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首页> 外文期刊>Journal of Biomechanics >LUMBAR FACET PAIN - BIOMECHANICS, NEUROANATOMY AND NEUROPHYSIOLOGY
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LUMBAR FACET PAIN - BIOMECHANICS, NEUROANATOMY AND NEUROPHYSIOLOGY

机译：腰痛面部疼痛-生物力学，神经解剖学和神经生理学

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摘要

Idiopathic low back pain has confounded health care practitioners for decades. Although there has been much advance in the understanding of the biomechanics of the lumbar spine over the past 25 years, the cellular and neural mechanisms that lead to Facet pain are not well understood. An extensive series of experiments was undertaken to help elucidate these mechanisms and gain a better understanding of lumbar facet pain. Biomechanic and neuroanatomic studies were performed in human cadaveric Facet joints and neurophysiologic studies were performed in New Zealand White rabbits. These studies provide the following evidence to help explain the mechanisms of lumbar facet pain: (1) The facet joint can carry a significant amount of the total compressive load on the spine when the human spine is hyperextended. (2) Extensive stretch of the human facet joint capsule occurs when the spine is in the physiologic range of extreme extension. (3) An extensive distribution of small nerve fibers and free and encapsulated nerve endings exists in the lumbar facet joint capsule, including nerves containing substance P, a putative neuromodulator of pain. (4) Low and high threshold mechanoreceptors fire when the facet joint capsule is stretched or is subject to localized compressive forces. (5) Sensitization and excitation of nerves in facet joint and surrounding muscle occur when the joint is inflamed or exposed to certain chemicals that are released during injury and inflammation. (6) Marked reduction in nerve activity occurs in Facet tissue injected with hydrocortisone and lidocaine. Thus, the facet joint is a heavily innervated area that is subject to high stress and strain. The resulting tissue damage or inflammation is likely to cause release of chemicals irritating to the nerve endings in these joints, resulting in low back pain. Copyright (C) 1996 Elsevier Science Ltd. [References: 57]
机译：数十年来，特发性下背痛使医疗保健从业人员感到困惑。尽管在过去的25年中，对腰椎生物力学的理解有了很大进步，但导致小平面疼痛的细胞和神经机制尚不十分清楚。进行了一系列广泛的实验，以帮助阐明这些机制并更好地理解腰椎小面疼痛。在人体尸体小平面关节中进行了生物力学和神经解剖学研究，在新西兰白兔中进行了神经生理学研究。这些研究提供以下证据来帮助解释腰椎小面疼痛的机制：（1）当人的脊柱过度伸展时，小面关节可承受脊柱上很大的总压缩负荷。 （2）当脊柱处于极度伸展的生理范围内时，人小关节囊被广泛拉伸。 （3）腰椎小关节囊中广泛分布着小神经纤维和游离的，包封的神经末梢，包括含有P物质的神经，P是推测的疼痛神经调节剂。 （4）当小关节囊被拉伸或受到局部压缩力时，低阈值和高阈值的机械感受器会发射声。 （5）当关节发炎或暴露于受伤和发炎期间释放的某些化学物质时，会发生小关节和周围肌肉神经的敏化和兴奋。 （6）注射氢化可的松和利多卡因的小平面组织中神经活动明显减少。因此，小关节是严重受神经支配的区域，容易受到高应力和高应变。所导致的组织损伤或炎症很可能导致释放刺激这些关节神经末梢的化学物质，从而导致腰痛。版权所有（C）1996 Elsevier Science Ltd. [参考：57]

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