It is speculated that the changes of sensory field and cortical reorganization observed after amputation are related to PLP. The sudden absence of afferent nerves following amputation resulted in many changes at the peripheral and spinal levels. On the other hand, the neural mechanism of PLP is closely related to the brain reorganization after denervation in the sensorimotor system. On the one hand, peripheral mechanisms include mechanical stimulation, circulating catecholamines, proinflammatory immune factors, and other sensitive neurochemicals activating the residual limb neuromas. The underlying mechanisms of PLP have commonly been classified according to the level of the nervous system: peripheral or central. Due to failure to respond to oral medication, we attempted the use of auricular therapy (AT) and achieved satisfactory symptom improvement in this patient. Hence, we presented a case of a 28-year-old female suffering from phantom pain accompanied by intermittent myoclonus in her residual limb after amputation. In clinical settings, PLP and jumping residual limb rarely occur at the same time. Similarly, the pathophysiology has not been completely elucidated and there are currently no guidelines or standardized treatment for it. The “jumping residual limb” syndrome is generally regarded as a form of spinal reflex myoclonus limited to the amputation site. Although it is reported that only 1% or less of these post-amputation patients experience spontaneous, involuntary, autonomous movements of the residual limb, it is significantly disturbing to patients when it does occur. On the other hand, movement disorders following amputation is a rare complication and can manifest as the jumping residual limb phenomenon, the nature of which is a form of peripheral myoclonus and is characterized by sudden, brief, and sometimes repetitive muscle contractions, jerking, tremulousness or spasms of the residual limb. At present, given to a lack of robust evidence to support the efficacy of many treatments, it remains difficult to effectively manage. Regarding etiology and pathogenesis, PLP is regarded as one kind of neuropathic pain and is caused by a lesion of the somatosensory nervous system.
Although the frequency and intensity of pain diminish over time in most PLP patients, severe pain can persist in about 5–10% of amputees, affecting individuals’ subjective well-being, as well as both physical and mental components of quality of life. The onset of pain may be elicited by environmental, emotional, or physical changes. Most of the amputees suffer from burning, cramping, pinprick, stabbing, itching, or other sensations of pain in the first few weeks following amputation. It is a common complication and the prevalence may be as high as 75–80% in amputees. Phantom limb pain (PLP) is defined as persistent painful sensations perceived in the missing portion of the amputated limb.
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