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      Cervical disc degeneration and neck pain

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          Abstract

          Cervical intervertebral disc has long been considered a common source of neck pain. However, the pain caused by the disc itself has not been clearly defined so far, and its diagnosis and treatment has always been controversial. Degenerative cervical disc has a rich supply of nerve fibers, is prone to inflammatory reactions, and is susceptible to pain that can be provoked by disc stimulation or distention, and can be eliminated by block. Overwhelming clinical evidence demonstrates that neck pain in patients with degenerative cervical radiculopathy or myelopathy can be subsided rapidly by anterior cervical surgery, further indicating that this neck pain stems from the pathology of cervical disc itself. Cervical discography is advocated as the only test that connects disease to symptoms, but the procedure remains controversial. If strict criteria and technique are maintained, discography can discriminate painful, symptomatic discs from nonpainful, asymptomatic discs. Discogenic neck pain alone without cervical disc herniation or cervical spondylosis accounts for a large proportion of chronic neck pain. For these patients who continue to have refractory neck pain and fail to respond to conservative treatment, anterior cervical fusion surgery or artificial cervical disc replacement may be a better choice, and preoperative cervical discography can guarantee the excellent surgical results. Existing basic and clinical studies have scientifically shown that cervical intervertebral disc degeneration can lead to neck pain.

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          Most cited references 29

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          Role of cytokines in intervertebral disc degeneration: pain and disc content.

          Degeneration of the intervertebral discs (IVDs) is a major contributor to back, neck and radicular pain. IVD degeneration is characterized by increases in levels of the proinflammatory cytokines TNF, IL-1α, IL-1β, IL-6 and IL-17 secreted by the IVD cells; these cytokines promote extracellular matrix degradation, chemokine production and changes in IVD cell phenotype. The resulting imbalance in catabolic and anabolic responses leads to the degeneration of IVD tissues, as well as disc herniation and radicular pain. The release of chemokines from degenerating discs promotes the infiltration and activation of immune cells, further amplifying the inflammatory cascade. Leukocyte migration into the IVD is accompanied by the appearance of microvasculature tissue and nerve fibres. Furthermore, neurogenic factors, generated by both disc and immune cells, induce expression of pain-associated cation channels in the dorsal root ganglion. Depolarization of these ion channels is likely to promote discogenic and radicular pain, and reinforce the cytokine-mediated degenerative cascade. Taken together, an enhanced understanding of the contribution of cytokines and immune cells to these catabolic, angiogenic and nociceptive processes could provide new targets for the treatment of symptomatic disc disease. In this Review, the role of key inflammatory cytokines during each of the individual phases of degenerative disc disease, as well as the outcomes of major clinical studies aimed at blocking cytokine function, are discussed.
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            Comprehensive evidence-based guidelines for interventional techniques in the management of chronic spinal pain.

            Comprehensive, evidence-based guidelines for interventional techniques in the management of chronic spinal pain are described here to provide recommendations for clinicians. To develop evidence-based clinical practice guidelines for interventional techniques in the diagnosis and treatment of chronic spinal pain. Systematic assessment of the literature. Strength of evidence was assessed by the U.S. Preventive Services Task Force (USPSTF) criteria utilizing 5 levels of evidence ranging from Level I to III with 3 subcategories in Level II. Short-term pain relief was defined as relief lasting at least 6 months and long-term relief was defined as longer than 6 months, except for intradiscal therapies, mechanical disc decompression, spinal cord stimulation and intrathecal infusion systems, wherein up to one year relief was considered as short-term. The indicated evidence for accuracy of diagnostic facet joint nerve blocks is Level I or II-1 in the diagnosis of lumbar, thoracic, and cervical facet joint pain. The evidence for lumbar and cervical provocation discography and sacroiliac joint injections is Level II-2, whereas it is Level II-3 for thoracic provocation discography. The indicated evidence for therapeutic interventions is Level I for caudal epidural steroid injections in managing disc herniation or radiculitis, and discogenic pain without disc herniation or radiculitis. The evidence is Level I or II-1 for percutaneous adhesiolysis in management of pain secondary to post-lumbar surgery syndrome. The evidence is Level II-1 or II-2 for therapeutic cervical, thoracic, and lumbar facet joint nerve blocks; for caudal epidural injections in managing pain of post-lumbar surgery syndrome, and lumbar spinal stenosis, for cervical interlaminar epidural injections in managing cervical pain (Level II-1); for lumbar transforaminal epidural injections; and spinal cord stimulation for post-lumbar surgery syndrome. The indicated evidence for intradiscal electrothermal therapy (IDET), mechanical disc decompression with automated percutaneous lumbar discectomy (APLD), and percutaneous lumbar laser discectomy (PLDD) is Level II-2. The limitations of these guidelines include a continued paucity of the literature, lack of updates, and conflicts in preparation of systematic reviews and guidelines by various organizations. The indicated evidence for diagnostic and therapeutic interventions is variable from Level I to III. These guidelines include the evaluation of evidence for diagnostic and therapeutic procedures in managing chronic spinal pain and recommendations for managing spinal pain. However, these guidelines do not constitute inflexible treatment recommendations. Further, these guidelines also do not represent "standard of care."
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              Intervertebral disc, sensory nerves and neurotrophins: who is who in discogenic pain?

              The normal intervertebral disc (IVD) is a poorly innervated organ supplied only by sensory (mainly nociceptive) and postganglionic sympathetic (vasomotor efferents) nerve fibers. Interestingly, upon degeneration, the IVD becomes densely innervated even in regions that in normal conditions lack innervation. This increased innervation has been associated with pain of IVD origin. The mechanisms responsible for nerve growth and hyperinnervation of pathological IVDs have not been fully elucidated. Among the molecules that are presumably involved in this process are some members of the family of neurotrophins (NTs), which are known to have both neurotrophic and neurotropic properties and regulate the density and distribution of nerve fibers in peripheral tissues. NTs and their receptors are expressed in healthy IVDs but much higher levels have been observed in pathological IVDs, thus suggesting a correlation between levels of expression of NTs and density of innervation in IVDs. In addition, NTs also play a role in inflammatory responses and pain transmission by increasing the expression of pain-related peptides and modulating synapses of nociceptive neurons at the spinal cord. This article reviews current knowledge about the innervation of IVDs, NTs and NT receptors, expression of NTs and their receptors in IVDs as well as in the sensory neurons innervating the IVDs, the proinflammatory role of NTs, NTs as nociception regulators, and the potential network of discogenic pain involving NTs.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2018
                14 November 2018
                : 11
                : 2853-2857
                Affiliations
                [1 ]Department of Spinal Surgery, General Hospital of Armed Police Force, Beijing 100039, People’s Republic of China, pengbaogan@ 123456163.com
                [2 ]Interventional Spine and Musculoskeletal Care, Virginia iSpine Physicians, PC Virginia Spine Research Institute, Inc Richmond, VA, USA
                Author notes
                Correspondence: Baogan Peng, Department of Spinal Surgery, Institute of Spinal Surgery, General Hospital of Armed Police Force, 69 Yongding Road, Beijing 100039, People’s Republic of China, Tel +86 10 5797 6611, Fax +86 10 5797 6937, Email pengbaogan@ 123456163.com
                Article
                jpr-11-2853
                10.2147/JPR.S180018
                6241687
                © 2018 Peng and DePalma. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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