The Journal of Bone and Joint Surgery (American). 2006;88:68-71.
doi:10.2106/JBJS.E.01282
© 2006 The Journal of Bone and Joint Surgery, Inc.
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Pathology and Possible Mechanisms of Nervous System Response to Disc Degeneration

Helena Brisby, MD, PhD

Corresponding author:
Helena Brisby, MD, PhD
Department of Orthopaedics, Sahlgrenska University Hospital/Sahlgrenska, SE-413 45, Göteborg, Sweden.
E-mail address: helena.brisby{at}vgregion.se

The author did not receive grants or outside funding in support of her research for or preparation of this manuscript. She did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the author is affiliated or associated.

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.


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