Low Back Pain Multidisciplinary Rehabilitation

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King and Bogduk[1] note that the original idea of MDT pain management was to utilise the skills of all potentially relevant health practitioners such as pain physicians, radiologists, surgeons, interventionalists, physiotherapists, psychologists, and occupational therapies. This concept has morphed into one where the biomedical aspects are largely ignored, and so the term "MDT" and "pain clinic" are really misnomers.

Frequently the culture in MDT clinics can lead to the individuals equating a surgeon saying "there is no surgical intervention" with there is "no structural pain generator", and presume the cause is primarily nociplastic in nature without actually testing for nociceptive pain. For example, in the past investigations such as medial branch blocks were offered in some areas of the country, but largely due to the changes in ideology, they are now no longer offered, and furthermore the MDT clinics may refuse to work alongside reductionist clinicians.


The premises that underlie multidisciplinary rehabilitation, as it is currently practiced (a primary focus on psychosocial intervention while ignoring nociceptive drivers), have no support in evidence based medicine.

False Premise 1: "It isn't possible to identify the source of the pain"

The source of pain can in fact be found in most patients with access to appropriate investigations.[2][3][4][5][6]

The false statement has persisted through a "telephone game of referencing" dating back to the 60s before the advent of modern investigations, while ignoring the copious literature to the contrary. See Non-Specific Chronic Low Back Pain for complete discussion on this topic.

False Premise 2: "The injury has healed but the brain has a memory of pain"

The evidence does not support chronic nociceptive becoming "engraved" into the central nervous system. There is some support for this idea in neuropathic pain, but not nociceptive pain.[7][8]

If this were not the case then then precision treatments wouldn't have the drastic effect on both pain and function seen in research, hip arthroplasty wouldn't work for chronic hip pain secondary to hip osteoarthritis, microdiscectomy wouldn't work for chronic lumbar radicular pain, omeprazole wouldn't work for chronic dyspepsia, corticosteroids wouldn't work for chronic de quervains tenosynovitis, and percutaneous intervention wouldn't work for chronic angina.

Furthermore if the pain was primarily central in origin (like phantom limb pain), the research on diagnostic blocks would have shown that they don't abolish the chronic pain even temporarily, which is of course contrary to what has been found.

These two premises frequently lead to pseudo-theological arguments such as "the pain must be accepted before you can move forward," and "we can't help you if you continue to look at biomedical factors."


With these patently false premises, it is not surprising that MDT as it is typically practised is not particularly effective (pain reduction 0.5-1.4 on 0-10 scale, and disability reduction 1.4-2.5 on 0-24 Roland-Morris scale), and is also extremely costly.[9]

MDT should be reserved for patients with widespread chronic pain and demonstrable central sensitisation (e.g. as identified through simplified bedside quantitative sensory testing), of which the standard chronic low back pain patient does not fit under.[10] Psychologically based programs may reduce distress and prevent deterioration, but there is no evidence that they help patients return to work and normal activities. MDT is at most a palliative treatment.

It may also be suitable for patients who are not interested in exploring the biomedical aspect of the biopsychosocial model, or who have a dual diagnosis of chronic low back pain and a mental health disorder or past trauma.

Future Directions

"Good" clinics are not defined by the use of "multidisciplinary" in their names, but rather by the outcomes they achieve. What percentage of patients achieve relief of pain, restoration of activities of daily living, return to work, reduction of psychological distress, and no further need for health care related to the pain.

A future research need is assessing the efficacy of MDT as it was originally envisaged: a truly multidisciplinary approach that is able to address all problems in the biomedical, psychological, and social domains of chronic low back pain. The biomedical domain should not be hamstrung and restricted to medication, but include the full suite of proven investigations and interventions.

See Also


  1. ↑ Wade King and Nikolai Bogduk. Chronic Low Back Pain In: Bonica's Management of Pain. 2018
  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. ↑ 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. ↑ Cohen M, Quintner J, Buchanan D. Is chronic pain a disease? Pain Med. 2013 Sep;14(9):1284-8. doi: 10.1111/pme.12025. Epub 2013 Jan 7. PMID: 23294511.
  8. ↑ Curatolo M, Arendt-Nielsen L, Petersen-Felix S. Central hypersensitivity in chronic pain: mechanisms and clinical implications. Phys Med Rehabil Clin N Am. 2006 May;17(2):287-302. doi: 10.1016/j.pmr.2005.12.010. PMID: 16616268.
  9. ↑ Kamper SJ, Apeldoorn AT, Chiarotto A, Smeets RJ.E.M., Ostelo RWJG, Guzman J, van Tulder MW. Multidisciplinary biopsychosocial rehabilitation for chronic low back pain. Cochrane Database of Systematic Reviews 2014, Issue 9. Art. No.: CD000963. DOI: 10.1002/14651858.CD000963.pub3
  10. ↑ 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.