Pathophysiology of disk-related sciatica: what the current evidences point to.

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Sciatica in patients with disk disease was long ascribed to pressure put on the sciatic nerve root by a herniated disk. Following is a review of Mulleman D et al (2006) on role for chemical factors acting in conjunction with this mechanical insult.
Suggestion of chemical factor involvement comes from a number of clinical observations:
1. Disk surgery does not consistently provide pain relief,
2. Large disk herniations are not always symptomatic,
3. Severe pain may be present in patients without imaging evidence of nerve root compression,
4. The severity of symptoms and neurological signs is not well correlated with the size of the disk herniation, and conservative therapy is often effective.
Experimental studies have provided further evidence for a chemical component:
1. Disk herniations can undergo spontaneous resorption,
2. The intervertebral disk is immunogenic,
3. And mediators for inflammation have been identified within intervertebral disk tissue.
The current pathophysiological theory incriminates proinflammatory substances secreted by the nucleus pulposus (NP). When preexisting or concomitant mechanical injury to a nerve root occurs, these substances can cause nerve root pain.
Available information points to tumor necrosis factor-alpha (TNF-alpha) as the main candidate among substances potentially responsible for nerve root pain. Therefore, trials of TNF-alpha antagonists in patients with disk-related sciatica are warranted.

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