THE ROLE OF INFLAMMATION IN DISK HERNIATION-ASSOCIATED RADICULOPATHY

Objective: The causes and physiopathology of low-back pain and acute l umbar radiculopathy remain unclear. A compression of the nerve root by protruded disk has been suggested but explains only partially the phy siopathology of radicular pain. This article provides an overview of t he role of inflammation in disk herniation-associated radiculopathy. M ethods: A review of the relevant literature in American and European m edical journals was performed. Results: Several studies have identifie d inflammatory mediators (phospholipase A(2), prostaglandin E-2, leuko trienes, nitric oxide, immunoglobulins, pro-inflammatory cytokines suc h as interleukin [IL]-1 alpha. IL-1 beta, IL-6, and tumor necrosis fac tor alpha [TNF alpha]) and autoimmune reaction (macrophages expressing IL-1 beta, intercellular adhesion molecules) in disk herniation. An a ppealing hypothesis is that the leakage of these agents may produce an excitation of the nociceptors, a direct neural injury, a nerve inflam mation, or an enhancement of sensitization to other pain-producing sub stances (such as bradykinin), leading to the nerve root pain. However, the role of these inflammatory mediators in the pathophysiology of lu mbar radiculopathy has not been proven. Several findings suggest that this inflammatory response, which occurs in the early stage of disk he rniation, is transient. Indeed, most studies of chronic disk herniatio n samples failed to demonstrate inflammation. Conclusion: Although inf lammation may partially explain lumbar radiculopathy, involvement of i nflammatory mediators in the physiopathology of disk herniation-associ ated radiculopathy has not been proven. Semin Arthritis Rheum 28:60-71 . Copyright (C) 1998 by W.B. Saunders Company.