What is the pathophysiology of diskogenic pain in low back pain (LBP) and sciatica?

Updated: Aug 22, 2018
  • Author: Jasvinder Chawla, MD, MBA; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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Answer

Answer

Many studies have demonstrated that the intervertebral disk and other structures of the spinal motion segment can cause pain.

Kuslich et al used regional anesthesia in 193 patients who were about to undergo lumbar decompressive surgery for disk herniation or spinal stenosis. [29] Pain was elicited by using blunt surgical instruments or an electrical current of low voltage in 30% of patients who had stimulation of the paracentral annulus fibrosis and in 15% with stimulation of the central annulus fibrosis. However, it is unclear why mechanical back pain syndromes commonly become chronic, with pain persisting beyond the normal healing period for most soft-tissue or joint injuries in the absence of nonphysical or operant influences.

In 1987, Mooney proposed that this LBP chronicity was best explained by a tissue component of the spine that obeyed physiological rules different from those of other connective tissues in the body. [19]

This divergent behavior is best illustrated in the intervertebral disk with its composition of large, unique, water-imbibing proteoglycan molecules. During adulthood, these large molecules break into small molecules that bind less water. Repair by means of proteoglycan synthesis is slow. Fissuring and disruption of the annular lamellae further exacerbate molecular breakdown and the dehydration of the disk. Arterial blood supply to the peripheral one third of the outer annulus is meager and inadequate to prevent subsequent internal degeneration. The annulus and nucleus pulposus are similarly compromised, as they receive nutrition only by means of diffusion through adjacent vertebral endplates. Although sluggish healing of the intervertebral disk may partially account for the tendency of a spinal lesion to lead to chronicity, a direct concordance between structural degeneration and spinal pain does not exist.

Recent elucidation of biochemical behaviors and neurophysiological factors affecting the disk and other regional pain-sensitive tissues may account for this discrepancy. In humans, painful disks have a lower pH than nonpainful disks. Also, experimental lowering of the pH in animal models induced pain-related behaviors and hyperalgesia. Diskography of canine disks that were normally or experimentally deformed seemed to show increased concentrations of neuropeptides, such as substance P (SP), calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP) in the dorsal root ganglion (DRG), implicating their possible role in the transmission or modulation of pain. SP probably modulates initial nociceptive signals received in the gray matter of the dorsal spinal cord.


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