自從羅馬學者Aulus Cornelius Celsus 在二千年前提出了發炎的表徵包括紅(Rubor)、腫(Tumor)、熱(Calor)、痛(Dolor)之後,疼痛與發炎的關係便牢不可破,加上急性受傷後之組織炎症現象,更加肯定了「受傷"發炎"疼痛」的關係。所以但凡急性或長期肌腱痛都一概被診為發炎。但除了發炎外,是否就沒有其他致痛原因?
甚麽叫炎症?
疼痛並非界定發炎的絕對準則,組織中有否炎症細胞(巨噬細胞、T淋巴細胞、肥大細胞)與及前列腺素(Prostaglandin E2)水平是否飊升,才是炎症的指標。近代研究更發現,創傷後的炎症反應是重要修復過程,並非要除之而後快(Chan, and Fu, 2009)。
其實早在一九七六年,義大利學者Giancarlo Puddu已發現長期疼痛肌腱中的膠原蛋白碎裂分離,卻沒有炎症細胞,並首先以“Tendinosis” (慢性肌腱病變)的名稱來形容此現象(Puddu, et al., 1976),可惜當時「炎症」的理論較易為人接受,Puddu的發現並未引起多大注意(現在也好不了多少!)
慢性肌腱病變-“Tendinosis”
大量研究發現長期疼痛肌腱中的膠原蛋白雜亂無章(Puddu, et al.,1976),纖維幼細及中斷,脆弱及鬆散的第三類膠原蛋白比例增加(Khan, et al., 1999),並有壞死及鈣化現象,肌腱的韌度及彈性也較差(Soslowsky, et al., 2000)。這就是為何肌腱變厚(不少人以為是骨頭變大)及活動初時肌腱繃緊疼痛的原因。簡單來說,就是肌腱霉爛、脆弱、無法復原,但絕非發炎。這些發現,完全推翻了一直流行的炎症理論,真是晴天霹靂,怎麼與聽到的不一樣!?
真正的肌腱炎並不常見,且在三至五星期內便自然痊癒(Khan, et al., 2000)。相反,慢性肌腱病變卻俯拾皆是,又難復原(Astrom, et al., 1995; Khan, and Cook, 2000)。
不少學者都認為應該放棄肌腱炎這名稱,免得誤導大眾及醫者以消炎的方法治療(Alfredson, 2005; Khan, and Cook, 2002; Sharma, and Maffulli, 2005)。
沒有發炎,痛從那裡來?
其實並非發炎才會致痛,慢性肌腱病變組織滲出的硫酸軟骨素(Chondroitin Sulphate)及神經傳導物質穀氨酸(Glutamate)也可刺激痛覺神經末梢產生痛楚(Alfredson, et al., 1999; Khan, et al., 2000)。同時,膠原蛋白排列紊亂,結構改變,承受張力時膠原蛋白異常變形,也可刺激肌腱之痛覺感受器致痛(Alfredson, et al., 1999; Khan, et al., 2000; Leadbetter, 1992)。
「肌肉肌腱適應差異」
肌肉是運動的力量來源,是故有大量細胞核支持其新陳代謝及有充足血液供應,所以肌纖維能夠每七至十五天便更新一半(Goldspink, 1992),這麼快的更新速度能讓肌肉快速生長以適應訓練。肌肉力量要靠肌腱傳導至骨骼,肌腱的主要成份是膠原蛋白,但製造膠原蛋白的細胞卻少得可憐,又因為要承受強大且持續的肌肉拉力,血液供應僅可維生。因此在正常情況下,需約一年才可替換半數膠原蛋白,是故肌腱生長極之緩慢,受傷後也極難復原(Hardingham, et al., 1974)。
八成慢性肌腱病變需時三至六個月才有望復原(Khan, et al., 2000),處理不當更可『至死不癒』。患者應有合理期望,不要以為塗些藥酒、服點藥物、敷敷冰便會在數天內復原。治療方向是要重新誘發修復程序及改善病變組織的微循環,而非盲目的消炎止痛敷冰(Almekinders, et al., 1995; Collins, 2008)。
十四年前,英國運動醫學期刊總編Karim Khan已說過:“It’s the time to abandon the tendonitis myth”. 『是時候摒棄肌腱炎神話。』(Khan, and Cook, 2002)時至今日,神話依然,要改變根深蒂固的觀念,難似登天。
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