A complete in-depth discussion of the various nonsurgical treatment modalities can be found in the subsequent chapters of this book. Overall, the predictors of success for nonsurgical therapies for LBP are not well understood [5, 6]. This is not surprising for many reasons. In the literature, there is a paucity of placebo-controlled randomized studies. When analyzing the prospective studies, the most obvious difficulty in generalization across studies is the lack of standardization of selection criteria, definitions of pain, and validated objective outcome measures for pain. The criteria for diagnosis and inclusion in most studies for facet and epidural injection differ, as well as the criteria for success ranging from 50 % or greater. Chapters 12, 13, and 14 will discuss in more detail the specifics of interventional, neuromodulation, and intrathecal drug therapies available for the nonsurgical treatment of LBP, respectively. However, the authors will highlight below some key points regarding patient selection and nonsurgical treatment of LBP below.

One common contributor to axial back pain LBP is facet arthropathy . The facet joints are richly innervated by a dual innervation of somatic, nociceptive, and autonomic pain fibers. Therefore, somatic fibers at each facet level are responsible for characteristically localized pain in tandem with referred pain due to a convergence of pathways with autonomic fibers either in the dorsal horns or thalamus in the second- or third-order ascending pathways, respectively [7]. It is important to consider facet arthropathy as a source of pain, particularly in the setting of axial LBP, without radicular symptoms. The diagnosis of facet joint pain is typically made by an interventional facet nerve block yielding symptomatic relief of LBP in the absence of radiculopathy [8]. Facet pain has been shown in studies by Manchikanti and colleagues to have a prevalence ranging from 20 to 40 % of all LBP [8–15]. There are no class A recommendations for the management of “facet-joint”-type pain. Instead, level II evidence supporting lumbar facet joint nerve blocks [8, 16, 17] and radiofrequency neurotomy [18, 19] has been previously published supporting these modalities of pain mediation. Furthermore, only level III evidence exists in support of intraarticular corticosteroid injections for chronic LBP thought to be due to facet arthropathy [20, 21]. Long-term benefit has been noted with the injection of anesthetics and most recently in 2014 the addition of corticosteroids yielded no added long-term pain relief beyond that provided by local anesthetics [8]. Overall, when facet joint pain is overlooked as an etiology of axial LBP, painful symptoms can persist after surgical decompression.

Internal disc disruption (IDD) resulting in discogenic pain is thought to be the most common cause of axial LBP [7]. IDD is defined as degeneration of the disc, desiccation, and disc height collapse, with annular tears in the absence of disc herniation and neural compression [22]. In the absence of radicular symptoms, an associated herniated disc is rarely thought to be the cause of axial pain. The characteristics of discogenic pain are often ill defined and the relative benefits of open spinal surgery are not as clear compared to interventional or rehabilitative measures. In a systematic review comparing five RCTs, no significant difference in ODI was found between spinal fusion and nonsurgical management [23]. In a long-term follow-up of three RCTs by Mannion and colleagues, no significant difference was seen between the surgical and nonsurgical groups as well [24]. One flaw in these studies is the lack of concordance between choice of nonsurgical therapy and specific surgical intervention. Overall, discogenic pain remains as the most common cause of back pain and a uniform surgical approach may not be the answer for each patient. Appropriate localization of the pain generator in the case of multilevel degenerative disc disease is often required.