Brisby Helena
Department of Orthopaedics, Sahlgrenska University Hospital/Sahlgrenska, SE-413 45, Göteborg, Sweden.
J Bone Joint Surg Am. 2006 Apr;88 Suppl 2:68-71. doi: 10.2106/JBJS.E.01282.
Degeneration of the intervertebral disc is clinically considered to be an important source of pain in patients with low-back pain. Disc deterioration and/or degeneration may influence the nervous system by stimulation of nociceptors in the anulus fibrosus, causing nociceptive pain that is often referred to as discogenic pain. The stimulation of the nociceptors may be of mechanical or inflammatory origin. Deterioration of a disc with loss of normal structure and weight-bearing properties may lead to abnormal motions that cause mechanical stimulation. This theory is supported by the fact that patients commonly experience an increase in pain with weight-bearing and certain movements. In addition, an ingrowth of vessels and nerve fibers into deeper layers of the anulus fibrosus has been observed in degenerated discs. A large number of inflammatory and signaling substances, such as tumor necrosis factor and interleukins (interleukin-1beta, interleukin-6, and interleukin-8), may also play a role in the development of back pain. Independent of stimulus of the nociceptors, the pain impulses are conducted through myelinated A delta fibers and unmyelinated C fibers to the dorsal root ganglion and continue by way of the spinothalamic tract to the thalamus and the somatosensory cortex. In response to stimulation of the nociceptors in the disc, the somatosensory system may increase its sensitivity, resulting in a nonfunctional response; that is, normally innocuous stimuli may generate an amplified response (peripheral sensitization). When disc degeneration leads to a disc herniation, the adjacent nervous system structures, such as the nerve roots or the dorsal root ganglion, can be affected, causing neuropathic pain of mechanical or biochemical origin. Disc deterioration also influences other spinal structures, such as facet joints, ligaments, and muscles, which can also become pain generators. Thus, disc degeneration may be responsible for the development of chronic low-back pain without being the actual pain focus. Both nociceptive and neuropathic pain can be modulated at higher centers, both at the spinal and the supraspinal levels (central sensitization). The altered magnitude of perceived pain is often referred to as neural plasticity and is considered to play a critical role in the evolution of chronic pain. Together with the complexity of the nervous system and pain modulation mechanisms, psychological aspects may also play a role in the response of the nervous system in patients with chronic low-back pain caused by disc degeneration.
椎间盘退变在临床上被认为是腰痛患者疼痛的一个重要来源。椎间盘退变和/或恶化可能通过刺激纤维环中的伤害感受器影响神经系统，引发伤害感受性疼痛，通常被称为椎间盘源性疼痛。伤害感受器的刺激可能源于机械性或炎症性。椎间盘结构和承重特性丧失导致的退变可能引发异常运动，从而产生机械性刺激。这一理论得到了患者在负重和某些运动时疼痛通常会加剧这一事实的支持。此外，在退变的椎间盘中已观察到血管和神经纤维长入纤维环深层。大量炎症和信号物质，如肿瘤坏死因子和白细胞介素（白细胞介素-1β、白细胞介素-6和白细胞介素-8），也可能在背痛的发生中起作用。独立于伤害感受器的刺激，疼痛冲动通过有髓鞘的Aδ纤维和无髓鞘的C纤维传导至背根神经节，并通过脊髓丘脑束继续传导至丘脑和躯体感觉皮层。响应椎间盘内伤害感受器的刺激，躯体感觉系统可能会提高其敏感性，导致功能失调反应；也就是说，通常无害的刺激可能会产生放大反应（外周敏化）。当椎间盘退变导致椎间盘突出时，相邻的神经系统结构，如神经根或背根神经节，可能会受到影响，引发机械性或生化性起源的神经性疼痛。椎间盘退变还会影响其他脊柱结构，如小关节、韧带和肌肉，这些结构也可能成为疼痛源。因此，椎间盘退变可能是慢性腰痛发生的原因，但并非实际的疼痛焦点。伤害感受性疼痛和神经性疼痛都可以在脊髓和脊髓上水平的高级中枢进行调节（中枢敏化）。感知疼痛程度的改变通常被称为神经可塑性，被认为在慢性疼痛的演变中起关键作用。连同神经系统和疼痛调节机制的复杂性，心理因素也可能在椎间盘退变引起的慢性腰痛患者的神经系统反应中起作用。
