who suffered from phantom limb syndrome – 16 in Albania and 15 in Israel – with local anesthetic near where the nerves from their amputated legs enter the spinal cord in the lower back. Within minutes, phantom limb sensation and pain was temporarily reduced or eliminated in all the amputees." [25]


Most approaches to treatment over the past two decades have not shown consistent symptom improvement. Treatment approaches have included drugs such as antidepressants, Spinal cord stimulation, Vibration therapy, acupuncture, hypnosis, and biofeedback.[26]

In 2006 Herta Flor, at the Department of Clinical Neuroscience, University of Heidelberg, stated that "Several studies, including large surveys of amputees, have shown that most currently available treatments for phantom limb pain, which range from analgesic and antidepressant medication to stimulation, are ineffective and fail to consider the mechanisms that underlie production of the pain".[27]

One approach that has gained a great deal of public attention is the mirror box developed by Vilayanur Ramachandran and colleagues.[28][29] Through the use of artificial visual feedback it becomes possible for the patient to "move" the phantom limb, and to unclench it from potentially painful positions.

Recently, graded motor imagery (which may incorporate mirror therapy) and sensory discrimination training have emerged as promising therapeutic tools in dealing with pathologic pain problems such as phantom limb pain and complex regional pain syndrome. However, Lorimer Mosely, who developed graded motor imagery, cautions "Although evidence is emerging that treatments such as graded motor imagery and sensory discrimination training can be effective for pathologic pain, further studies are needed to replicate the current data and elucidate the mechanisms involved."[30]

See also

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  1. ^ Mitchell, S. W. (1871). "Phantom limbs". Lippincott's Magazine of Popular Literature and Science 8: 563–569. 
  2. ^ Melzack, R. (1992). "Phantom limbs" (PDF). Scientific American (April): 120–126. 
  3. ^ a b c d Ramchandran, VS; Hirstein, William (1998). "The perception of phantom limbs" (PDF). Brain 121 (9): 1603–1630. PMID 9762952. doi:10.1093/brain/121.9.1603. 
  4. ^ Sherman, R. A., Sherman, C.J. & Parker, L. (1984). "Chronic phantom and stump pain among American veterans: Results of a survey". Pain 18: 83–95. doi:10.1016/0304-3959(84)90128-3. 
  5. ^
  6. ^ Nikolajsen, L. & Jensen, T. S. (2006). McMahon S, Koltzenburg M, ed. Wall & Melzack's Textbook of Pain (5th ed.). Elsevier. pp. 961–971. 
  7. ^ a b c d Ramachandran, V. S. & Blakeslee, S. (1998). Phantoms in the Brain: Probing the Mysteries of the Human Mind. William Morrow & Company. ISBN 0-688-15247-3. 
  8. ^ Saadah, E. S. & Melzack, R. (1994). "Phantom limb experiences in congenital limb-deficient adults". Cortex 30 (3): 479–485. doi:10.1016/s0010-9452(13)80343-7. 
  9. ^ Canadian Psychology, 1989, 30:1{\[1]
  10. ^ Pons TP, Garraghty PE, Ommaya AK, Kaas JH, Taub E, Mishkin M. (1991). "Massive cortical reorganization after sensory deafferentation in adult macaques.". Science 252 (5014): 1857–1860. PMID 1843843. doi:10.1126/science.1843843. 
  11. ^ Ramachandran, V. S., Rogers-Ramachandran, D. C. & Stewart, M. (1992). "Perceptual correlates of massive cortical reorganization" (PDF). Science 258 (5085): 1159–1160. PMID 1439826. doi:10.1126/science.1439826. 
  12. ^ Flor H, Elbert T, Knecht S, Wienbruch C, Pantev C, Birbaumer N, Phantom-limb pain as a perceptual correlate of cortical reorganization following arm amputation. Nature 1995; 375: 482–484.
  13. ^ Knecht,S,Henningsen,H,Elbert,T,Flor,H,Hohling,C,Pantev,C,Taub,E, Reorganizational and perceptional changes after amputation, Brain,1996,119,1213-1219 [2]
  14. ^ Handbook of Neuropsychology: Plasticity and rehabilitation, Jordan Grafman, Chapter 9, page 187
  15. ^ Epoch Times website, July 16,2014
  16. ^ a b Peripheral nervous system origin of phantom limb pain, Pain, Vol. 155, Issue 7, pages 1384-1391 [3]
  17. ^ Moseley, Brugger, Interdependence of movement and anatomy persists when amputees learn a physiologically impossible movement of their phantom limb, PNAS, Sept 16, 2009,[4]
  18. ^ McGeoch, P., and Ramachandran, V., (2012), The appearance of new phantom fingers post-amputation in a phocomelus, Neurocase, 18 (2), 95-97.
  19. ^ The moving phantom. Motor execution or motor imagery?, Lorimer Moseley, Body in Mind blog site, July 20, 2012 [5]
  20. ^ Bolognini N, Olgiati E, Maravita A, Ferraro F, Fregni F (August 2013). "Motor and parietal cortex stimulation for phantom limb pain and sensations". Pain 154 (8): 1274–80. PMID 23707312. doi:10.1016/j.pain.2013.03.040. 
  21. ^ Phantom limb pain, Wellcome Trust Web site article on Pain by Jonathan Cole [6]
  22. ^ Subedi B, Grossberg GT (2011). "Phantom limb pain: mechanisms and treatment approaches". Pain Research and Treatment 2011: 864605. PMC 3198614. PMID 22110933. doi:10.1155/2011/864605. 
  23. ^ Elizabeth A. Franz1. "Bimanual coupling in amputees with phantom limb." Nature Neuroscience. [7]
  24. ^ A New Challenge to the Maladaptive Plasticity Theory of Phantom Limb Pain, David Holzman, March 21, 2013,Pain Research Form web site [8]
  25. ^ Solved: Mystery of phantom limb pain,May 28, 2014
  26. ^ Foell, Jens; Bekrater-Bodmann, Robin; Flor, Herta; Cole, Jonathan (December 2011). "Phantom Limb Pain After Lower Limb Trauma: Origins and Treatments". International Journal of Lower Extremity Wounds 10: 224–235. doi:10.1177/1534734611428730. 
  27. ^ Flor, H; Nikolajsen, L; Jensn, T (November 2006). "Phantom limb pain: a case of maladaptive CNS plasticity?" (PDF). Nature Reviews Neuroscience 7: 873. doi:10.1038/nrn1991. 
  28. ^ Ramachandran, V. S., Rogers-Ramachandran, D. C., Cobb, S. (1995). "Touching the phantom". Nature 377 (6549): 489–490. PMID 7566144. doi:10.1038/377489a0. 
  29. ^ Ramachandran, V. S., Rogers-Ramachandran, D. C. (1996). "Synaesthesia in phantom limbs induced with mirrors" (PDF). Proceedings of the Royal Society of London 263 (1369): 377–386. PMID 8637922. doi:10.1098/rspb.1996.0058. 
  30. ^ Reuters Health, U.S. Edition, Jan. 12

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