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Non-Specific Chronic Low Back Pain

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It is often incorrectly stated that the cause of chronic low back pain cannot be diagnosed in 85% of cases with exact figure differing with different publications (some say 80%, some say 90%)[1] This "convenient truth" has been proven to be false time and time again. Unlike acute low back pain where the causes and sources are largely unknown (around 95% of cases are unknown), The sources of chronic low back pain are largely known (see Causes and Sources of Chronic Low Back Pain). History and examination are insufficient for diagnosis, but the source can be established with at least moderate certainty in around 90% of cases as long as there is access to appropriate investigations and the investigations are done in a logical manner.[2][3][4][5][6]

The Origin of the Myth

The fact that some authors and clinicians continue to perpetuate the myth that most chronic low back pain is "non-specific low back pain" is likely ideological in nature, rather than based on evidence. Typically the review articles reference yet further review articles, misleadingly only reference red flag prevalence data, or simply make ex cathedra proclamations.

An example of this "train of intellectual dishonesty" regarding the prevalence of "non-specific back pain" is presented here for illustration. The lancet review by Hartvigsen 2018[7] ("nearly all") which has been cited 416 times as of writing references a review by Maher from 2017 ("90%")[8], which in turn references a review by Koes from 2006 ("90%"),[9] which in turn references a review by Deyo from 1992 ("85%"),[10] which in turn references an expert opinion workshop by White from 1982 ("20% to 85%")[11] and speech by Nachemson from 1984.[12] The 1982 workshop figure is unreferenced, and I am unable to access the full 1984 speech. The 2017 review by Maher also dishonestly references a study on acute low back pain,[13] another review by Deyo from 2001 ("85%") which in turn does not reference their figure[14], and another study of older adults that only looked for vertebral fracture in patients with mixed acute and chronic back pain.[15] The reference train runs dry at that point, but note how the 1982 expert opinion figure of "20-85%" became "nearly all," without further appropriate primary references to support this updated figure, and the literature on precision diagnosis has been completely ignored.

Sometimes we find that the reference train leads to a report by the Quebec Task Force in 1987.[16] Another possible source of the 80-90% figure is a 1966 study of British General Practice patients with acute low back pain, where no cause was evident in 79% of men and 88% of women.[17] It goes without saying that history, exam, and plain films were the only tools of diagnosis at that time.

Generally the reviews on the topic display several flaws in logical thinking.

  1. They reference information about the very low rate of red flag conditions, and conclude therefore most causes of low back pain are unknown. The one does not follow the other. A lack of red flag conditions does not equal a lack of a structural source. To diagnose the structural source you need to follow a particular process which has been painstakingly validated over the last 30 years by many researchers.[6]
  2. The fact that in many cases the cause of the chronic low back pain can't be cured does not mean that it is "non-specific." The one does not follow the other. Bacterial infections weren't "non-specific" before the advent of antibiotics. Croup wasn't "non-specific" before it was discovered that oral steroids worked.
  3. They dishonestly ignore the research on precision diagnosis, which shows the extreme limitations of conventional methods of assessment and investigation, and the referencing train leads to articles published at a time before the advent of this methodology, and so the false-negative rate would have been very high. These older articles also commonly confused sciatica, spondylosis, spondylolisthesis, and spondylolysis with causes of low back pain, and so false-positives were likely also common.

In the last 30 years imaging and investigation techniques have drastically improved, and it is now possible to determine the cause in the majority but not all cases.[18] In New Zealand it is usually lack of funding for access to the appropriate diagnostic tools that renders diagnosis impossible, rather than the tools themselves not existing. The forces driving the overdiagnosis of "non-specific low back pain" are likely complex. There may be strong beliefs in the importance of avoiding biomedical diagnoses and a desire to maintain the status quo. Allowing precision diagnosis in chronic low back pain may be unappealing to a range of different stakeholders including DHBs, pharmaceutical and biotechnology companies that target chronic pain, professional societies, funding agencies, MDT clinics, and the psychosocial academic system. Allowing bio to be part of biopsychosocial management does not lessen the importance of the psychosocial aspects. Yet some proponents of the non-specific model use the almost theological reasoning that pain must be accepted as central sensitisation before it can be managed, and incorrectly lump nociplastic conditions like fibromyalgia with most chronic low back pain.[19][1]

Utility of Precision Diagnoses

Whether the cause should be diagnosed, and whether the cause can be cured are two entirely separate questions from whether it can be diagnosed. Bogduk has presented the value of making a biomedical diagnosis as being viewed from three lenses: positive therapeutic value (does making a diagnosis lead to improved outcomes), negative therapeutic value (does making a diagnosis prevent inappropriate treatment), and diagnostic utility (is making a diagnosis helpful in itself without treatment being available).[20]

  • Positive therapeutic utility: for confirmed facet joint mediated pain (two positive blocks) there is a treatment called medial branch radiofrequency neurotomy that has a good chance of working.[21][22][23][24] For pure discogenic pain there is no good proven therapy. For vertebrogenic pain (modic changes), there is basivertebral nerve ablation.[25] For proven sacroiliac joint pain and sacroiliac ligament pain, there is evidence for sacroiliac joint fusion[26][27] and lateral branch cooled radiofrequency neurotomy.[28][29]
  • Negative therapeutic utility: Providing a diagnosis may stop a potentially inappropriate intervention. For example, if provocation discography is negative or indeterminate then it may not be appropriate to have spinal fusion.
  • Diagnostic utility: Making a diagnosis provides an explanation, and reduces the fear around not knowing what is causing the pain. It also serves to inform treating clinicians that the patient doesn't have primary nociplastic pain, which otherwise may lead to the patient not being taken seriously.

IASP Definition

When a diagnosis of non-specific low back pain is made, the IASP term can be used which is "Lumbar Spinal Pain of Unknown or Uncertain Origin."

The diagnostic criteria for this are "Lumbar spinal pain for which no other cause has been found or can be attributed." This term is intended for use when the complaints defy conventional diagnosis, but can also be used as a temporary label before more a more definitive diagnosis is made. In other cases a decision may be made not to pursue definitive diagnosis.

See Also

References

  1. ↑ 1.0 1.1 Fitzcharles MA, Cohen SP, Clauw DJ, Littlejohn G, Usui C, Häuser W. Nociplastic pain: towards an understanding of prevalent pain conditions. Lancet. 2021 May 29;397(10289):2098-2110. doi: 10.1016/S0140-6736(21)00392-5. PMID: 34062144.
  2. ↑ DePalma et al.. What is the source of chronic low back pain and does age play a role?. Pain medicine (Malden, Mass.) 2011. 12:224-33. PMID: 21266006. DOI.
  3. ↑ DePalma et al.. Etiology of chronic low back pain in patients having undergone lumbar fusion. Pain medicine (Malden, Mass.) 2011. 12:732-9. PMID: 21481166. DOI.
  4. ↑ DePalma et al.. Multivariable analyses of the relationships between age, gender, and body mass index and the source of chronic low back pain. Pain medicine (Malden, Mass.) 2012. 13:498-506. PMID: 22390231. DOI.
  5. ↑ DePalma et al.. Structural etiology of chronic low back pain due to motor vehicle collision. Pain medicine (Malden, Mass.) 2011. 12:1622-7. PMID: 21958329. DOI.
  6. ↑ 6.0 6.1 DePalma. Diagnostic Nihilism Toward Low Back Pain: What Once Was Accepted, Should No Longer Be. Pain medicine (Malden, Mass.) 2015. 16:1453-4. PMID: 26218010. DOI.
  7. ↑ Hartvigsen J, Hancock MJ, Kongsted A, Louw Q, Ferreira ML, Genevay S, Hoy D, Karppinen J, Pransky G, Sieper J, Smeets RJ, Underwood M; Lancet Low Back Pain Series Working Group. What low back pain is and why we need to pay attention. Lancet. 2018 Jun 9;391(10137):2356-2367. doi: 10.1016/S0140-6736(18)30480-X. Epub 2018 Mar 21. PMID: 29573870.
  8. ↑ Maher C, Underwood M, Buchbinder R. Non-specific low back pain. Lancet. 2017 Feb 18;389(10070):736-747. doi: 10.1016/S0140-6736(16)30970-9. Epub 2016 Oct 11. PMID: 27745712.
  9. ↑ Koes BW, van Tulder MW, Thomas S. Diagnosis and treatment of low back pain. BMJ. 2006 Jun 17;332(7555):1430-4. doi: 10.1136/bmj.332.7555.1430. PMID: 16777886; PMCID: PMC1479671.
  10. ↑ Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992 Aug 12;268(6):760-5. PMID: 1386391.
  11. ↑ White AA 3rd, Gordon SL. Synopsis: workshop on idiopathic low-back pain. Spine (Phila Pa 1976). 1982 Mar-Apr;7(2):141-9. doi: 10.1097/00007632-198203000-00009. PMID: 6211779.
  12. ↑ Nachemson AL. Prevention of chronic back pain. The orthopaedic challenge for the 80's. Bull Hosp Jt Dis Orthop Inst. 1984 Spring;44(1):1-15. PMID: 6326902.
  13. ↑ Henschke N, Maher CG, Refshauge KM, Herbert RD, Cumming RG, Bleasel J, York J, Das A, McAuley JH. Prevalence of and screening for serious spinal pathology in patients presenting to primary care settings with acute low back pain. Arthritis Rheum. 2009 Oct;60(10):3072-80. doi: 10.1002/art.24853. PMID: 19790051.
  14. ↑ Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001 Feb 1;344(5):363-70. doi: 10.1056/NEJM200102013440508. PMID: 11172169.
  15. ↑ Enthoven WT, Geuze J, Scheele J, Bierma-Zeinstra SM, Bueving HJ, Bohnen AM, Peul WC, van Tulder MW, Berger MY, Koes BW, Luijsterburg PA. Prevalence and "Red Flags" Regarding Specified Causes of Back Pain in Older Adults Presenting in General Practice. Phys Ther. 2016 Mar;96(3):305-12. doi: 10.2522/ptj.20140525. Epub 2015 Jul 16. PMID: 26183589.
  16. ↑ Scientific approach to the assessment and management of activity-related spinal disorders. A monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spine (Phila Pa 1976). 1987 Sep;12(7 Suppl):S1-59. PMID: 2961086.
  17. ↑ Dillane JB, Fry J, Kalton G. Acute back syndrome-a study from general practice. Br Med J. 1966 Jul 9;2(5505):82-4. doi: 10.1136/bmj.2.5505.82. PMID: 20791052; PMCID: PMC1943081.
  18. ↑ Knezevic NN, Candido KD, Vlaeyen JWS, Van Zundert J, Cohen SP. Low back pain. Lancet. 2021 Jul 3;398(10294):78-92. doi: 10.1016/S0140-6736(21)00733-9. Epub 2021 Jun 8. PMID: 34115979.
  19. ↑ Julien N, Goffaux P, Arsenault P, Marchand S. Widespread pain in fibromyalgia is related to a deficit of endogenous pain inhibition. Pain. 2005 Mar;114(1-2):295-302. doi: 10.1016/j.pain.2004.12.032. PMID: 15733656.
  20. ↑ Bogduk N, Aprill C, Derby R. Lumbar discogenic pain: state-of-the-art review. Pain Med. 2013 Jun;14(6):813-36. doi: 10.1111/pme.12082. Epub 2013 Apr 8. PMID: 23566298.
  21. ↑ Cohen SP, Williams KA, Kurihara C, Nguyen C, Shields C, Kim P, Griffith SR, Larkin TM, Crooks M, Williams N, Morlando B, Strassels SA. Multicenter, randomized, comparative cost-effectiveness study comparing 0, 1, and 2 diagnostic medial branch (facet joint nerve) block treatment paradigms before lumbar facet radiofrequency denervation. Anesthesiology. 2010 Aug;113(2):395-405. doi: 10.1097/ALN.0b013e3181e33ae5. PMID: 20613471.
  22. ↑ Nath S, Nath CA, Pettersson K. Percutaneous lumbar zygapophysial (Facet) joint neurotomy using radiofrequency current, in the management of chronic low back pain: a randomized double-blind trial. Spine (Phila Pa 1976). 2008 May 20;33(12):1291-7; discussion 1298. doi: 10.1097/BRS.0b013e31817329f0. PMID: 18496338.
  23. ↑ Moussa WM, Khedr W. Percutaneous radiofrequency facet capsule denervation as an alternative target in lumbar facet syndrome. Clin Neurol Neurosurg. 2016 Nov;150:96-104. doi: 10.1016/j.clineuro.2016.09.004. Epub 2016 Sep 5. PMID: 27618781.
  24. ↑ MacVicar J, Borowczyk JM, MacVicar AM, Loughnan BM, Bogduk N. Lumbar medial branch radiofrequency neurotomy in New Zealand. Pain Med. 2013 May;14(5):639-45. doi: 10.1111/pme.12000. Epub 2012 Dec 28. PMID: 23279154.
  25. ↑ Fischgrund JS, et al. Intraosseous Basivertebral Nerve Ablation for the Treatment of Chronic Low Back Pain: 2-Year Results From a Prospective Randomized Double-Blind Sham-Controlled Multicenter Study. Int J Spine Surg. 2019 Apr 30;13(2):110-119. doi: 10.14444/6015. PMID: 31131209; PMCID: PMC6510180.
  26. ↑ Polly DW, et al. Two-Year Outcomes from a Randomized Controlled Trial of Minimally Invasive Sacroiliac Joint Fusion vs. Non-Surgical Management for Sacroiliac Joint Dysfunction. Int J Spine Surg. 2016 Aug 23;10:28. doi: 10.14444/3028. PMID: 27652199; PMCID: PMC5027818.
  27. ↑ Dengler J, et al. Randomized Trial of Sacroiliac Joint Arthrodesis Compared with Conservative Management for Chronic Low Back Pain Attributed to the Sacroiliac Joint. J Bone Joint Surg Am. 2019 Mar 6;101(5):400-411. doi: 10.2106/JBJS.18.00022. PMID: 30845034; PMCID: PMC6467578.
  28. ↑ Cohen SP, Hurley RW, Buckenmaier CC 3rd, Kurihara C, Morlando B, Dragovich A. Randomized placebo-controlled study evaluating lateral branch radiofrequency denervation for sacroiliac joint pain. Anesthesiology. 2008 Aug;109(2):279-88. doi: 10.1097/ALN.0b013e31817f4c7c. PMID: 18648237; PMCID: PMC2666931.
  29. ↑ Patel N. Twelve-Month Follow-Up of a Randomized Trial Assessing Cooled Radiofrequency Denervation as a Treatment for Sacroiliac Region Pain. Pain Pract. 2016 Feb;16(2):154-67. doi: 10.1111/papr.12269. Epub 2015 Jan 7. PMID: 25565322.
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