Anosognosia and Phantom Limb Syndrome - Essay Example

Anosognosia and Phantom Limb Syndrome Name: University: Date: Anosognosia and Phantom Limb Syndrome Introduction Phantom limb pain according to Chahine and Kanazi (2007) is a neuropathic pain whose recommendations for treatment are similar to the neuropathic pain syndromes’ recommendations. Essentially, Phantom limb syndrome is a medical condition whereby patients experience some sort of sensations in non-existing limb. Normally, it takes place in 80 to 100 per cent of amputees, and sometimes results in resistant to treatment. Some risk factors of Phantom limb pain include traumatic amputation, preoperative pain, as well as a form of anesthetic procedure utilised during the amputation. In this case, a number of pathophysiologic theories such as somatosensory cortical rearrangements, central sensitization as well as spinal mechanisms have been proposed. On the other hand, anosognosia can be defined as lack of awareness about impairment, failure to recognise that an illness or deficit exists, in body function such as memory (Ramachandran, 1996). Classically, anosognosia takes place amongst patients who have had stroke in the brain’s right parietal lobe; thus, generating left hemiplegia. The affected person can deny that there is something wrong in their body, in spite of the fact that their left side has been paralyzed. Anosognosia as mentioned by Prigatano (2010) is not a simple denial; instead, it is a subconscious psychological mechanism utilised by people from time to time. This is bodily damage to brain part that people use to think about themselves. Therefore anosognosia is anatomical while denial is psychological. The essay seeks to offer details about phantom limb and Anosognosia and discuss some of the prevalent etiological theories for these bizarre syndromes. Discussion Phantom-limb pain is normally considered neuropathic, and is associated with damage of peripheral or central neurons. Even though this pain commonly occurs following an amputation of a leg or arm, it may as well take place after some body parts such as penis, rectum, breast or teeth are removed through surgical procedures. Lesions of the central nervous system or the peripheral nerves may as well bring about phantom-limb syndrome. The syndrome is more likely to happen to people who had chronic pain prior to the amputation, but it is less likely to occur to people who had amputation while they were very young. According to Flor (2002), high frequency of phantom-limb pain is reported amongst older children. Even though phantom sensations appear to take place amongst individuals born with no limb, pain in the non-existing limb appears to be extremely rare in such circumstances. Phantom-limb pain long-term course is not clear because the majority of the existing studies as cited by Flor (2002) show that between 80 and 100 per cent of amputees experience phantom sensations that are non-painful. Phantom limb pain frequency has been reported to be between 60 and 80 per cent during the early postoperative period. The number of patients having this type of pain reduces as time passes, but is still significant; the intensity as well as duration of painful incidences does drop for most patients. Phantom limb syndrome affects adults more as compared to children. Chances of developing phantom limb syndrome are increased by pre-amputation infection, pre-amputation pain, traumatic amputation, blood clot within the amputated limb, among other factors (Crawford, 2014). The anosognosia anatomical basis in patients with stroke has been described by a number of studies. Anosognosia according to Pia, Neppi-Mòdona, Ricci, and Berti (2004) appears to be similarly frequent when the damage is continued to temporal, parietal or frontal cortical structures, but it is very high when the lesions involve a combination of frontal as well as parietal structures. Normally, people suffering from anosognosia often confabulate. According to Baddeley, Kopelman, and Wilson (2003), confabulation is coming up with an answer that connect pieces of people, time, information and places that do not fit together. Occasionally the affected persons would combine memories from different occasions and maintain that the incident unfolded that way. Sometimes they insist that the event took place recently while actually it occurred decades ago with different individuals. At times, they combine information from the television or newspaper with their event. Still, anosognosia as mentioned by reference is not a problem denial, but rather a sincere incapability to recognize the existing problem. It is mainly attributed to brain injuries, and takes place at different degrees in disorders like Alzheimer's disease, bipolar disorder and schizophrenia. A person suffering from anosognosia cannot be considered as difficult and is not declining to face the truth; instead, he/she is literally not able to believe that his sickness is, actually, a disease. Consequently, he/she fails to see the essence of taking medication so as to control his/her illness. A lot of individuals with anosognosia decline to take medication for bipolar disorder or schizophrenia, because they believe they are not ill. If coerced, they may pretend to cooperate, while they discard their medication in secret. Cortical Reorganization theory as mentioned by reference is the most cited etiological theories that explain phantom limb syndrome. Cortical reorganization theory rationality was examined by Merzerich et al, and they established that after deafferentation and amputation, cortical changes were displayed by the adult monkeys in the somatosensory homunculus. The finding resulted to the belief that cortical reorganization is a key component that produces phantom limb sensations. According to cortical reorganization theory, maladaptive cortical reorganization takes place in the motor cortex and somatosensory cortex. Besides that, maladaptive reorganization takes place when the control of the missing limb’s motor and somatosensory representations is taken over by the surrounding areas take over. Reference posits that the face, normally, take over homunculi regions related to the arm for people whose upper limb have been amputated. It is suggested that cortical reorganization as well as maladaptive plasticity in phantom limb patients expounds the cause of phantom limb syndrome. Functional MRI data demonstrates that phantom limb syndrome patients have higher activation in motor and somatosensory cortices, while amputees with no healthy controls and pain show no increased activation. Cortical reorganization theory has strongly been supported, and has facilitated in developing possible treatment techniques that try to reduce decrease maladaptive cortical reorganization amongst amputees. Besides that, Ronald Melzack established the neurosigniture or neuromatrix theory of phantom limb syndrome, and the theory is associated closely with the body schema concept. Neuromatrix as described by reference is a neural network, which generates different patterns of impulse depending on the received input from different cortical areas as well as the relationship created between different neural circuits. Such cortical inputs come from visual areas, limbic system circuits, thalamocortical circuits as well as the somatosensory cortex. Basically, inputs from such areas are synthesized and processed so as to create a distinctive, integrated output. According to the neuromatrix theory, the nerve impulses are produced from the self-body schema’s cortical inputs forming the basis of self-awareness. In this case, the integrated output is considered a neurosigniture and is believed to be a hardwired. Therefore, after amputation the hardwired neurosigniture can generate problems due to conflict between perceptions concerning the body’s post-operational state. After amputation, the static neurosigniture remains unchanged even if there is input signifying non-existence of the phantom limb. The input differences from the body and the neurosigniture results in an overriding response, which leads to the perception that the body is unchanged; therefore, an intact limb perception, irrespective of conflicting sensory input from the body, can be the main cause of phantom limb syndrome. Given that psychological denial, confabulation, confusion, defective feedback and disconnection failed to completely explain anosognosia, a feedforward theory of anosognosia was proposed by Heilman (1991) (Heilman, Barrett, & Adair, 1998). Basically, the theory is associated with expectations. Generally, recognize can be recognised through expectations, and so the feedforward theory suggests that anosognosia is an intentional system deficit in the formulation of movement expectations. According to the theory, the patient intentional system is simultaneously activated with his/her motor system so that a movement can occur. A representation of the body with regard to a particular movement is constantly contrasted with afferent information. For patients knowing their hemiplegia, the body representation as well as comparator system identify a mismatch between the movement expectations and the actual unsuccessful performance of movement. Still, for patients with anosognosia, their intentional-preparatory system is damaged and this results in lack of expectations in moving their paretic limb (Gerafi, 2011). Therefore, the comparator system becomes unable to identify any mismatch, leading to the unawareness of detecting their movement failure. With regard to the confabulation theory, confabulation as described earlier is whereby a spontaneous false response that is not associated with reality is created by a person. For anosognosia patients, they normally create confabulations because of neurological impairment. Therefore, anosognosia is considered as a form of confabulation (Ramachandran, 1996). From an evolutionary point of view, confabulations exist so as to generate a coherent belief system as well as certainly maintain balance and control to the patient’s behaviour. According to confabulation theory, the coping strategies of right and left hemispheres are very different. The right hemisphere detects if anomalous information surpasses a particular threshold before forcing for a review of the maintained model by the left hemisphere (Gerafi, 2011). The left hemisphere, on the other hand, produces a model and tries to maintain it constantly. In case new information put this maintained model at risk, it will lead to confabulation or denial; thus, stabilisation of the model. Therefore, this results in a conflict between left and right hemispheres because of the left hemisphere attempt to maintain the original model while simultaneously the right hemisphere tries to force modification of the model. Therefore, patients with anosognosia have lost this mechanism because their right hemisphere has been damaged, and therefore, cannot detect anomalous information. As a result, the left hemisphere continually denies as well as confabulates the hemiplegia with no modification of the model, which could otherwise be recreated into a different model by utilising the same data. Without a doubt, it is alluring to believe that because the bodies are so close to the owners, the scope for delusions will be minimal. However, for some bodily experiences the satisfaction conditions are not easy to articulate. People through body senses can access their body, and this privileged is the main source of infallible knowledge (Ramachandran, Krause, & Case, 2011). A number of studies as cited by Besharati, Crucianelli, and Fotopoulou (2014) have similarly come to a conclusion that patients suffering from anosognosia are more inclined to recognise their deficit when asked in third-person questions. More studies have also pointed out that patients with such bizarre syndromes may originally come to understand their sickness through encounters with a third person. For instance, a patient can only comprehend and later internalize that he/she had a stroke through a third-person observation. Intellectualising conscious awareness as a first-person phenomenon has to a large extent resulted in side-lining of its scientific examination (Besharati, Crucianelli, & Fotopoulou, 2014). Still, being unaware of illness, particularly in the early critical stages, can considerably hamper efforts for rehabilitation. Conclusion In conclusion, the essay has offered details about phantom limb and anosognosia and has also discussed some of the prevalent etiological theories for these bizarre syndromes. As mentioned in the essay, patients suffering from anosognosia normally fail to acknowledge their illness or impairment. Anosognosia as defined in the essay is the neuropsychological self-awareness deficit and normally related to both subcortical as well as cortical lesions that are distributed in the right hemisphere, leading to a left hemiplegia. Body awareness disturbances provide crucial perspectives into neurocognitive processes that are involved in making of the bodily self. Generally, anosognosia is a complex phenomenon that involves a multifaceted interplay between behavioral, emotional as well as neurological components. Some of etiological theories that discuss about anosognosia include confabulation theory and feedforward theory. On the other hand, phantom-limb syndrome is common sequelae of amputation that affects almost 80 per cent of individuals who undergo the procedure. As argued in the essay, central changes are the key determinant of phantom-limb syndrome; but still, psychological as well as peripheral factors can contribute to it. Some of theories that discuss the etiology of phantom-limb syndrome include; Cortical Reorganization theory and neuromatrix theory. References Baddeley, A. D., Kopelman, M. D., & Wilson, B. A. (2003). The Handbook of Memory Disorders. New York: John Wiley & Sons. Besharati, S., Crucianelli, L., & Fotopoulou, A. (2014). Restoring awareness: a review of rehabilitation in anosognosia for hemiplegia. Rev. Chil. Neuropsicol, 9, 31-37. Chahine, L., & Kanazi, G. (2007). Phantom limb syndrome: a review. Middle East J Anaesthesiol, 19(2), 345-355. Crawford, C. (2014). Phantom Limb: Amputation, Embodiment, and Prosthetic Technology. New York: NYU Press. Flor, H. (2002). Phantom-limb pain: characteristics, causes, and treatment. THE LANCET Neurology, 1, 182-189. Gerafi, J. (2011). Anosognosia for Hemiplegia: Theoretical, Clinical, and Neural Aspects. University of Skövde. Skövde, Sweden: Joel Gerafi. Heilman, K. M., Barrett, A. M., & Adair, J. C. (1998). Possible mechanisms of anosognosia: a defect in self-awareness. Philosophical Transactions of the Royal Society, 353, 1903-1909. Pia, L., Neppi-Mòdona, M., Ricci, R., & Berti, A. (2004). The Anatomy of Anosognosia for Hemiplegia: A Meta-Analysis. Cortex, 40(2), 367-377. Prigatano, G. P. (2010). The Study of Anosognosia. Oxford : Oxford University Press. Ramachandran, V. S. (1996). What neurological syndromes can tell us about human nature: some lessons from phantom limbs, capgras syndrome, and anosognosia. Cold Spring Harbor Symposia on Quantitative Biology, 61, 115-134. Ramachandran, V. S., Krause, B., & Case, L. K. (2011). The phantom head. Perception, 40, 367-370. Read More