在脊椎手術如此普遍的今天，脊椎術後失敗症候群可稱得上是一個相當嚴重的問題。估計在美國每年約有25,000至50,000個新病例產生。脊椎術後失敗症候群，並不全然是指手術本身失敗而言，在學術研究上更包括了凡是脊椎手術後症狀仍然持續，或是再度發生新的症狀之病症。另外，也包括手術後其他未經手術的脊椎新產生的退化性椎間盤疾症，均統稱為脊椎術後失敗症候群。而脊椎術後失敗症候群的病人，通常在手術後仍然持續出現背痛、坐骨神經痛，甚至造成生活功能障礙等等症狀。雖然嚴重程度不一，但是病人幾乎是無法正常工作，或是必須更換工作，甚至必須提前從職場退休。這對病人、家庭及社會無疑是一項嚴重的損失和打擊。在眾多造成脊椎術後失敗症候群之原因中，脊椎術後瘢痕組織之形成，可視為一個重要的病因。脊椎術後瘢痕組織，主要是由於手術中受到創傷的骨膜和脊旁肌群中的纖維母細胞侵入術後所殘留的血塊中，經過一段時期逐漸轉化而成脊椎術後瘢痕組織。MRI對於術後脊椎的檢查有很大的助益，但深入的研究後，對於脊椎術後瘢痕組織是否會造成脊椎術後失敗症候群，卻產生了疑問和爭論。即便是被大多數學者所接受的主流學說；主張脊椎術後瘢痕組織確實引起脊椎手術後的背痛與坐骨神經痛。但它究竟是如何引起術後疼痛及其確實的機轉，至今仍無定論。我們根據多數學者研究的結果，提出實驗假說，認為脊椎術後瘢痕組織的生長與脊椎術後失敗症候群，應有相當程度的關聯。脊椎術後瘢痕組織與脊椎術後失敗症候群之關聯，可能不僅是因為脊椎術後瘢痕組織對周邊神經組織所產生的機械式的壓迫和牽扯作用而已。因此我們利用一般研究脊椎術後瘢痕組織的動物實驗模式，進一步去探討脊椎術後瘢痕組織與脊椎術後失敗症候群在病態生理學上的關聯性。而根據實驗結果發現，脊椎術後瘢痕組織，延著術後椎板缺口進入脊柱管腔內，並與脊椎管腔內的神經組織形成沾黏。而此沾黏延伸的範圍，隨著椎板缺口加大，和術後時間的增長，而出現遞增的情形。脊椎術後瘢痕組織與脊椎硬腦膜形成沾黏，不僅使得與之沾黏的脊椎硬腦膜出現增厚，同時亦使馬尾內之神經根產生病理性變化。傳統上認為術後瘢痕組織，經由對脊柱內神經組織壓迫造成損傷，進而引發脊椎術後失敗症候群之症狀。但本實驗發現術後瘢痕組織本身對脊椎硬腦膜只形成沾黏，並無產生明顯壓迫之效應。且由DRG結構相對完整，認為術後瘢痕組織對於脊柱內神經組織之損傷，除了壓迫的作用外，應該還有其它的致痛機轉參與。而為了更進一步探討脊椎術後瘢痕組織，在脊椎術後失敗症候群中所扮演的角色，未來將結合應用電子顯微鏡和免疫染色之技術深入探究。

Degenerative conditions of the lumbar spine include degenerative disc disease, herniated nucleus pulposus (HNP), lumbar canal stenosis, and degenerative instability. As many as 40% of patients, however, fail to experience satisfactory long-term relief of symptoms after primary procedures. Failed back surgery syndrom (FBSS) has become a common entity. FBSS is a group of disorders with persistent or recurrent symptoms following spinal surgery, with the hallmarks of back pain, sciatica, and functional impairment. FBSS is characterized by severe chronic and disabling pain that generally is resistant to physiotherapy and pharrmacologic treatment. There are many causes of FBSS; among of the most common is epidural fibrosis. There are numerous reports suggesting that fibrosis and adhesions can cause compression or tethering of nerve root, which may cause recurrent radicular pain and physical impairment. However, the importance of epidural scarring in relation to persistent neurological deficits or post-surgical pain is debatable. Recently it has been suggested that mechanical compression of nerve roots in lumbar disc herniation may not be the only cause of clinical symptoms such as radicular pain and dysfunction. Therefore, we make hypotheses that epidural fibrosis can induce post surgical pain but the cause may be not due to the mechanical compression of spinal nerve or cauda equina only. We performed an experimental study of morphological analysis in post operative spinal tissue using animal models of Wistar mouse which were applied to study FBSS in many other laboratories. Under light microscopy screening exam with H & E stain, we found (1) The scar formation and adhesion is increasing with time course and size of lamina opening, (2) The scar adhesion has minimal dura compression effect, (3) The scar adhesion may induce neovascularization and axon swelling in cauda equina area, (4) The pathological effects are time, volume and distance dependent, (5) The scar adhesion can induce dura mater thickening and the thickness difference between dura-adhesion(-) and dura-adhesiion (+) is statistical significantly, (6) The scar adhesion has no pathological effect to DRG , the relative normal DRG implicate that the post operation recurrent neuropathic pain may be not due to DRG injury or damage by scar adhesion. In our current study, we found that the post operative scarring tissue has no apparent compression effect to spinal tissue, but it can really induce some pathological change to dura mater and nerve root in cauda equina area. We conclude that epidural fibrosis may relate to FBSS but the cause may be not due to the mechanical compression of spinal nerve or cauda equina only.

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