Phantom limb pain: A literature review - 0 views
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. The purpose of this review article is to summarize recent researches focusing on phantom limb in order to discuss its definition, mechanisms, and treatments.
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The incidence of phantom limb pain has varied from 2% in earlier records to higher rates today. Initially, patients were less likely to mention pain symptoms than today which is a potential explanation for the discrepancy in incidence rates. However, Sherman et al.4 discuss that only 17% phantom limb complaints were initiated treated by physicians. Consequently, it is important to determine what constitutes phantom pain in order to provide efficacious care. Phantom pain is pain sensation to a limb, organ or other tissue after amputation and/or nerve injury.5 In podiatry, the predominant cause of phantom limb pain is after limb amputation due to diseased state presenting with an unsalvageable limb. Postoperative pain sensations from stump neuroma pain, prosthesis, fibrosis, and residual local tissue inflammation can be similar to phantom limb pain (PLP). Patients with PLP complain of various sensations including burning, stinging, aching, and piercing pain with changing warmth and cold sensation to the amputated area which waxes and wanes.6 Onset of symptoms may be elicited by environmental, emotional, or physical changes.
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The human body encompasses various neurologic mechanisms allowing reception, transport, recognition, and response to numerous stimuli. Pain, temperature, crude touch, and pressure sensory information are carried to the central nervous system via the anterolateral system, with pain & temperature information transfer via lateral spinothalamic tracts to the parietal lobe. In detail, pain sensation from the lower extremity is transported from a peripheral receptor to a first degree pseudounipolar neurons in the dorsal root ganglion and decussate and ascend to the third-degree neurons within the thalamus.7 This sensory information will finally arrive at the primary sensory cortex in the postcentral gyrus of the parietal lobe which houses the sensory homunculus.8 It is unsurprising that with an amputation that such an intricate highway of information transport to and from the periphery may have the potential for problematic neurologic developments.
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