Why does my neck or back hurt when the damaged disc is not pressing on a nerve ? What can be done about it (other than surgery) ?

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One could argue that scientific evidence supporting the efficacy of epidural steroid injection indirectly supports the efficacy of epidural administration by any route of administration. This argument makes sense in view of the anatomy of the epidural space and the pathophysiology of radiculopathy. To elaborate, the epidural space is a continuous anatomic compartment extending from the base of the skull to the sacrum that can be entered at various levels and by various routes to achieve the same end. The space itself consists of adipose (fat) tissue interspersed with random bands of fibrous tissue and venous vessels. The ventral epidural space is closest to the posterior disc margin and the traversing nerve root, which is the presumed site of pathology (i.e., pain) in lumbar radiculopathy. Although the most direct method to deposit medication into this region is by using a transforaminal approach to needle insertion, it is conceivable that medication may reach this target equally well using a caudal, interlaminar, or other approaches.

Regarding pathophysiology, investigations into the biochemistry of disc degeneration and herniation indicate that intraspinal inflammation is a major cause of radicular pain. The neurotoxic, inflammatory mediator phospholipase A2 (PLA2) is contained within the disc nucleus and is released after annular injury. PLA2 in turn triggers the arachidonic acid cascade, leading to localized inflammation mediated by prostaglandins and leukotrienes. Inflammatory neuropeptides such as calcitonin gene-related peptide (CGrP) and substance P are contained within the dorsal root ganglion and perpetuate inflammation as they are released from irritated nerve roots. Corticosteroids have powerful anti-inflammatory effects, which include inhibition of prostaglandin synthesis, blockade of PLA2 activity, and stabilization of inflammatory cell membranes. Injecting corticosteroids into the epidural space should result in higher concentrations of the active medication at the site of inflammation when compared to oral or parenteral routes of steroid administration. The spinal injection route of administration is the only method of drug delivery that does not rely on blood flow to deliver the medication to its site of action and blood flow may be impaired in the region of compressive disc herniation. Even with normal spinal circulation, blood flow delivers steroid preferentially to high blood flow organs with presumably low concentrations arriving at the site of spinal pathology.

Excerpted from: Pain Physician: January 2007 10:185-212, at p.204. www.painphysicianjournal.com

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