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Pathophysiology of Reflex Sympathetic Dystrophy

交感神經反射失養症的病生理學

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摘要


交感神經反射失養症常發生於外傷之後,它的臨床症狀包括了肢體持續性的燒灼痛,觸、痛覺敏感,腫脹,皮膚顏色及溫度改變,流汗改變及關節活動度受限等。較有效的治療方法包括了早期交感神經阻斷,肌膜引痛點局部注射,口服類固醇及物理治療等。其致病機轉目前仍不清楚,但認為和交感神經活性過高有關;早期的研究以為於神經受傷處形成感覺神經和交感神經突觸,並造成脊髓反射異常,如此形成一惡性循環所致。之後的研究則認為可能是感覺神經末稍阿爾發一受體(alpha-1)被活化,並發展出對交感神經傳導物質過度敏感性,此種變化並可往上傳至脊髓,造成脊髓反射異常,臨床上,交感神經反射失養症常可見合併有肌膜引痛點,而肌膜症候群亦可見交感神經反射異常之現象;肌膜引痛點局部注射對交感神經反射失養症亦是一相當有效的治療方法。目前的研究認為肌膜引痛點和交感神經反射失養症,於治病機轉及臨床表現方面有相關性,它們均和交感神經及脊隨反射異常有關。但二者詳細的作用機制仍需要進一部的研究探討。

並列摘要


Reflex sympathetic dystrophy (RSD) usually develops in a limb after an injury. It is characterized by constant burning pain, allodynia, hyperalgesia, swelling, vasomotor and sudomotor changes. Once RSD is established, successful outcome depends upon early recognition and therapy. The therapies include sympathetic blockade, myofascial trigger point injection, physical therapy, oral corticosteroid, etc. Many hypotheses have been proposed to explain the mechanism responsible for RSD. However, no single hypothesis proposed to date explains all of the features of RSD. It has been recognized for decades that pain may in certain instances be dependent on sympathetic innervation of the area afflicted with pain. Sympathetically maintained pain (SMP), a term that describes the intimate interrelationship of pain and autonomic dysfunction, is recognized by many to be an aspect (or even a defining characteristic) of causalgia and RSD. It seems that alpha-1 receptors expressed on the terminals of sensory nerve fibers develops the capacity, when activated, to evoke pain. Further studies are needed to elucidate the pathogenesis of the RSD.

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