The role of inflammation in disk herniation-associated radiculopathy

The causes and physiopathology of low-back pain and acute lumbar radiculopathy remain unclear. A compression of the nerve root by protruded disk has been suggested but explains only partially the physiopathology of radicular pain. This article provides an overview of the role of inflammation in disk herniation-associated radiculopathy.

A review of the relevant literature in American and European medical journals was performed.

Several studies have identified inflammatory mediators (phospholipase A2, prostaglandin E2, leukotrienes, nitric oxide, immunoglobulins, pro-inflammatory cytokines such as interleukin [IL]-1alpha, IL-1beta, IL-6, and tumor necrosis factor alpha [TNFalpha]) and autoimmune reaction (macrophages expressing IL-1beta, intercellular adhesion molecules) in disk herniation. An appealing hypothesis is that the leakage of these agents may produce an excitation of the nociceptors, a direct neural injury, a nerve inflammation, or an enhancement of sensitization to other pain-producing substances (such as bradykinin), leading to the nerve root pain. However, the role of these inflammatory mediators in the pathophysiology of lumbar radiculopathy has not been proven. Several findings suggest that this inflammatory response, which occurs in the early stage of disk herniation, is transient. Indeed, most studies of chronic disk herniation samples failed to demonstrate inflammation.

Although inflammation may partially explain lumbar radiculopathy, involvement of inflammatory mediators in the physiopathology of disk herniation-associated radiculopathy has not been proven.