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An Overview of Chronic Spinal Pain

Revisiting Diagnostic Categories and Exploring an Evolving Role for Neurostimulation

Sharan, Ashwini MD, FACS; Riley, Jonathan MD; Hoelscher, Christian MD

doi: 10.1097/BRS.0000000000002212

Study Design. Topic overview.

Objective. To describe the varied etiologies resulting in chronic spinal pain and review the current available evidence for treatments.

Summary of Background Data. Chronic pain conditions, especially those that affect the axial back and radiate to the extremities, affect a large population. This results in pronounced disability and a high socioeconomic burden. Our understanding of the underlying mechanisms for chronic pain is limited. This prevents a comprehensive diagnostic approach. Evidence from high-level clinical trials supporting treatments for chronic spinal pain is also limited.

Methods. Articles were identified through PubMed searches or already known to the author. The literature was reviewed and summarized, indicating the strength of evidence available for many treatment modalities.

Results. There are very few studies published that evaluate behavioral modifications for chronic spinal pain and only one long-term study investigating chronic pharmacological treatments. The data on the success of spinal surgeries to relieve chronic spinal pain suggest an unacceptably high failure rate. The best evidence (Level I) currently available suggests that spinal cord stimulation is a safe, effective, and durable treatment for chronic spinal pain. Recent clinical data support further investigation of new innovations and earlier therapeutic consideration of currently employed approaches.

Conclusion. Currently, physicians are limited in the practice of evidence-based medicine regarding chronic spinal pain treatments due to both the paucity of data available and an inconsistent diagnostic nomenclature. The introduction of new neurostimulation modalities is promising but requires better characterization through ongoing prospective clinical investigation.

Level of Evidence: 5

Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, PA.

Address correspondence and reprint requests to Ashwini Sharan, MD, FACS, Department of Neurological Surgery, Thomas Jefferson University and Jefferson Hospital for Neuroscience, 909 Walnut Street, Clinical Office Building, 2nd Floor, Philadelphia, PA; E-mail:

Received 18 November, 2016

Revised 4 April, 2017

Accepted 17 April, 2017

The manuscript submitted does not contain information about medical device(s)/drug(s).

No funds were received in support of this work.

No relevant financial activities outside the submitted work.

Chronic pain affects approximately 30% of all adults in the United States.1 Back pain constitutes the most frequent reason for patients seeking medical care with 15% to 20% of adults experiencing back pain in any given year and 50% to 80% of the population experiencing back pain in their lifetime.2–4 This common ailment is the leading cause of disability worldwide5,6 and places a tremendous strain on the healthcare system as well as loss of workforce productivity.1,7–11 In severe cases, it has the potential to interfere with every aspect of life, including disrupting sleep, work, family life, and even self-care.12 Treatments for back pain include physical therapy, pain medications, implanted medical devices, and surgery; however, effective, long-term pain relief eludes many patients. Herein, we briefly review the constellation of pathologies that contribute to experience of spinal pain and outline the diagnostic and therapeutic challenges that arise in the treatment of these patients.

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An optimized therapeutic plan should be identified for the patient with spinal pain when it arrives at a specific diagnosis that simultaneously: identifies whether the patient has axial symptoms, appendicular symptoms, or a combination of both; excludes a nonspinal mimic as the primary pain generator; identifies whether the underlying symptoms are of a nociceptive or neuropathic origin; accounts for the chronicity and severity of the symptoms; and establishes patient goals and expectations.

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First, Overcoming Diagnostic Imprecision

Overly broad, overlapping, and sometimes inconsistently used terminologies are major contributors to diagnostic imprecision. Examples of terms that are both broadly and inconsistently utilized include “low back pain,” “postlaminectomy syndrome,” and “failed back surgery syndrome” (FBSS). These are not actionable terms on which a course of treatment can be based. A physician's differential diagnosis is necessary to illuminate the cause of axial and/or appendicular symptoms. In addition to the history and physical examination, imaging-based evaluation, attempted interventions (e.g., physical therapy), and development of a longitudinal relationship may be required to arrive at an accurate diagnosis and therefore an optimized treatment regimen.

The first step in arriving at a specific diagnosis is effective communication between healthcare providers and patients. Our group13 has attempted to prospectively assess the inter-rater reliability of a pain map with defined anatomic boundary landmarks. While the pain boundaries were based on easily palpable surface landmarks, inter-rater reliability was unacceptable low between all groups: patients and physicians (36%), patients and nurses (65%), and physicians and nurses (29%). In the absence of a specific and detailed nomenclature, we use a map that is completed by the patient to describe the location of his/her symptoms, as shown in Figure 1. This helps to improve clarity of communication as opposed to reliance on broad and imprecise terms.

Figure 1

Figure 1

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Spinal Pain, a Constellation of Pathologic Entities

Spinal pain is a broad term, but generally refers to pain originating in the spine that may be felt in the axial skeleton or in the extremities (appendicular pain). Mechanical etiologies of spinal pain that result in axial symptoms include stretch injuries of the back muscles, ligaments and/or tendons, spondylolisthesis, vertebral fracture, and spinal deformity (scoliosis and kyphosis). Mechanical etiologies that result in appendicular symptoms include herniated discs, spinal stenosis, and cauda equina syndrome. Nonmechanical spinal pain that can result in either axial or appendicular symptoms results from arthropathies (such as ankylosing spondylitis and rheumatoid arthritis), infection of the bone, disc, or spinal cord, arachnoiditis, and cancerous involvement of the spinal elements. As described earlier, diagnoses such as FBSS and postlaminectomy syndrome do not by themselves provide a precise etiology as to a patient's axial or appendicular symptoms and should be avoided as a final diagnosis. Some conditions with nonspinal origins can mimic back and lower extremity pain characteristic of the mechanical and nonmechanical spinal pain disorders listed previously, such as bursitis, piriformis syndrome, spasticity, fibromyalgia, abnormal gait, poor posture, and obesity.

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Understanding Pain Type, Severity, and Chronicity

In addition to confirming a spinal origin, and assessing the balance of axial to appendicular symptoms, arrival at an optimized treatment plan should also assess whether the patient has nociceptive or neuropathic pain and should consider the severity and chronicity of a patient's symptoms.

Nociceptors relay information to the brain about mechanical and inflammatory processes via small-diameter afferents. The experience of painful nociceptive sensation is recognized to be a physiologically adaptive mechanism to guard against further tissue injury. Treatments for nociceptive pain focus on alleviating the localized mechanical or inflammatory insult. Alternatively, neuropathic pain is generated and maintained by the nervous system itself, often as a result of injury to a nerve and self-reinforcing changes in the pain pathways that heighten sensitivity to stimuli.14 Neuropathic pain is typically a chronic condition that may increase in severity over time, often after a dermatomal distribution, and may result in hyperalgesia and/or allodynia. In conjunction with a thorough medical history and physical examination, separate clinical evaluation tools can be used to assist in the diagnosis of a neuropathic pain component: the Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale15 and the painDETECT scale.16

Spinal pain may be designated as a chronic disorder based on the duration and severity of the symptoms, as well as the functional impairments resulting from the condition.17 The International Association for the Study of Pain defines chronic pain as “pain that persists beyond normal tissue healing time, which is assumed to be three months.”18 While there are no objective measures of chronic pain severity, a patient with pain intensity severe enough to seek medical treatment can be considered clinically significant.19 Chronic pain typically also results in severe functional limitations for the patient, such as limited range of motion and inability to exercise or perform physical activities required for work.20,21

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There is currently no “cure” for chronic neuropathic pain. Longitudinal management of the pain symptoms often occurs in the setting of a multidisciplinary effort. The care team must set expectations that patients are unlikely to be fully pain-free. Instead, appropriate expectations acknowledge a dynamic process between the patient and physician(s) in which various treatments are applied and titrated until achieving a combination of optimal pain relief and improving the patient's ability to work and engage in normal daily activities. This multimodal approach may include a constellation of physical and occupational therapy, cognitive therapy, pharmacological agents, and neuromodulation-based surgical interventions (e.g., neurostimulation, intrathecal pain pump). There are limited high-quality studies of behavior modifications for chronic spinal pain, with mixed results.22,23

First-line pharmacological interventions often involve nonsteroidal anti-inflammatory drugs. If the patient's pain does not respond to initial conservative treatments, the physician may prescribe more potent pharmacological treatments, including muscle relaxants, membrane stabilizers, antidepressants, and opiates, or minimally invasive interventions, such as epidural steroid injections,24–26 radiofrequency ablation, and adhesiolysis.27–31 Of studies evaluating pharmacological treatments of chronic spinal pain, there are very few with long-term follow-up to ascertain whether these medications have sustained efficacy. One long-term study found that gabapentin provided more significant pain relief than naproxen.32 Another evaluated whether perioperative pregabalin could prevent FBSS, but found it to be ineffective.33,34 A systematic review of opioid treatment for chronic low back pain found some evidence for the effectiveness of opioids compared to placebo in the short term but no difference between opioids and nonsteroidal anti-inflammatory drugs or antidepressants as well as no long-term data to evaluate the safety or effectiveness of chronic opioid therapy.35 It is important for the physician to develop methods to identify patients with drug-seeking behavior, significant psychological comorbidities, or motivation for prolonged disability. These patients may exaggerate their symptoms or lack of response to treatment, either knowingly or unknowingly.

While spinal surgery is not used as a treatment for the vast majority of chronic spinal pain patients, it is estimated that between 300,000 and 400,000 back pain patients will have surgery per year, with limited success. Approximately 20% to 50% of patients who undergo lumbar spinal surgery will develop FBSS.36–38 In addition, an estimated 19% to 23% of patients who have had lumbar surgery will undergo repeat operations,39,40 with the success rate declining with multiple surgeries.41 Data support a low success rate of additional decompression or fusion operations in FBSS patients.41,42 The high incidence of FBSS suggests that the parameters for a chronic spinal pain patient's surgical candidacy should be more clearly defined.

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Neurostimulation, an Evolving Technology and Therapy

A Case for Earlier Intervention

While there is a paucity of data supporting the effectiveness of continuing to use serial pharmacological agents for patients with uncontrolled chronic neuropathic spinal pain, data do support consideration of early neuromodulatory intervention. Lad et al43 have recently published data examining US Medicare patient claims data over a recent 7-year period (2008–2013). In a retrospective review of 762 patients, they showed a lower rate of subsequent hospitalizations and clinic visit utilization in patients who underwent spinal cord stimulation (SCS) implantation earlier after diagnosis. Using a larger dataset from the same source, the same group noted trends toward decreased postprocedural healthcare utilization when undergoing SCS as compared to decompressive or fusion surgeries.44 Together, these studies support earlier diagnosis as an important factor to optimize patient outcome and reduce long-term healthcare utilization.

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Prospective Neurostimulation Data

There are three high-quality randomized controlled trials assessing SCS. Both North et al and Kumar et al have explored SCS as a long-term treatment for the radicular symptoms of FBSS patients and, respectively, found it superior to either reoperation or conventional medical management.45–48 Follow-up analyses by North et al also support a substantial cost savings, and early consideration of SCS, given the high proportion of patients crossed over from reoperation to SCS. Kapural et al report the results of a randomized controlled trial that found high-frequency (10 kHz) SCS to be superior to traditional, low-frequency SCS for patients with chronic back and leg pain.49 While leg pain outcome pain measures were improved, compellingly a substantial improvement in axial back pain coverage was also observed. These results mimicked findings of previously published noncontrolled observational studies for high-frequency SCS.

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Evolving Role for Neurostimulation

Axial back pain has been notoriously difficult to treat with SCS,50,51 as it is difficult to achieve coverage overlap between the induced paresthesia in standard SCS and the back pain distribution. Some success has been found with peripheral nerve field stimulation or the combination of SCS and peripheral nerve field stimulation,52,53 but effective back pain treatments are still lacking. Recent advances in this field include the introduction of high-frequency (10 kHz) SCS, which has shown long-term benefits for subjects with chronic back pain.49,54,55 The data published thus far for high-frequency SCS suggest that this therapy is superior to traditional SCS in providing pain relief and that these results are sustained for at least 2 years. This new technology may function through entirely different mechanisms from traditional SCS as there is no induction of paresthesia necessary for the patient to achieve significant pain relief. This is distinct from traditional SCS that requires paresthesia in the same distribution as pain for effective treatment.

In addition to high-frequency SCS, recent studies have explored novel stimulation parameters such as burst stimulation56 and adaptive stimulation that is capable of position-dependent stimulation alteration. Additionally, novel targets such as the dorsal root ganglion56–58 are being attempted.

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Ongoing Challenges and Opportunities

Emerging data for the clinical efficacy of high-frequency SCS raise the possibility of a novel therapeutic mechanism of action of how stimulation interacts with neural structures. This underscores a need to have improved nomenclature for localization of epidural lead placement to best understand the relationship between the lead and underlying neural anatomy. Out of convenience, lead placement is identified relative to the adjacent bony spinal anatomy. However, the conus medullaris has a known variability in location that results in termination between approximately the midbody of T12 and the rostral portion of the L2 vertebral body. Especially as newer high-frequency SCS is able to generate improvements in patient's back pain, an improved understanding of lead placement with respect to the respective neural elements will be of increased importance to optimize the understanding of this therapy.

In the current setting of both technology improvements and a reconsideration of the mechanisms by which neurostimulation alleviates spinal pain, the entire patient evaluation process should be viewed through the lens of opportunities to optimize the application of neurostimulation technologies. Spratt's A-D-T-O model (assessment, diagnosis, treatment, outcome) provides a useful guide.59,60 The linkages between the steps of clinical care (assessment–diagnosis, diagnosis–treatment, and treatment–outcome) each serve as opportunities to identify patient subgroups that may benefit either earlier or more substantively from neurostimulation-based intervention.

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Chronic spinal pain is a pervasive problem with an enormous economic burden for society that can impose extreme limitations to the individual patient. Development of an optimized therapeutic plan begins with optimized communications between the physician and the patient with the underlying goal of arriving at the most specific possible accurate diagnosis. For patients with chronic neuropathic spinal pain with axial and/or appendicular symptoms, the best evidence to date supports multimodal treatment and consideration of early intervention with neurostimulation. High-frequency SCS has recently shown promise in multiple prospective studies to have improved outcomes data for both radicular and axial symptoms of being an important step toward improved treatments; however, there is a clear need for more long-term studies to evaluate many of the treatments routinely employed for chronic spinal pain.

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1. Institute of Medicine (U.S.) Committee on Advancing Pain Research Care and Education. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. 2011; Washington, DC: National Academies Press, xvii, 364 pp.
2. Lanes TC, Gauron EF, Spratt KF, et al. Long-term follow-up of patients with chronic back pain treated in a multidisciplinary rehabilitation program. Spine (Phila Pa 1976) 1995; 20:801–806.
3. Deyo RA, Mirza SK, Martin BI. Back pain prevalence and visit rates: estimates from U.S. national surveys, 2002. Spine (Phila Pa 1976) 2006; 31:2724–2727.
4. Rubin DI. Epidemiology and risk factors for spine pain. Neurol Clin 2007; 25:353–371.
5. Vos T, Flaxman AD, Naghavi M, et al. Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012; 380:2163–2196.
6. Hoy D, March L, Brooks P, et al. The global burden of low back pain: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis 2014; 73:968–974.
7. Luo X, Pietrobon R, Sun SX, et al. Estimates and patterns of direct health care expenditures among individuals with back pain in the United States. Spine (Phila Pa 1976) 2004; 29:79–86.
8. Burton AK, Balagué F, Cardon G, et al. Chapter 2. European guidelines for prevention in low back pain: November 2004. Eur Spine J 2006; 15 (suppl 2):S136–S168.
9. Dagenais S, Caro J, Haldeman S. A systematic review of low back pain cost of illness studies in the United States and internationally. Spine J 2008; 8:8–20.
10. Manchikanti L, Singh V, Falco FJ, et al. Epidemiology of low back pain in adults. Neuromodulation 2014; 17 (suppl 2):3–10.
11. Shmagel A, Foley R, Ibrahim H. Epidemiology of chronic low back pain in US adults: data from the 2009–2010 National Health and Nutrition Examination Survey. Arthritis Care Res (Hoboken) 2016; 68:1688–1694.
12. Turk DC, Melzack R. Handbook of Pain Assessment. 3rd ed.2011; New York: Guilford Press, xvii, 542 pp.
13. Wu C, Mehdi M, Maulucci CM, et al. Inter-rater variability in the assessment of low back and lower extremity pain. 17th Annual Meeting of the North American Neuromodulation Society; Las Vegas, NV. 2013.
14. Jensen TS, Baron R, Haanpää M, et al. A new definition of neuropathic pain. Pain 2011; 152:2204–2205.
15. Bennett M. The LANSS Pain Scale: the Leeds assessment of neuropathic symptoms and signs. Pain 2001; 92:147–157.
16. Freynhagen R, Baron R, Gockel U, et al. painDETECT: a new screening questionnaire to identify neuropathic components in patients with back pain. Curr Med Res Opin 2006; 22:1911–1920.
17. Von Korff M, Dworkin SF, Le Resche L. Graded chronic pain status: an epidemiologic evaluation. Pain 1990; 40:279–291.
18. Classification of chronic pain. Descriptions of chronic pain syndromes and definitions of pain terms. Prepared by the International Association for the Study of Pain, Subcommittee on Taxonomy. Pain Suppl 1986; 3:S1–S226.
19. Purves AM, Penny KI, Munro C, et al. Defining chronic pain for epidemiological research—assessing a subjective definition. Pain Clin 1998; 10:139–147.
20. Riley JF, Ahern DK, Follick MJ. Chronic pain and functional impairment: assessing beliefs about their relationship. Arch Phys Med Rehabil 1988; 69:579–582.
21. Dansie EJ, Turk DC. Assessment of patients with chronic pain. Br J Anaesth 2013; 111:19–25.
22. Timm KE. A randomized-control study of active and passive treatments for chronic low back pain following L5 laminectomy. J Orthop Sports Phys Ther 1994; 20:276–286.
23. Cramer H, Haller H, Lauche R, et al. Mindfulness-based stress reduction for low back pain. A systematic review. BMC Complement Altern Med 2012; 12:162.
24. Parr AT, Manchikanti L, Hameed H, et al. Caudal epidural injections in the management of chronic low back pain: a systematic appraisal of the literature. Pain Physician 2012; 15:E159–E198.
25. Manchikanti L, Falco FJ, Pampati V, et al. Cost utility analysis of caudal of caudal epidural injections in the treatment of lumbar disc herniation, axial or discogenic low back pain, central spinal stenosis, and post lumber surgery syndrome. Pain Physician 2013; 16:E129–E143.
26. Kaye AD, Manchikanti L, Abdi S, et al. Efficacy of epidural injections in managing chronic spinal pain: a best evidence synthesis. Pain Physician 2015; 18:E939–E1004.
27. Hayek SM, Helm S, Benyamin RM, et al. Effectiveness of spinal endoscopic adhesiolysis in post lumbar surgery syndrome: a systematic review. Pain Physician 2009; 12:419–435.
28. Epter RS, Helm S 2nd, Hayek SM, et al. Systematic review of percutaneous adhesiolysis and management of chronic low back pain in post lumbar surgery syndrome. Pain Physician 2009; 12:361–378.
29. Helm S 2nd, Benyamin RM, Chopra P, et al. Percutaneous adhesiolysis in the management of chronic low back pain in post lumbar surgery syndrome and spinal stenosis: a systematic review. Pain Physician 2012; 15:E435–E462.
30. Helm S 2nd, Hayek SM, Colson J, et al. Spinal endoscopic adhesiolysis in post lumbar surgery syndrome: an update to the assessment of the evidence. Pain Physician 2013; 16:SE125–SE150.
31. Helm S 2nd, Racz GB, Gerdesmeyer L, et al. Percutaneous and endoscopic adhesiolysis in managing low back and lower extremity pain: a systematic review and meta-analysis. Pain Physician 2016; 19:E245–E281.
32. Khosravi MB, Azemati S, Sahmeddini MA. Gabapentin versus naproxen in the management of failed back surgery syndrome; a randomized controlled trial. Acta Anaesthesiol Belg 2014; 65:31–37.
33. Gianesello L, Pavoni V, Barboni E, et al. Perioperative pregabalin for postoperative pain control and quality of life after major spinal surgery. J Neurosurg Anesthesiol 2012; 24:121–126.
34. Chaparro LE, Smith SA, Moore RA, et al. Pharmacotherapy for the prevention of chronic pain after surgery in adults. Cochrane Database Syst Rev 2013; CD008307.
35. Chaparro LE, Furlan AD, Deshpande A, et al. Opioids compared to placebo or other treatments for chronic low-back pain. Cochrane Database Syst Rev 2013; CD004959.
36. North RB, Kidd DH, Zahurak M, et al. Spinal cord stimulation for chronic, intractable pain: experience over two decades. Neurosurgery 1993; 32:384–394. [discussion 394–5].
37. Manchikanti L, Pampati V, Bakhit CE, et al. Non-endoscopic and endoscopic adhesiolysis in post-lumbar laminectomy syndrome: a one-year outcome study and cost effectiveness analysis. Pain Physician 1999; 2:52–58.
38. Deyo RA, Nachemson A, Mirza SK. Spinal-fusion surgery—the case for restraint. N Engl J Med 2004; 350:722–726.
39. Franklin GM, Haug J, Heyer NJ, et al. Outcome of lumbar fusion in Washington State workers’ compensation. Spine (Phila Pa 1976) 1994; 19:1897–1903. [discussion 1904].
40. Martin BI, Mirza SK, Comstock BA, et al. Reoperation rates following lumbar spine surgery and the influence of spinal fusion procedures. Spine 2007; 32:382–387.
41. North RB, Campbell JN, James CS, et al. Failed back surgery syndrome: 5-year follow-up in 102 patients undergoing repeated operation. Neurosurgery 1991; 28:685–690. [discussion 690–1].
42. Fritsch EW, Heisel J, Rupp S. The failed back surgery syndrome: reasons, intraoperative findings, and long-term results: a report of 182 operative treatments. Spine (Phila Pa 1976) 1996; 21:626–633.
43. Lad SP, Petraglia FW 3rd, Kent AR, et al. Longer delay from chronic pain to spinal cord stimulation results in higher healthcare resource utilization. Neuromodulation 2016; 19:469–476.
44. Sharan A, et al. Comparing changes in healthcare utilization following back surgery and spinal cord stimulation for chronic pain. 20th Annual Meeting of the North American Neuromodulation Society; Las Vegas, NV 2016.
45. North RB, Kidd DH, Lee MS, et al. A prospective, randomized study of spinal cord stimulation versus reoperation for failed back surgery syndrome: initial results. Stereotact Funct Neurosurg 1994; 62:267–272.
46. North RB, Kidd DH, Farrokhi F, et al. Spinal cord stimulation versus repeated lumbosacral spine surgery for chronic pain: a randomized, controlled trial. Neurosurgery 2005; 56:98–107.
47. Kumar K, Taylor RS, Jacques L, et al. Spinal cord stimulation versus conventional medical management for neuropathic pain: a multicentre randomised controlled trial in patients with failed back surgery syndrome. Pain 2007; 132:179–188.
48. Kumar K, Taylor RS, Jacques L, et al. The effects of spinal cord stimulation in neuropathic pain are sustained: a 24-month follow-up of the prospective randomized controlled multicenter trial of the effectiveness of spinal cord stimulation. Neurosurgery 2008; 63:762–770. [discussion 770].
49. Kapural L, Yu C, Doust MW, et al. Novel 10-kHz high-frequency therapy (HF10 therapy) is superior to traditional low-frequency spinal cord stimulation for the treatment of chronic back and leg pain: the SENZA-RCT randomized controlled trial. Anesthesiology 2015; 123:851–860.
50. Kumar K, Nath R, Wyant GM. Treatment of chronic pain by epidural spinal cord stimulation: a 10-year experience. J Neurosurg 1991; 75:402–407.
51. Oakley J. Spinal cord stimulation in axial low back pain: solving the dilemma. Pain Med 2006; 7 (S1):58–63.
52. Kloimstein H, Likar R, Kern M, et al. Peripheral nerve field stimulation (PNFS) in chronic low back pain: a prospective multicenter study. Neuromodulation 2014; 17:180–187.
53. Hamm-Faber TE, Aukes H, van Gorp EJ, et al. Subcutaneous stimulation as an additional therapy to spinal cord stimulation for the treatment of low back pain and leg pain in failed back surgery syndrome: four-year follow-up. Neuromodulation 2015; 18:618–622. [discussion 622].
54. Van Buyten JP, Al-Kaisy A, Smet I, et al. High-frequency spinal cord stimulation for the treatment of chronic back pain patients: results of a prospective multicenter European clinical study. Neuromodulation 2013; 16:59–65. [discussion 65–6].
55. Al-Kaisy A, Van Buyten JP, Smet I, et al. Sustained effectiveness of 10 kHz high-frequency spinal cord stimulation for patients with chronic, low back pain: 24-month results of a prospective multicenter study. Pain Med 2014; 15:347–354.
56. Schu S, Slotty PJ, Bara G, et al. A prospective, randomised, double-blind, placebo-controlled study to examine the effectiveness of burst spinal cord stimulation patterns for the treatment of failed back surgery syndrome. Neuromodulation 2014; 17:443–450.
57. De Ridder D, Plazier M, Kamerling N, et al. Burst spinal cord stimulation for limb and back pain. World Neurosurg 2013; 80:642.e1–649.e1.
58. Liem L. Stimulation of the dorsal root ganglion. Prog Neurol Surg 2015; 29:213–224.
59. FDA Approval Letter for HIFU. 3.16.2017. Available from: Accessed March 16, 2017.
60. Spratt KF. Use of the assessment–diagnosis–treatment–outcomes model to improve patient care. Mil Med 2013; 178 (10 suppl):121–131.

back pain; chronic spinal pain; high-frequency SCS; spinal cord stimulation

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