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Use of Temporary Implantable Biomaterials to Reduce Leg Pain and Back Pain in Patients with Sciatica and Lumbar Disc Herniation

机译:使用临时植入的生物材料减轻坐骨神经痛和腰椎间盘突出症患者的腿痛和腰痛

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摘要

The principle etiology of leg pain (sciatica) from lumbar disc herniation is mechanical compression of the nerve root. Sciatica is reduced by decompression of the herniated disc, i.e., removing mechanical compression of the nerve root. Decompression surgery typically reduces sciatica more than lumbar back pain (LBP). Decompression surgery reduces mechanical compression of the nerve root. However, decompression surgery does not directly reduce sensitization of the sensory nerves in the epidural space and disc. In addition, sensory nerves in the annulus fibrosus and epidural space are not protected from topical interaction with pain mediators induced by decompression surgery. The secondary etiology of sciatica from lumbar disc herniation is sensitization of the nerve root. Sensitization of the nerve root results from a) mechanical compression, b) exposure to cellular pain mediators, and/or c) exposure to biochemical pain mediators. Although decompression surgery reduces nerve root compression, sensory nerve sensitization often persists. These observations are consistent with continued exposure of tissue in the epidural space, including the nerve root, to increased cellular and biochemical pain mediators following surgery. A potential contributor to lumbar back pain (LBP) is stimulation of sensory nerves in the annulus fibrosus by a) cellular pain mediators and/or b) biochemical pain mediators that accompany annular tears or disruption. Sensory fibers located in the outer one-third of the annulus fibrosus increase in number and depth as a result of disc herniation. The nucleus pulposus is comprised of material that can produce an autoimmune stimulation of the sensory nerves located in the annulus and epidural space leading to LBP. The sensory nerves of the annulus fibrosus and epidural space may be sensitized by topical exposure to cellular and biochemical pain mediators induced by lumbar surgery. Annulotomy or annular rupture allows the nucleus pulposus topical access to sensory nerve fibers, thereby leading to LBP. Coverage of the annulus and adjacent structures in the epidural space by absorbable viscoelastic gels appears to reduce LBP following surgery by protecting sensory fibers from cellular and biochemical pain mediators.
机译:腰椎间盘突出症引起的腿痛(坐骨神经痛)的主要病因是对神经根的机械压迫。通过对椎间盘减压,即去除神经根的机械压迫,可以减少坐骨神经痛。减压手术通常比腰背痛(LBP)更能减轻坐骨神经痛。减压手术减少了神经根的机械压迫。但是,减压手术并不能直接降低硬膜外腔和椎间盘中感觉神经的敏感性。此外,纤维环和硬膜外间隙的感觉神经不受保护,不会与减压手术引起的疼痛介质发生局部相互作用。腰椎间盘突出症的坐骨神经痛的次要病因是神经根的致敏。神经根的敏化是由于a)机械压迫,b)暴露于细胞疼痛介质和/或c)暴露于生化疼痛介质。尽管减压手术减少了神经根受压,但感觉神经敏化常持续存在。这些观察结果与手术后硬膜外腔组织(包括神经根)持续暴露于增加的细胞和生化疼痛介质有关。腰背痛(LBP)的潜在诱因是a)细胞痛介质和/或b)伴有环状眼泪或破裂的生化痛介质刺激纤维环中的感觉神经。由于椎间盘突出,位于纤维环外侧三分之一的感觉纤维数量和深度增加。髓核由可对位于环和硬膜外腔的感觉神经产生自体免疫刺激的物质组成,导致LBP。纤维环和硬膜外间隙的感觉神经可通过局部暴露于腰椎手术引起的细胞和生化疼痛介质而敏化。瓣环切开术或环形破裂允许髓核局部进入感觉神经纤维,从而导致LBP。可吸收的粘弹性凝胶覆盖硬膜外间隙中的环面和相邻结构,似乎在手术后通过保护感觉纤维免受细胞和生化疼痛介质的作用而降低了LBP。

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