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The Phantom Limb Pain

Generally, theories are based on neurological pathway and cortical re-organisation based on amputated people. Neurobiological ideas proposed up to now are divided into peripheral, vertebral and central system, which all overlap one another to a certain degree. Peripheral mechanism says that impulses created by neuromas at the stump are identified by the brain as pain. Alternatively, the central device explains phantom pain in conditions of central sensitisation. Whilst, spinal mechanism details phantom limb pain as found in the mind itself.

On the other side, some researchers assume that there are psychological explanations to phantom limb pain. Analysts have proposed that phantom limb pain can be described by learning the personality of the amputee. Yet analysts have also tried out to check that phantom limb pain is a result of amputated people using defence mechanisms to handle their reduction.

Peripheral system:

According to this device, pain is perceived in the mind as neuromas are developed in the tip of the stump, which create impulses that travel in the spinal-cord.

After amputation, fibres of the nerve endings form neuromas that induce abnormal impulses travel to the brain. There is good data to suggest that neuromas are able to spontaneously flame impulses, it is also known that neuromas improve the sensitivity of mechanised and other stimuli received.

Chabal et al (1989) in an experiment demonstrated that when gallamine, a potassium programs blocker was injected into the neuromas of amputees, their stump pain increased. He recommended that the permeability in ion route within neuromas added to phantom limb pain. This shows that neuromas are a possible cause for phantom limb pain, this provides evidence for the peripheral device. More experimental studies support this mechanism, as when neuromas are surgical removed, the pain is reduced at the phantom limb. Again, signifying neuromas are involved in phantom limb pain.

However, there are a great number of observational and experimental studies that not support the peripheral device. Physical stimulation of neuromas can increase C-fiber activity, therefore the degree of phantom pain increase, however, after the neuromas have ended firing, action potentials pain still persists.

As when peripheral nerves treated with conduction blocking brokers, the pain is not completely eliminated, it is merely reduced (2), which shows that neuromas aren't the sole cause for phantom limb pain but there are other factors included.

Furthermore, studies also show that pain can occur in the lack of the stump (7), hence, lack of neuromas, which empathises the view that neuromas are not the sole reason.

In addition to the, pain can occur when limb is congenitally absent. Weinstein and Sersen (1961) identified five children with congenital absence who experienced phantom limb aches and pains on a limb that never existed (8). In a very follow-up study, Weinstein et al (1964) reported another 18 situations in which phantoms were experienced in congenitally absent limbs. This shows that neuromas and the stump may well not even be engaged in phantom limb pain but may be a factor that escalates the sensation noticed by patients (9). Moreover, phantom limb pain is present immediately after amputation, this rules out the causal role of neuromas, as the amputated stump have not yet shaped neuromas.

More recent research has verified these findings suggesting strong facts for choice explanations of phantom limb pain, as merely studying the peripheral system may well not be sufficient to detailing phantom limb (10-11).

Central device:

According to this device, phantom pain is a result of central sensitisation. Central sensitisation is where sensory neurons in the dorsal horns of the spinal cord become sensitised by peripheral injury or inflammation. This sort of sensitisation has been suggested just as one causal mechanism for persistent pain conditions. It is also suggested by research workers to describe phantom limb pain.

The loss of afferent source from periphery brings about irritations in dorsal horn or in the central anxious system resulting in everlasting changes in synaptic structure and reduced inhibitory functions and increased excitability functions is seen in the dorsal horn.

Under normal circumstances, circuitry in the brain remains largely steady throughout life. However, useful MRI studies in patients with amputated limbs show that almost all patients have had a motor unit cortical reorganisation.

Cortical corporation is defined in terms of maps known as homunculus. For example, sensory information from the ft. projects to 1 cortical site and the projections from the hand target to some other site. As the result of this Organisation predicated on anatomical connection of sensory inputs to the cortex, cortical representation of the body resembles a homunculus. (Illustration of sensory homunculus).

The phantom limb experience, which is considered to result from disorganisation in the mind homunculus and the inability to receive source from the targeted area. Studies show that there is a high relationship with the degree of physical re-organisation and the amount of phantom pain.

Major engine re-organisation occurs in a downward move from the hand section of the cortex to the face area, especially the lips. Sometimes there is a side move of the hands electric motor cortex to the ipsilateral cortex. In patients with phantom limb pain, the reorganisation was great enough to cause a change in cortical lip representation in to the side areas which occurred during lip movements (14).

There have been many ideas proposed to make clear this cortical re-mapping but nothing have been recognized. This suggests that the concept of central mechanism can't be accepted as the only real causal element in contributing to phantom limb because of its insufficient experimental data.

Spinal system:

According to this mechanism, phantom limb pain is found in the brain itself. Davies et al (1998) reported that thalamic excitement evokes phantom pain (15). Holmes (1911) identified a case in which a patient reported the total disappearance of kept lower leg phantom pain carrying out a lesion in the patient's right hemisphere, (39) suggesting that the pain is found in the mind. Merzenich et al (1984) amputated fingers in monkeys, which lead to a 1-2mm invasion into cortical representation of amputated finger in most important somatosensory cortex suggesting that pain didn't involve the amputated limb but was a lot to do with the company of the mind (16). Pons et al (1991) reported an identical finding, but a larger invasion in adult macaques (18). Ramachandran (2000) proved this using MEG, where he viewed the re-organisation in the top limb of amputees, and he discovered that the sensory type from face activated the side area in the mind, a 2-3cm invasion (19-21). This provided strong proof for the vertebral mechanism.

Livingston (1943) completed a report on thirty six amputated people who suffered from phantom limb pain. They were given local anaesthetic into spinal cord, and it was found that nine out of the thirty-six patients said their pain was permanently gone and over two-thirds said they thought temporarily reduced pain. He recommended that 'closed down, self-sustaining, reverberating circuits' are setup by persistent peripheral irritations or by release of spinal-cord skin cells from inhibitory control through the loss of afferent suggestions (31). Furthermore, once these circuits are set up, surgery of the peripheral source has no effect on them and, therefore, won't abolish the pain, suggesting more proof for the spinal mechanism.

The device of dis-inhibition in the spinal-cord resulting in phantom limb pain was evaluated by Wall (1981). He proposed that the quick lack of afferent input following amputation results in a number of changes at both peripheral and vertebral level.

Furthermore, Wall proposed that we now have both immediate and long-term changes. Such functions described by Wall membrane suggest that the consequences of peripheral nerve lesions spread beyond the broken cells into the spinal-cord itself. Therefore, it addresses some of the observations on phantom phenomena not discussed by peripheral theories (41). Thus recommending a more valid theory of justification of phantom limb pain.

Neuromatrix theory:

The neuromatrix theory was proposed by Melzack (1990), which followed the spinal mechanism. He argues that people have an integral matrix of neurons which is spread around the mind. When the active matrix is deprived of input from the limbs, phantom pain develops as the neuromatrix produces abnormal firing as an alternative (17). The idea shows that the conscious consciousness and belief of self is established in the brain, that can be changed by different perceptual inputs (22). Melzack explains the basic result from the neuromatrix as a "neurosignature" which is particular to the individual. The matrix is genetically motivated but is customized throughout life, to make a neurosignature. It really is this neurosignature of an body part that decides how it is consciously identified (4).

In the situation of amputated patients, irregular type to the matrix after amputation results pain. This abnormal input is because insufficient normal suggestions or high degrees of input induced by abnormal firing of damaged nerves.

Melzack also suggested that neuromatrix extends to three major neural circuits. The input systems contributing to the neurosignature are mainly the somatosensory, limbic, and thalamocortical systems. Studies completed on brain-damaged patients have shown that the ones that refused to accept their limbs within their body show to have destruction in their somatosensory systems (25). Outcome is moved into conscious consciousness by integration of most these system. It is suggested that the pain aspect of output occurs for several reasons. For example, cramping might occur because limb movement is the pre-wired part of neuromatrix. Thus, after amputation, neuromatrix gets no signal from periphery that the limb is moving, so neuromatrix outcome will include the basic neurosignature. This may send strong messages for the limb to go so patients record cramping (23, 26).

Somatosensory pain ram illustrates how encounters can shape the pattern produced by neuromatrix (24). This suggests that neural representation of pre-amputation pain is formed after one very powerful pain experience, since pain memory space is experienced as both sensory and affective events. We presume that both experiences are encoded in neuromatrix (27).

This neuromatrix theory is consistent with the vertebral, central and peripheral device. The idea also suggests that psychological factors may also produce source that triggers the matrix and brings about pain by dread, insomnia, stress, and fatigue (28-29).

The neuromatrix theory is similar to the gate control theory and can be applied to persistent pain not simply phantom pain. Gate control theory proposes that pain is the understanding whose quality and intensity is influenced by the individual's background and their state of mind.

However, the neuromatrix theory does not explain the way the pain can spontaneously end and how some amputees do not have problems with phantom limb pain. This is a major criticism, which consequently reduces the theory's power. The theory also does not make clear how these factors influence pain. The theory is also very hard to check, although pet models have been useful, they do not provide great support. However, the neuromatrix does provide a device to explain understanding of pain and also psychological management of pain. (30). Overall, it is clear that further research is necessary in this area.

Psychological explanations:

There are lots of emotional explanations that contain been proposed. Some researchers have proposed that phantom limb pain can be explained by taking into consideration the personality of the amputee. For example, Parkes (1973) found that those who have a prolonged phantom pain obtained on top of personality measure of 'compulsive self-reliance' and 'rigidity'. This suggests that there is something about these personality qualities that cause amputated people to have a higher chance of experiencing phantom pain than those who obtained lower on the questionnaire test 'compulsive self-reliance' and 'rigidity'. Parkes also advised that those who find themselves rigid dislike and resist change, so experience phantom pain as they find it difficult to accept the loss of a limb. Those who are compulsive self-reliance also get pain because they feel helpless. Patients become distressed needing to rely on someone else (32). However, Sherman said that mental health explanations of phantom pain have less regarding personality but more regarding after amputation experience. He said that treatment success rate is low so this will cause stress in every but the most prolonged, self-reliant individuals to insist treatment (28, 33). Contradicting this Shukla et al (1982) found no difference in personality in amputated people who experience phantom limb pain and the ones that not experience phantom limb (40).

Another psychological reason is the fact that pain is because the utilization of defence mechanisms such as denial or repression (34-37). Weiss and fishman (1963) advised that patients may deny limb loss therefore pain is a reinforcement of the living of the limb (36). Kolb further areas that, the more important your body part is to the average person emotionally, a lot more the individual will maintain denial of losing (34). However, Simmel (1958) argues that phantom pain occurs as folks are flooded with emotions and anxiety from the loss of the body part (35). However, this idea is difficult to test, as the causal hyperlink between denial, despair and phantom limb pain cannot be established.

Further difficulty in establishing the role of mental health distress comes from symptoms overlapping, as it is difficult to determine which symptom is reflected where disorder. For instance, difficulty in addressing sleep is regarded as a symptom of melancholy. Yet, additionally it is a feature of serious pain. In the same way, endorsement of items associated with tiredness is indicative of depressive disorder, but is also associated with persistent pain in the absence of depression.

Relationship between phantom limb and subconscious distress is confounded by a number of post-amputation factors. Also, research in this field didn't differentiate between acute adjustment response and chronic problems (28), for example it's quite common to feel reactions of surprise, grief and denial, for individuals who just underwent amputation, (38) and this is expected within the post-amputation period.

Conclusion:

Overall both neurobiological and psycho explanations are key to detailing phantom limb pain. Yet, the neurological basis and mechanisms for phantom limb pain given in this article are all based mostly from experimental theories and observations. Our knowledge in this field is little. There is bound empirical evidence to support studies carried on amputated patients. Also, we've a limited understanding of the true mechanism causing phantom pains which suggests that it's difficult to establish an explanation for phantom limb pain. However, a number of the have been suggested and many ideas highly overlap, making it difficult to reach a conclusion.

One of the major weaknesses to the peripheral mechanism is that it has failed to discuss how it is possible for the stump to be manipulated and the effect sensation thought are pain rather than any other discomfort such as touch, pressure or itchiness (5-6). Using the info provided, I do not believe that phantom limb pain can be discussed by peripheral system. Yet, I really do believe that it does have a role in increasing phantom limb pain.

Spinal mechanism does indeed provide a much better description for phantom limb pain. However, it didn't describe why phantom limb pain in addition has been reported where there is absolutely no nerve damage and where there has been a complete business deal of the spinal-cord (23).

On the other side, strong evidence facilitates the psychological justification for phantom limb pain but recent study suggests that mental factors do not play causal role in phantom pain but do increase degrees of pain experience (28). It is also interesting to notice that research on "personality types" are associated with an increase of phantom limb pain, whereas nothing discuss personality types that are less likely to experience phantom limb pain. Yet, it could be argued that the neurobiological mechanism has stronger research to aid phantom limb pain, recommending a better justification.

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