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Excerpt
It is becoming more clear that the pathophysiology of lumbar radiculopathy does indeed involve a biochemical process. As the authors point out, other studies have shown that pure mechanical compression alone is not sufficient to cause lumbar radiculopathy. Because all of the agents that were detected are proinflammatory, the most likely pathophysiology of lumbar radiculopathy is that an acute inflammatory process produces a hypersensitive dorsal root ganglion or a spinal nerve root, making the neural structures more sensitive to mechanical deformation.
I would caution the readers about IL-1α, the main instigator in terms of starting the inflammatory cycle with the production of prostaglandin E2. The biochemistry of acute inflammation is extremely complex with multiple cytokines involved, and previously published literature has shown that these cytokines autoregulate in multiple and different manners. The most likely scenerio is that there are other cytokines that are involved intimately with the inflammatory process and that the production of IL-1α and the increased production of PGE2 is only a part of the answer. More research needs to be performed in this area to further elucidate the complex regulatory mechanisms involved with lumbar radiculopathy.
Finally, an interesting question to ponder is whether or not the cytokines and prostaglandins are being produced during the degenerative cycle of the disc. If these agents are already being produced to a significant degree in a degenerating disc before the herniation event, it may mean that these cytokines are involved in the degradation of the intervertebral disc matrix. There is ample evidence in the articular cartilage literature to substantiate that interleukin-1 and TNF-α, prostaglandin E2, and IL-6 are involved in the possible regulatory mechanisms of protoglycan synthesis.
