Instruct: Given a question, retrieve relevant documents that answer the question.
Query: Is phantom pain experienced by amputees neurological?
Phantom limb sensation is any sensory phenomenon (except pain) which is felt at an absent limb or a portion of the limb. It has been known that at least 80% of amputees experience phantom sensations at some time of their lives. Some experience some level of this phantom pain and feeling in the missing limb for the rest of their lives.
Phantom limb pain is a type of tactile hallucination because it creates a sensation of excruciating pain in a limb that has been amputated. In 1996, VS Ramachandran conducted a research on several amputees to pinpoint the neural reasons behind these illusionary pains. Most of these amputees that had an unbearable phantom limb pain are reported by patients whose limb was paralyzed before amputation. VS Ramachandran proposed the "learned paralysis" hypothesis. The hypothesis suggested that every time the patients tried to move their paralyzed limb, they received sensory feedback (through vision and proprioception) that the limb did not move. This feedback hardwired itself into the brain circuitry, so that, even when the limb was no longer present, the brain had learned that the phantom limb was paralyzed. As a treatment for phantom limb pains, VS Ramachandran devised a mirror box that would superimpose the mirror image of the normal arm in place of the missing arm and the patient would immediately be relieved of the pain. This suggested that the brain had a plastic nature in the somatosensory system and the brain had reorganized its somatosensory region to accommodate for this new change. Patients that experience this phantom limb pain are very important in research studies for their role in determining brain plasticity. The vivid tactile sensation of the arm that is no longer present suggest the highly complex nature of the brain to reorganize different functions which were once thought to be hardwired to specific regions (localization).
In addition to peripheral mechanisms, spinal mechanisms are thought to have an influencing role in phantom pains. 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.[3] 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.[3] This leads to hyperexcitability of the spinal cord, which usually occurs only in the presence of noxious stimuli. Because patients with complete spinal cord injury have experienced phantom pains, there must be an underlying central mechanism responsible for the generation of phantom pains.
The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72% of patients had phantom limb pain, and six months later, 67% reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts of pain per day, or it may reoccur less often. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb. Phantom limb pain may accompany urination or defecation.
Phantom limbs are a phenomenon which occurs following amputation of a limb from an individual. In 90–98% of cases, amputees report feeling all or part of the limb or body part still there, taking up space. The amputee may perceive a limb under full control, or paralyzed. A common side effect of phantom limbs is phantom limb pain. The neurophysiological mechanisms by which phantom limbs occur is still under debate. A common theory posits that the afferent neurons, since deafferented due to amputation, typically remap to adjacent cortical regions within the brain. This can cause amputees to report feeling their missing limb being touched when a seemingly unrelated part of the body is stimulated (such as if the face is touched, but the amputee also feels their missing arm being stroked in a specific location). Another facet of phantom limbs is that the efferent copy (motor feedback) responsible for reporting on position to the body schema does not attenuate quickly. Thus the missing body part may be attributed by the amputee to still be in a fixed or movable position.
In limb amputees, some, but not all, studies have found a correlation between preoperative pain in the affected limb and postoperative phantom pain. There is a significant association between painful and non-painful phantom experiences, preoperative pain in the symptomatic eye and headache. Based on the present data, it is difficult to determine if headaches or preoperative eye pain play a causal role in the development of phantom phenomena or if headache, preoperative eye pain, and postoperative phantom eye experiences are only epiphenomena of an underlying factor. However, a study in humans demonstrated that experimental pain leads to a rapid reorganization of the somatosensory cortex. This study suggests that preoperative and postoperative pain may be an important co-factor for somatosensory reorganization and the development of phantom experiences.
Davis has also worked on variety of chronic pain conditions, concussion, and phantom pain. She has demonstrated that findings support the hypothesis that the thalamic representation of the amputated limb remains functional in amputees with phantoms Through several studies, she has shown important interactions between pain and cognition, by studying how brain networks shift their function towards pain while multitasking on cognitive tasks (Seminowicz et al., 2007; Erpelding et al., 2013) or when processing multimodal sensory information (Downar et al., 2000) or during mind wandering (Kucyi et al., 2013). She has introduced two influential theories that builds on the neuromatrix concept of Melzack. In the "pain switch" concept (Davis et al., 2015), she emphasizes the basic feeling of "ouch" that must be represented by a core brain mechanism, regardless of pain intensity or quality. The other concept is called the Dynamic Pain Connectome which emphasizes that spatiotemporal representation of pain in the brain is dynamic and includes activity in the salience and default mode network as well as the ascending nociceptive and antinociceptive pathways.
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.
Phantom pain and non-painful phantom sensations result from changes in the central nervous system due to denervation of a body part. Phantom eye pain is considerably less common than phantom limb pain. The prevalence of phantom pain after limb amputation ranged from 50% to 78%. The prevalence of phantom eye pain, in contrast, is about 30%.
Severe beak trimming, or beak trimming birds at an older age is thought to cause chronic pain. Following beak trimming of older or adult hens, the nociceptors in the beak stump show abnormal patterns of neural discharge, which indicate acute pain. Neuromas, tangled masses of swollen regenerating axon sprouts, are found in the healed stumps of birds beak trimmed at 5 weeks of age or older and in severely beak trimmed birds. Neuromas have been associated with phantom pain in human amputees and have therefore been linked to chronic pain in beak trimmed birds. If beak trimming is severe because of improper procedure or done in older birds, the neuromas will persist which suggests that beak trimmed older birds experience chronic pain, although this has been debated.
A large proportion of amputees (50–80%) experience the phenomenon of phantom limbs; they feel body parts that are no longer there. These limbs can itch, ache, burn, feel tense, dry or wet, locked in or trapped or they can feel as if they are moving. Some scientists believe it has to do with a kind of neural map that the brain has of the body, which sends information to the rest of the brain about limbs regardless of their existence. Phantom sensations and phantom pain 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).
Sensations related to the phantom limb's posture, length and volume e.g. feeling that the phantom limb is behaving just like a normal limb like sitting with the knee bent or feeling that the phantom limb is as heavy as the other limb. Sometimes, an amputee will experience a sensation called telescoping. This is the feeling that the phantom limb is gradually shortening over time. Sensations of movement (e.g. feeling that the phantom foot is moving). Sensations of touch, temperature, pressure and itchiness. Many amputees report of feeling heat, tingling, itchiness, and pain.
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.[3] 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.[1]
Neuromas, tangled masses of swollen regenerating axon sprouts, are found in the healed stumps of birds beak trimmed at 5 weeks of age or older and in severely beak trimmed birds. Neuromas have been associated with phantom pain in human amputees and have therefore been linked to chronic pain in beak trimmed birds. If beak trimming is severe because of improper procedure or done in older birds, the neuromas will persist which suggests that beak trimmed older birds experience chronic pain, although this has been debated.
Flor (2002) trained amputees to detect the location and frequency of shocks delivered to their stumps, which resulted in an expansion of corresponding cortical regions and significant reduction of their phantom limb pain.
An interesting phenomenon involving plasticity of cortical maps is the phenomenon of phantom-limb sensation. Phantom-limb sensation is experienced by people who have undergone amputations in hands, arms, and legs, but it is not limited to extremities. Although the neurological basis of phantom-limb sensation is still not entirely understood, it is believed that cortical reorganization plays an important role.[13]
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.
Paré also reintroduced the ligature of arteries (first used by Galen) instead of cauterization during amputation. The usual method of sealing wounds by searing with a red-hot iron often failed to arrest the bleeding and caused patients to die of shock. For the ligature technique he designed the ""Bec de Corbeau"" ("crow's beak"), a predecessor to modern haemostats. Although ligatures often spread infection, it was still an important breakthrough in surgical practice. Paré detailed the technique of using ligatures to prevent hemorrhaging during amputation in his 1564 book "Treatise on Surgery". During his work with injured soldiers, Paré documented the pain experienced by amputees which they perceive as sensation in the 'phantom' amputated limb. Paré believed that phantom pains occur in the brain (the consensus of the medical community today) and not in remnants of the limb. He also performed many neurosurgical procedures.
In 1542, during the siege of Perpignan, Paré, accompanying the French army, employed a novel technique to aid in bullet extraction. During a battle, Maréchal de Brissac was wounded, having been shot in the shoulder. When finding the bullet seemed impossible, Paré had the idea to ask the victim to put himself in the exact position he was in when shot. The bullet was then found and removed by Henry's personal surgeon, Nicole Lavernault.
V. S. Ramachandran, a neuroscientist, was also fascinated with amputees and their phantom pains. One of his patients was a man with insistent pain in his arm, an arm that was in fact removed many years prior. Ramachandran proceeded to test out a treatment of his own creation. He made the man place his arms into a box, the one arm that was still attached surrounded by mirrors. The box and the mirror together provided the illusion that his arm was still intact. Then, he made the man move his hands around as if he still had both. It is after this ritual of moving his ands about that the man exclaims that he feels his pain subsiding, that he feels his phantom fist unclench for the first time in many years. Thus concludes the chapter about the brain and its motor, which essentially is responsible for every part working correctly.
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.[5] 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.[6] Of those experiencing innocuous sensations, a majority of patients also report distinct painful sensations.
One novel use of this test has been to provide temporary pain relief from phantom limb pains in amputees and paraplegics. It can also induce a temporary remission of anosognosia, the visual and personal aspects of hemispatial neglect, hemianesthesia, and other consequences of right hemispheric damage.
People with amputations have reported phantom limbs. This serves as evidence that the brain is hard-wired to perceive body image, making it notable that sensory input and proprioceptive feedback are not essential in its formation. Losing an anatomical part through amputation sets a person up for complex perceptual, emotional, and psychological responses. Such responses include phantom limb pain, which is the painful feeling some amputees incur after amputation in the area lost. Phantom limb pain permits a natural acceptance and use of prosthetic limbs.
Phantom limbs are sensations felt by amputees that make it feel like their amputated extremity is still there. Sometimes amputees can experience pain from their phantom limbs; this is called phantom limb pain (PLP).
Neuromas formed from injured nerve endings at the stump site are able to fire abnormal action potentials, and were historically thought to be the main cause of phantom limb pain. Although neuromas are able to contribute to phantom pain, pain is not completely eliminated when peripheral nerves are treated with conduction blocking agents.[6] Physical stimulation of neuromas can increase C fiber activity, thus increasing phantom pain, but pain still persists once the neuromas have ceased firing action potentials. The peripheral nervous system is thought to have at most a modulation effect on phantom limb pain.[3]
It has been suggested that symptoms of mirror-touch synesthesia can occur in amputees. 98% of amputees report phantom sensations in their amputated limb, and one of the studied treatments for phantom limb pain has involved a mirror box. In this treatment, the amputee places their good arm into a mirror box, allowing the image of the arm to reflect where the amputated arm normally would be. When touch is applied to the good arm, amputees have reported corresponding sensations in their phantom limb. These cases can be considered mirror-touch synesthesia because a visual stimulus was able to elicit a tactile sensation. Studies have looked further into determining whether amputees actually experience mirror touch synesthesia. Four amputees were recruited in a study and asked to observe an assistant's arm being touched at various angles. 61 out of the 64 trials experienced mirror-touch sensations, and when the arm was wiggled, the sensations were enhanced. Finally, one amputee experienced a cold sensation when observing ice cubes touching the assistant's arm. Although there is evidence that mirror-touch synesthesia occurs in amputees, recent data has been inconclusive.