Phantom pain

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Phantom pain is described as a perception that the individual's experience is related to limbs or organs that are not part of the body physically. Loss of limbs is a result of either elimination by amputation or deficiency of limbs. However, the sensation of ghost limbs can also occur after nerve avulsion or spinal cord injury.

Sensation is noted most often following arms or leg amputations, but may also occur after removal of the breast, teeth, or internal organs. Phantom limb pain is pain in the limb that is missing or part of the body. Pain sensitivity varies from individual to individual.

The sensation of the ghost limb is any sensory phenomenon (except pain) that is felt in the limb that is absent or part of the body. It is known that at least 80% of amputees experience a phantom sensation at some point in their life. Some experience some degree of pain and feelings of this ghost in lost limbs for the rest of their lives.

The term "ghost limb" was first coined by the American neurologist Silas Weir Mitchell in 1871. Mitchell described that "thousands of limbs haunt many good soldiers, every now and then torture them". However, in 1551, the French military surgeon Ambroise ParÃÆ' © recording the first documentation of ghost limb pain when he reported that, "For patients, long after amputation is made, say that they still feel pain on the amputated part".

Video Phantom pain

Jenis

There are different types of sensations that may be felt:

• Sensations related to posture, ghost length and volume, for example. feel that ghostly boughs behave like normal limbs like sitting with knees bent or feeling that a ghost limb is as heavy as other limbs. Sometimes, an amputee will experience a sensation called telescoping. This is the feeling that the phantom limb gradually shortens from time to time.
• Motion sensations (eg the feeling that the ghost's legs are moving).
• Touch sensation, temperature, pressure and itching. Many amputees report feelings of heat, tingling, itching, and pain.

Maps Phantom pain

Signs and symptoms

Phantom pain involves the sensation of pain in the part of the body that has been removed.

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Epidemiology

Pain of limbs and the sensation of phantom extremities are interrelated, but must be distinguished from each other. While the sensations of ghost limbs are experienced by those with congenital limb deficiency, spinal cord injury, and amputations, ghost pain pain occurs almost exclusively as a result of amputations. Almost immediately after limb amputation, 90-98% of patients reported experiencing a ghostly sensation. Nearly 75% of individuals experience phantom as soon as anesthesia is exhausted, and the remaining 25% of patients experience ghosts within days or weeks. Of those who experience a harmless sensation, the majority of patients also report different pain sensations.

Age and sex have not been shown to affect the onset or duration of ghost pain. Although not yet fully explored, an investigation of lower limb amputations observed that when stumps decreased, there was a greater incidence of moderate and severe phantom pain.

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Pathophysiology

The neurological basis and mechanism for ghost pain are all derived from experimental theories and observations. Little is known about the actual mechanisms that cause pain, and many theories overlap. Historically, phantom pain was thought to have originated from neuromas located at the end of the stump. Traumatic neuromas, or non-tumor nerve injuries, often arise from surgery and result from abnormal growth of injured nerve fibers. Although stump neuromas contribute to phantom pain, they are not the only cause. This is because patients with congenital limb deficiency sometimes, though rarely, have phantom pain. This suggests that there is a central representation of the limbs responsible for painful sensations. Today, the theory is based on changes in neurological pathways and cortical reorganization.

The peripheral mechanism

Neuromas are formed from the wounded nerve endings at the stump site that are capable of firing the potential for abnormal action, and are historically regarded as the main cause of ghost pain. Although neuromas may contribute to phantom pain, pain is not completely eliminated when peripheral nerves are treated with conducting inhibitors. Physical stimulation of neuromas can increase the activity of fiber C, thus increasing phantom pain, but the pain still persists after neuromas stop performing the firing action potential. The peripheral nervous system is thought to have the most modulation effect on ghost pain.

Spinal mechanism

In addition to peripheral mechanisms, spinal mechanisms are considered to have a role that affects phantom pain. Edge neural injury can cause degeneration of fibers C in the dorsal horn of the spinal cord, and ending fibers A can then branch off into the same lamina. If this happens, A fiber input can be reported as a dangerous stimulus. Substance P, involved in the transmission of pain signals, usually expressed by A? and fiber C, but after peripheral nerve damage, the substance P is expressed by A? fibers. This causes the hyperexitability of the spinal cord, which usually only occurs when there is dangerous stimulation. Because patients with complete spinal cord injuries experience phantom pain, there must be a central underlying mechanism responsible for generation of ghost pain.

Central mechanism and cortical remapping

Under ordinary circumstances, genetically determined circuits in the brain remain stable throughout life. It is estimated, until about 30 years ago, no new neural circuitry could form in the adult mammalian brain. More recently, functional MRI studies in amputees have shown that almost all patients undergo motor cortical remapping. The majority of motor reorganizations have taken place as a shift under the area of ​​the hand from the cortex to the facial representation area, especially the lips. Sometimes there is a shift in the side from the motor of the hand cortex to the ipsilateral cortex. In patients with ghost pain, reorganization is large enough to cause cortical lipid representation changes to the area of ​​the hands only during lips movements. It has also been found that there is a high correlation between the extent of extremity limb pain and the extent to which shift of the cortical representation from the mouth to the hand area of ​​the motor and the somatosensory cortical reorganization has occurred. In addition, since phantom pain in upper limb amputations increases, there is a higher degree of shift from facial motor representation. There are several theories that try to explain how cortical mapping occurs in amputations, but none is supported for the most part.

Neuromatriks

Neuromatriks theory proposes that there is a wide web connecting the thalamus and cortex, and the cortex and limbic system. This is a theory that goes beyond the body schema theory and incorporates awareness of self-consciousness. This theory proposes that conscious awareness and self-perception are produced in the brain through input patterns that can be modified by different perceptual inputs. This tissue has been genetically determined, and modified throughout one's life by various sensory inputs to create neurosignature. It is the neurosignature of a particular part of the body that determines how it is consciously perceived. Input systems that contribute to neurosignature are especially somatosensory, limbic, and thalamocortical systems. Neuromatriks theory aims to explain how certain pain-related activities lead to a conscious perception of phantom pain. The persistence of neurosignature, even after amputation of the limbs, can be a cause of sensation and pain. Phantom pain may arise from abnormal reorganization in neuromatrics to a pre-existing pain state.

Opposition to the theory of neuromatriks exists largely because it fails to explain why the aid of a phantom sensation seldom relieves the ghost pain. It also does not discuss how sensations can spontaneously end and how some amputees do not experience the sensation of ghosts at all. Moreover, the main limitation of neuromatriks theory is that it also widely takes into account various aspects of the perception of ghost limbs. It may also be too difficult to test empirically, especially when testing the phantom sensation without pain.

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Management

Various methods have been used to treat ghost pain legs. Your doctor may prescribe medications to relieve pain. Some antidepressants or antiepilepsy have been shown to have beneficial effects for reducing ghost pain. Often physical methods such as light massage, electrical stimulation, and hot and cold therapy have been used with varying results.

There are many different treatment options for ghost pain limbs that are actively being studied. Most treatments do not take into account the underlying mechanisms of phantom pain, and are therefore ineffective. However, there are several treatment options that have been shown to reduce pain in some patients, but this treatment option usually has a success rate of less than 30%. It is important to note that this success rate does not exceed the placebo effect. It is also important to note that because the rate of cortical reorganization is proportional to ghost pain, any disturbance to the amputated area can improve the perception of pain.

Non-surgical technique

Mirrored box therapy

Mirrored box therapy allows the illusion of movement and touching ghostly boughs by inducing a somatosensory and motor clutch between the fantom and the real limb. Many patients experience pain due to clotted ghost limbs, and since ghost limbs are not under voluntary control, opening the lid becomes impossible. This theory proposes that the ghost limbs feel paralyzed because there is no feedback from the ghosts back to the brain to inform the opposite. Vilayanur S. Ramachandran believes that if the brain receives visual feedback that the limbs have moved, the phantom limbs will become untouched.

Although the use of mirror therapy has proven effective in some cases there is still no widely accepted theory of how it works. In a 2010 study of ghostly ghost pain, Martin Diers and his colleagues found that "In randomized controlled trials using graded motor images... and mirror training, patients with complex regional pain syndromes or ghost pain pain showed decreased pain as well as improved post-treatment function and at 6 months of follow-up, and it indicates that the order of treatment is important. "The study found that mirror imaging did not produce significant cortical activity in patients with ghost pain and concluded that" the optimal method for altering pain and brain representation, and the brain mechanisms underlying the effects of mirror training or motor image, are still unclear. "

A number of small-scale studies have shown encouraging results, but there is no current consensus on the effectiveness of mirror therapy. Recent reviews of the research literature published by Mosely and Ezendam conclude that much of the evidence supporting mirror therapy is anecdotal or derived from studies that have weak methodological qualities. In 2011, a large-scale review of the literature on mirror therapy by Rothgangel summarizes the current research as follows:

"For stroke there is evidence of moderate quality that MT [Mirror Therapy] as an additional intervention improves arm function recovery, and low quality: evidence of lower extremity and pain function after stroke Quality of evidence in patients with complex regional pain syndrome and ghost pain are also low: Company conclusions can not be drawn Little is known about which patients are most likely to benefit from MT, and how MTs should be applied: with a clear description of the intervention protocols should focus on standard outcome measures and systematically note the side effects. "

Pharmacological treatments

Pharmacological techniques are often followed by other treatment options. The required dose of pain medication often drops substantially when combined with other techniques, but is rarely discontinued completely. Tricyclic antidepressants, such as amitriptyline, and sodium channel blockers, especially carbamazepine, are often used to relieve chronic pain, and have recently been used in an effort to reduce phantom pain. Pain relief can also be achieved through the use of opioids, ketamine, calcitonin, and lidocaine.

Surgical technique

Brain stimulation in

Deep brain stimulation is a surgical technique used to relieve patients from ghost pain. Prior to surgery, patients underwent functional brain imaging techniques such as PET scans and functional MRIs to determine the exact trajectory at which pain originated. Surgery is then performed under local anesthesia, because patient feedback during surgery is required. In a study conducted by Bittar et al., Radio frequency electrodes with four contact points were placed in the brain. Once the electrode is in place, the contact location is slightly altered according to where the patient feels the greatest relief from the pain. Once the maximum relief location is determined, the electrode is implanted and secured to the skull. After major surgery, secondary surgery under general anesthesia is performed. The subcutaneous pulse generator is implanted into the pectoral pocket under the clavicle to stimulate the electrode. It was found that all three patients studied had received satisfactory painkillers from deep brain stimulation. The pain has not been completely removed, but the intensity has been reduced by more than 50% and the burned component has completely disappeared.

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See also

• Phantom limb
• Phantom eye syndrome
• Frieder Kempe

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References

• MacLachlan, Malcolm; McDonald, Dympna; Waloch, Justine (2004), "Mirror Treatment of Phantom Pain Lower Limbs: Case Study", Disability and Rehabilitation , 26 (14/15): 901-904, doi: 10.1080/09638280410001708913, PMIDÃ,15497919

• Richardson, Cliff; Glenn, Sheila; Horgan, Maureen; Nurmikko, Turo (October 2007), "A Study of Prospective Factors Associated with Phantom Paste Massage Presence Six Months After Major Limb Amputation in Patients with Vascular Disease Edges", The Journal of Pain , 8 (10): 793-801, doi: 10.1016/j.jpain.2007.05.007, PMID 17631056 Ã,

Source of the article : Wikipedia