Abstract

307 ISSN 1758-1869 10.2217/PMT.12.32 © 2012 Future Medicine Ltd Pain Manage. (2012) 2(4), 307–309 Solutions containing steroids have been injected into the epidural space for the treatment of chronic back pain for over 50 years. Currently, epidural steroid injections (ESIs) are the most commonly performed intervention in pain clinics worldwide [1]. However, despite the widespread use of ESIs, the efficacy of this procedure remains controversial. Whereas a wealth of controlled and anecdotal evidence supports their use, dozens of other studies have attempted and failed to conclusively prove that ESIs are an effective means of analgesia in patients with chronic back pain [2]. This poses a dilemma for the modern pain practitioner and begs the question as to why the efficacy of such a ubiquitous intervention remains unproven in the literature. In all likelihood, this apparent paradox arises partly from an oversimplification of the question itself. As most practitioners are aware, the term ‘chronic back pain’ is one that encompasses a vast array of etiologies that are often difficult to distinguish from one another due to significant overlap in symptoms [3]. Even in patients with classical radiculopathy, these symptoms rarely occur in isolation (i.e., without concomitant mechanical low back pain). From a pathophysiological standpoint, the theoretical benefit of ESIs is in patients with neuropathic spinal pain (NSP). The most widely supported mechanism of analgesia in these patients is ascribed to the anti-inflammatory properties of cortico steroids counteracting the high concentrations of inflammatory enzymes that are often found at the site of pathology [4]. Although other mechanisms have been postulated, such as a direct anti nociceptive action [5] and osmotic dilution of inflammatory cytokines [6], epidural steroids should not be expected to be as efficacious in patients without an inflammatory component to their pain. Even differentiating between NSP and mechanical back pain can be difficult, as factors that predispose to NSP also result in changes in regional biomechanics leading to nociceptive pain [7]. For example, the presence of facet joint arthritis predisposes patients to radiculopathy secondary

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