Phantom pain

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This article is about the medical condition. For the video game, see Metal Gear Solid V: The Phantom Pain.
Phantom pain
SpecialtyNeurology

Phantom pain is a painful perception that an individual experiences relating to a limb or an organ that is not physically part of the body, either because it was removed or was never there in the first place.[1]

Sensations are reported most frequently following the amputation of a limb, but may also occur following the removal of a breast, tongue, or internal organ.[2] Phantom eye syndrome can occur after eye loss. The pain sensation and its duration and frequency varies from individual to individual.

Phantom pain should be distinguished from other conditions that may present similarly, such as phantom limb sensation and residual limb pain. Phantom limb sensation is any sensory phenomenon, except pain, which is felt at an absent limb or a portion of the limb.[3] It is estimated that up to 80% of amputees experience phantom limb sensations at some time of their lives.[4] Some experience some level of this phantom feeling in the missing limb for the rest of their lives. Residual limb pain, also referred to as stump pain, is a painful perception that originates from the residual limb, or stump, itself.[2] It is typically a manifestation of an underlying source, such as surgical trauma, neuroma formation, infection, or an improperly fitted prosthetic device.[5] Although these are different clinical conditions, individuals with phantom pain are more likely to concomitantly experience residual limb pain as well.[6]

The term "phantom limb" was first coined by American neurologist Silas Weir Mitchell in 1871.[7] Mitchell described that "thousands of spirit limbs were haunting as many good soldiers, every now and then tormenting them".[8] However, in 1551, French military surgeon Ambroise Paré recorded the first documentation of phantom limb pain when he reported that "for the patients, long after the amputation is made, say that they still feel pain in the amputated part".[8]

Signs and symptoms[edit]

The symptomatic course of phantom pain is widely variable, but the onset often presents within the first week after amputation.[2] The reported pain may be intermittent and lasting seconds to minutes, but can be continuous with acute exacerbations.[9] The duration of symptoms varies among individuals, with some reporting decreased pain over time and others reporting a more stable or even increasing trajectory.[10] Sensations may be described as shooting, stabbing, squeezing, throbbing, tingling, or burning, and sometimes feels as if the phantom part is being forced into an uncomfortable position.[11]

Visual representation of body parts within the somatosensory cortex

While the sensation often affects the part of the limb farthest from the body, such as the fingers or toes, other body parts closer to the brain, such as the arm or leg, can still experience similar sensations.[12] It is thought that phantom pain more commonly involves the part of the limb farthest from the body because of its larger cortical representation within the somatosensory cortex [citation needed]. Sensations on smaller limbs and digits such as toes or fingers tend to be less severe [citation needed].

Overall, the sensations may be triggered by pressure on the remaining part of the limb, emotional stress, or changes in temperature.[13]

Causes[edit]

Individuals may experience phantom pain following surgical or traumatic amputation of a limb, removal of an organ, or in instances of congenital limb deficiency. It is most commonly observed after amputation, although less frequent cases have been reported following the removal of a breast, tongue, or eye.[2] Phantom pain is seen more often in older adults as compared to individuals with congenital limb deficiency or amputation at an early age.[14] It has also been reported that individuals with a prior history of chronic pain, anxiety, or depression are more likely to develop phantom pain than those without these risk factors.[15]

Pathophysiology[edit]

The neurological basis and mechanisms for phantom pain are all derived from experimental theories and observations. Little is known about the true mechanisms causing phantom pain, and many theories highly overlap. Historically, phantom pains were thought to originate from neuromas located at the stump tip.[1] Traumatic neuromas, or non-tumor nerve injuries, often arise from surgeries and result from the abnormal growth of injured nerve fibers.[11] Although stump neuromas may contribute to phantom pains, they are not the sole cause. This is because patients with congenital limb deficiency can sometimes, although much less frequently, experience phantom pains.[14] This suggests that there is also a central representation of the limb responsible for generating painful sensations.[16] Currently, theories are based on altered neurological pathways within the peripheral nervous system and spinal cord, as well as cortical reorganization within the brain.

Peripheral mechanisms[edit]

Neuromas formed from injured nerve endings at the stump site show increased sodium channel expression and are able to spontaneously fire abnormal action potentials.[17] This increased activity of Aδ and C fibers, which are involved in pain and temperature sensation, can contribute to phantom pain. However, it has been noted that pain still persists once the neuromas have ceased firing action potentials or when peripheral nerves are treated with conduction blocking agents.[16] The peripheral nervous system is therefore thought to have at most a modulation effect on phantom limb pain.[8]

Spinal mechanisms[edit]

In addition to peripheral mechanisms, spinal mechanisms are thought to have an influencing role in the development of phantom pain. Peripheral nerve injury can lead to the degeneration of C fibers in the dorsal horn of the spinal cord, and terminating A fibers may subsequently branch into the same lamina.[8] If this occurs, A fiber inputs could be reported as noxious stimuli. Substance P, involved in the transmission of pain signals, is usually expressed by Aδ and C fibers, but following peripheral nerve damage, substance P is expressed by Aβ fibers.[8] This leads to hyperexcitability of the spinal cord, which usually occurs only in the presence of noxious stimuli. These changes to the nerve fiber inputs may also lead to an expansion of the neuronal receptive fields, such that previously non-noxious stimuli are now interpreted as noxious.[11] This process of hyperexcitability and receptive field changes is broadly referred to as central sensitization.[1] It is also known that increased expression of glutamate and NMDA, coupled with decreased inhibition from GABAergic neurons, further contributes to the mechanism of central sensitization.[18] However, because patients with complete spinal cord injury have experienced phantom pain, there must also be an underlying central mechanism within the brain.

Central mechanisms[edit]

Under ordinary circumstances, the genetically determined circuitry in the brain remains largely stable throughout life. For much of the twentieth century, it was believed that no new neural circuits could be formed in the adult mammalian brain, but experiments from the 1980s onward cast this into doubt.[16] For instance, functional MRI studies in amputees have shown that almost all patients have experienced cortical remapping.[19] After amputation, cortical remapping is the process by which areas of the somatosensory and primary motor cortices representing the loss limb are invaded by nearby regions.[20] This leads to areas of the brain formerly receiving input from the lost limb now able to be stimulated from the nearby invading cortical regions.

Most of the studies using functional MRI to investigate cortical remapping in humans have been in upper limb amputees. Following the loss of an arm, the majority of motor reorganization occurred as a downward shift of the hand area of the cortex onto the area of face representation, especially the lips.[20] In individuals with phantom limb pain, the reorganization was great enough to cause a change in cortical lip representation into the hand areas only during lip movements.[16] Additionally, as phantom pains in upper extremity amputees increased, there was a higher degree of medial shift of the facial motor representation.[21] It has also been found that there is a high correlation between the severity of phantom limb pain and the extent to which cortical reorganization has occurred.[21]

The neuromatrix[edit]

The neuromatrix theory, initially coined by psychologist Ronald Melzack in the 1990s, proposes that there is an extensive network connecting the thalamus and the cortex, and the cortex and the limbic system.[8] It is a theory that extends beyond body schema theory and incorporates the conscious awareness of oneself. This theory proposes that conscious awareness and the perception of self are generated in the brain via patterns of input that can be modified by different perceptual inputs.[22] The network is genetically predetermined, and is modified throughout one’s lifetime by various sensory inputs to create a neurosignature.[23] It is the neurosignature of a specific body part that determines how it is consciously perceived.[8] The input systems contributing to the neurosignature are primarily the somatosensory, limbic, and thalamocortical systems. The neuromatrix theory aims to explain how certain activities associated with pain lead to the conscious perception of phantom pain. The persistence of the neurosignature, even after limb amputation, may be the cause of phantom sensations and pain. Phantom pain may arise from abnormal reorganization in the neuromatrix to a pre-existing pain state.[24]

Opposition to the neuromatrix theory exists largely because it fails to explain why relief from phantom sensations rarely eliminates phantom pains. It also does not address how sensations can spontaneously end and how some amputees do not experience phantom sensations at all.[8] In addition, a major limitation of the neuromatrix theory is that it too broadly accounts for various aspects of phantom limb perception. It is also likely that it is too difficult to be tested empirically, especially when testing painless phantom sensations.[22]

Management[edit]

Various methods have been used to treat phantom limb pain. Doctors may prescribe medications to reduce the pain. Some antidepressants or antiepileptics have been shown to have a beneficial effect on reducing phantom limb pain. Often physical methods such as light massage, electrical stimulation, and hot and cold therapy have been used with variable results.

There are many different treatment options for phantom limb pain that are actively being researched. Most treatments do not take into account the mechanisms underlying phantom pains, and are therefore ineffective. However, there are a few treatment options that have been shown to alleviate pain in some patients, but these treatment options usually have a success rate less than 30%.[8] It is important to note that this rate of success does not exceed the placebo effect. It is also important to note that because the degree of cortical reorganization is proportional to phantom limb pains, any perturbations to the amputated regions may increase pain perception.[8]

Mirror therapy[edit]

Ramachandran (right) with his original mirror box

Mirror box therapy allows for illusions of movement and touch in a phantom limb by inducing somatosensory and motor pathway coupling between the phantom and real limb.[22] Many patients experience pain as a result of a clenched phantom limb, and because phantom limbs are not under voluntary control, unclenching becomes impossible.[25] This theory proposes that the phantom limb feels paralyzed because there is no feedback from the phantom back to the brain to inform it otherwise. Vilayanur S. Ramachandran believes that if the brain received visual feedback that the limb had moved, then the phantom limb would become unparalyzed.[25]

Although the use of mirror therapy has been shown to be effective in some cases there is still no widely accepted theory of how it works. According to 2017 paper that reviewed a wide range of studies of mirror therapy, "Research evidence suggests that a course of treatment (four weeks) of mirror therapy may reduce chronic pain. Contraindications and side effects are few. The mechanism of action of mirror therapy remains uncertain, with reintegration of motor and sensory systems, restored body image and control over fear-avoidance likely to influence outcome. The evidence for clinical efficacy of mirror therapy is encouraging, but not yet definitive. Nevertheless, mirror therapy is inexpensive, safe and easy for the patient to self-administer."[26]

Little research was published on MT before 2009, and much of the research since then has been of low quality.[27] Out of 115 publications between 2012 and 2017 about using mirror therapy to treat phantom limb pain, a 2018 review, found only 15 studies whose scientific results should be considered. From these 15 studies, the reviewers concluded that "MT seems to be effective in relieving PLP, reducing the intensity and duration of daily pain episodes. It is a valid, simple, and inexpensive treatment for PLP."[28]

Medication[edit]

Pharmacological techniques are often continued in conjunction with other treatment options. Doses of pain medications needed often drop substantially when combined with other techniques, but rarely are discontinued completely. Tricyclic antidepressants, such as amitriptyline, and sodium channel blockers, mainly carbamazepine, are often used to relieve chronic pain, and recently have been used in an attempt to reduce phantom pains. Pain relief may also be achieved through use of opioids, ketamine, calcitonin, and lidocaine.[8]

Deep-brain stimulation[edit]

Deep brain stimulation is a surgical technique used to alleviate patients from phantom limb pain. Prior to surgery, patients undergo functional brain imaging techniques such as PET scans and functional MRI to determine an appropriate trajectory of where pain is originating. Surgery is then carried out under local anesthetic, because patient feedback during the operation is needed. In the study conducted by Bittar et al., a radiofrequency electrode with four contact points was placed on the brain. Once the electrode was in place, the contact locations were altered slightly according to where the patient felt the greatest relief from pain. Once the location of maximal relief was determined, the electrode was implanted and secured to the skull. After the primary surgery, a secondary surgery under general anesthesia was conducted. A subcutaneous pulse generator was implanted into a pectoral pocket below the clavicle to stimulate the electrode.[8] It was found that all three patients studied had gained satisfactory pain relief from the deep brain stimulation. Pain had not been completely eliminated, but the intensity had been reduced by over 50% and the burning component had completely vanished.[8]

Epidemiology[edit]

Phantom limb pain and phantom limb sensations are linked, but must be differentiated from one another. While phantom limb sensations are experienced by those with congenital limb deficiency, spinal cord injury, and amputation, phantom limb pain occurs almost exclusively as a result of amputation.[29] Almost immediately following the amputation of a limb, 90–98% of patients report experiencing a phantom sensation. Nearly 75% of individuals experience the phantom as soon as anesthesia wears off, and the remaining 25% of patients experience phantoms within a few days or weeks.[16] Of those experiencing innocuous sensations, a majority of patients also report distinct painful sensations.

Age and gender have not been shown to affect the onset or duration of phantom limb pain. Although it has not been fully explored, one investigation of lower limb amputation observed that as stump length decreased, there was a greater incidence of moderate and severe phantom pain.[8]

See also[edit]

References[edit]

  1. ^ a b c Hanyu-Deutmeyer, Aaron A.; Cascella, Marco; Varacallo, Matthew (2023), "Phantom Limb Pain", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 28846343, retrieved 2024-01-19
  2. ^ a b c d knadmin (2017-03-03). "Phantom Pain". PM&R KnowledgeNow. Retrieved 2024-01-19.
  3. ^ Poor Zamany Nejatkermany, Mahtab; Modirian, Ehsan; Soroush, Mohammadreza; Masoumi, Mehdi; Hosseini, Maryam (2016). "Phantom Limb Sensation (PLS) and Phantom Limb Pain (PLP) among Young Landmine Amputees". Iranian Journal of Child Neurology. 10 (3): 42–47. ISSN 1735-4668. PMC 4928615. PMID 27375755.
  4. ^ Kaur, Amreet; Guan, Yuxi (December 2018). "Phantom limb pain: A literature review". Chinese Journal of Traumatology. 21 (6): 366–368. doi:10.1016/j.cjtee.2018.04.006. PMC 6354174. PMID 30583983.
  5. ^ Stover, Gary; Prahlow, Nathan (2020). "Residual limb pain: An evidence-based review". NeuroRehabilitation. 47 (3): 315–325. doi:10.3233/NRE-208005. ISSN 1878-6448. PMID 32986622.
  6. ^ Srivastava, Devjit (November 2017). "Chronic post-amputation pain: peri-operative management - Review". British Journal of Pain. 11 (4): 192–202. doi:10.1177/2049463717736492. ISSN 2049-4637. PMC 5661696. PMID 29123664.
  7. ^ Halligan, P. W. (2002). "Phantom limbs: The body in mind". Cognitive Neuropsychiatry. 7 (3): 251–269. doi:10.1080/13546800244000111. PMID 16571541. S2CID 31375410.
  8. ^ a b c d e f g h i j k l m n Bittar, R. G.; Otero, S.; Carter, H.; Aziz, T. Z. (2005). "Deep brain stimulation for phantom limb pain". Journal of Clinical Neuroscience. 12 (4): 399–404. doi:10.1016/j.jocn.2004.07.013. PMID 15925769. S2CID 42653229.
  9. ^ Sherman, R. A.; Sherman, C. J. (October 1983). "Prevalence and characteristics of chronic phantom limb pain among American veterans. Results of a trial survey". American Journal of Physical Medicine. 62 (5): 227–238. ISSN 0002-9491. PMID 6624883.
  10. ^ Sherman, Richard A.; Sherman, Crystal J.; Parker, Laura (January 1984). "Chronic phantom and stump pain among american veterans: results of a survey". Pain. 18 (1): 83–95. doi:10.1016/0304-3959(84)90128-3. ISSN 0304-3959.
  11. ^ a b c Culp, Clayton J.; Abdi, Salahadin (October 2022). "Current Understanding of Phantom Pain and its Treatment". Pain Physician. 25 (7): E941–E957. ISSN 2150-1149. PMID 36288580.
  12. ^ "Phantom Limb Pain". Physiopedia. Retrieved 2024-01-19.
  13. ^ "Phantom Limb Pain: What is It, Causes, Treatment & Outcome". Cleveland Clinic. Retrieved 2024-01-17.
  14. ^ a b Diers, Martin; Fuchs, Xaver; Bekrater-Bodmann, Robin; Flor, Herta (March 2023). "Prevalence of Phantom Phenomena in Congenital and Early-Life Amputees". The Journal of Pain. 24 (3): 502–508. doi:10.1016/j.jpain.2022.10.010.
  15. ^ Larbig, Wolfgang; Andoh, Jamila; Huse, Ellena; Stahl-Corino, Dietlinde; Montoya, Pedro; Seltzer, Ze'ev; Flor, Herta (2019-05-29). "Pre- and postoperative predictors of phantom limb pain". Neuroscience Letters. 702: 44–50. doi:10.1016/j.neulet.2018.11.044. ISSN 1872-7972. PMID 30503915.
  16. ^ a b c d e Ramachandran, V. S.; Hirstein, W. (1998). "The perception of phantom limbs. The D. O. Hebb lecture". Brain: A Journal of Neurology. 121 (9): 1603–1630. doi:10.1093/brain/121.9.1603. PMID 9762952.
  17. ^ Bennett, David L.; Clark, Alex J.; Huang, Jianying; Waxman, Stephen G.; Dib-Hajj, Sulayman D. (2019-04-01). "The Role of Voltage-Gated Sodium Channels in Pain Signaling". Physiological Reviews. 99 (2): 1079–1151. doi:10.1152/physrev.00052.2017. ISSN 0031-9333.
  18. ^ Koga, Kohei; Li, Shermaine; Zhuo, Min (2016-06-01). "Metabotropic Glutamate Receptor Dependent Cortical Plasticity in Chronic Pain". Current Neuropharmacology. 14 (5): 427–434. doi:10.2174/1570159X13666150425002304. PMC 4983748. PMID 27296638.
  19. ^ Cruz, V. T.; Nunes, B.; Reis, A. M.; Pereira, J. R. (2003). "Cortical remapping in amputees and dysmelic patients: A functional MRI study". NeuroRehabilitation. 18 (4): 299–305. doi:10.3233/NRE-2003-18404. PMID 14757926.
  20. ^ a b Makin, Tamar R.; Flor, Herta (2020-09-01). "Brain (re)organisation following amputation: Implications for phantom limb pain". NeuroImage. 218: 116943. doi:10.1016/j.neuroimage.2020.116943. ISSN 1053-8119.
  21. ^ a b Karl, A.; Birbaumer, N.; Lutzenberger, W.; Cohen, L. G.; Flor, H. (2001). "Reorganization of motor and somatosensory cortex in upper extremity amputees with phantom limb pain". The Journal of Neuroscience. 21 (10): 3609–3618. doi:10.1523/JNEUROSCI.21-10-03609.2001. PMC 6762494. PMID 11331390.
  22. ^ a b c Giummarra, M. J.; Gibson, S. J.; Georgiou-Karistianis, N.; Bradshaw, J. L. (2007). "Central mechanisms in phantom limb perception: The past, present and future". Brain Research Reviews. 54 (1): 219–232. doi:10.1016/j.brainresrev.2007.01.009. PMID 17500095. S2CID 42209339.
  23. ^ Melzack, Ronald (August 1999). "From the gate to the neuromatrix". Pain. Suppl 6: S121–S126. doi:10.1016/S0304-3959(99)00145-1. ISSN 0304-3959. PMID 10491980.
  24. ^ Melzack, R. (1992). "Phantom limbs". Scientific American. 266 (4): 120–126. Bibcode:1992SciAm.266d.120M. doi:10.1038/scientificamerican0492-120. PMID 1566028.
  25. ^ a b Ramachandran, V. S.; Rogers-Ramachandran, D. (1996). "Synaesthesia in Phantom Limbs Induced with Mirrors". Proceedings of the Royal Society B: Biological Sciences. 263 (1369): 377–386. Bibcode:1996RSPSB.263..377R. doi:10.1098/rspb.1996.0058. PMID 8637922. S2CID 4819370.
  26. ^ Mirror therapy: A potential intervention for pain management, Wittkopf,Johnson,2017 Nov;63(11):[1]
  27. ^ Jessie, Barbin; Seetha, Vanessa (2016). "The effects of mirror therapy on pain and motor control of phantom limb in amputees: A systematic review". Annals of Physical and Rehabilitation Medicine. 59 (4): 270–275. doi:10.1016/j.rehab.2016.04.001. PMID 27256539. Up to the 26th November 2015, 85 articles were retrieved on the Medline, Cochrane and Embase databases with using the keywords phantom limb and mirror therapy. It was noted that from 2009, the number of articles increased markedly (Fig. 1), showing increased interest in MT following amputation.
  28. ^ Campo-Prieto, P; Rodríguez-Fuentes, G (November 14, 2018). "Effectiveness of mirror therapy in phantom limb pain: A literature review". Neurologia. doi:10.1016/j.nrl.2018.08.003. PMID 30447854. It is a valid, simple, and inexpensive treatment for PLP. The methodological quality of most publications in this field is very limited, highlighting the need for additional, high-quality studies to develop clinical protocols that could maximise the benefits of MT for patients with PLP.
  29. ^ Kooijman, C. M.; Dijkstra, P. U.; Geertzen, J. H.; Elzinga, A.; Van Der Schans, C. P. (2000). "Phantom pain and phantom sensations in upper limb amputees: An epidemiological study". Pain. 87 (1): 33–41. doi:10.1016/S0304-3959(00)00264-5. PMID 10863043. S2CID 7565030.

External links[edit]

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