Is Mechanical Back Pain an Unscientific Myth that Should be Abandoned?
FEATURE
David Seaman
DC
Origins of mechanical back pain
Dr. Gordon Waddell, author of The Back Pain Revolution, is well known to evidencebased chiropractors. In both the first (1) and second (2) editions of his text, Waddell explains that the term “mechanical pain” was invented in 1980 based on a survey given to the members of the International Society for the Study of the Lumbar Spine, all of whom were orthopedic surgeons. No chiropractors were allowed, and orthopedic surgeons back then, in particular, were outspoken in their disdain of chiropractic. Two types of pain were described by the surgeons in this survey. One related to nerve tension with “radicular pain” being the most common term used to characterize the pain experienced. The other was pain that was relieved or increased by movement and position, which became known as “mechanical back pain.” Not a shred of scientific investigation was performed to confirm that such an entity existed in the physiological sense.
In other words, mechanical back pain is an unscientific concept that was invented by outspoken critics of the chiropractic profession and subsequently embraced by chiropractors who refer to themselves as being “scientific” and “evidence-based.” This sect of chiropractors ceaselessly criticizes the “straights” for being unscientific, which is somewhat shameful, in my opinion.
Why mechanical pain “fails”
Mechanical pain merely means musculoskeletal pain and nothing more, so why not just use the accurate and descriptive term “musculoskeletal pain” instead? The problem is that mechanical pain has morphed, without scientific evidence, into a pain classification category often contrasted with another clinician-invented pain category called “inflammatory pain,” which is synonymous with pain caused by ankylosing spondylitis(3). First, this is not remotely how pain scientists look at pain; they view pain from the perspective of nociception physiology, which should also be the foundation upon which clinicians view pain. Second, patients with so-called “mechanical back pain” often have varying degrees of relief by taking nonsteroidal, anti-inflammatory drugs, which speaks to the fact that inflammation exists in patients with back pain who do not have ankylosing spondylitis or other autoimmune diseases.
The situation is made worse by clinicians who incor-
rectly conceptualize mechanical pain as a type ot pain syndrome that involves the “mechanical” stimulation of nociceptors, without the involvement of biochemistry. For this to be true, there would have to be a subset of mechanical receptors on the nociceptive membrane that exclusively responds to noxious mechanical stimuli to generate pain in the absence of local biochemical changes. First, such a receptor has yet to be identified. Second, nociception can only be generated in the laboratory setting when inflammation is present, relegating mechanical pain into the category where it belongs—a purely speculative entity.
Three types of pain
Pain can be generated in only three ways, so there are only three types of pain syndromes from a physiological perspective. The first scientific paper I wrote on this topic to further my own understanding (4) demonstrated that healthcare professionals, in general, are poorly informed about pain mechanisms in their educational training. Consider the following quotation in a paper written by the director of pain management at Brigham and Women’s Hospital (Harvard University)(5):
Pain can be classified according to etiology and physiology. When used, this classification scheme can
be used to provide a rational treatment approach that is based on physiology and the rational use of pharmacology.
The reference for this statement was my spinal pain syndromes article mentioned earlier (4), which explained how pain can only be nociceptive or neuropathic. We now know there are two subtypes of nociceptive pain. The first involves the activation of nociceptors in the tissue that a patient experiences as painful, such as a painful tendon, muscle, joint, disc, ligament, or visceral tissue, which is called nociceptive pain (4). Mechanical pain and the pain of ankylosing spondylitis should be viewed properly as diagnostic terms, but from a physiological perspective, they are both nociceptive pains with different causes.
The second type of nociceptive pain involves the activation of nociceptive axons, which occurs with disc herniation. Axons fire spontaneously wherever they are exposed to inflammation, and so this pain has been termed “ectopic nociceptive pain”(6). Geoff Bove, a DC and PhD, has spent his entire research career inflaming midaxonal regions of neurons and recording their related neuronal hyerexcitability (7). Anytime a nerve tension test generates painful symptoms, it should be referred to physiologically as ectopic nociceptive pain.
Neuropathic pain is very different and caused by injured axons that never heal and become spontaneously active in the area of injury. This pain is so severe that the area of pain cannot be touched. Even putting on clothes can be excruciating, which means such patients are not going to see a chiropractor for fear of a physical examination (4> 6). Clearly, the only types of pain we deal with as DCs are nociceptive pain (95% of the time) and ectopic nociceptive pain (5% of the time). These percentages can vary based on the type of practice you have.
Treating nociceptive and ectopic nociceptive pain
Research has identified patient presentations and examinations that help guide back pain care. In my opinion,
Jeff Hebert’s article (8) and Don Murphy’s books(9-10) are the most useful. They clearly describe patients who will best respond to manipulation, end-range loading, postural changes, traction, or stabilization exercises.
When patients do not respond to manual and self-care approaches, the patient should be classified as a “nonresponder,” and further consideration should be given to the patient’s physiological status. In most cases, nonresponders are suffering from chronic inflammation, which promotes nociception and pain(11).
The most common causes of chronic inflammation are stress, a lack of sleep, sedentary living, and a proinflammatory diet(n-12). The outcome of these unhealthy lifestyle factors can be both physiological, such as metabolic syndrome, and psychological, such as depression and catastrophizing. Various promoters of chronic inflammation should be assessed and addressed in any nonresponding patient, and in this regard, there is no need to make interventions complicated or confusing for the patient(41M4).
Conclusion
When pain physiology is understood from a clinical perspective, it becomes obvious that mechanical back pain dramatically fails to capture what is actually wrong with
a patient, particularly a nonresponder. My suggestion is to abandon the term “mechanical back pain.”
The only consequence of doing this would be better patient care and better clinical thinking because spinal pain and its perpetuators will be better understood. Most treatments used by chiropractors will not change. Billing will not change; diagnostic codes will not change; and clinical practice operating procedures will not change. The primary change required of a practitioner, and the most difficult to do, is to abandon nonphysiological language and engage in proper communication with the patient about the actual physiologic nature of the painful condition.
References
1. Waddell G. The Back Pain Revolution. 2nd ed. New York: Churchill Livingstone; 1998. p.10-11, 135-36.
2. Waddell G. The Back Pain Revolution. 2nd ed. New York: Churchill Livingstone; 2004. p.10-11, 154.
3. Riksman JS et al. Delineating inflammatory and mechanical sub-types of low back pain: a pilot survey of fifty low back pain patients in a chiropractic setting. Chiropr Man Therap. 2011 ;19(1):5.
4. Seaman DR, Cleveland C. Spinal pain syndromes: nociceptive, ne uropathic, and psychologic mechanisms. JManip Physio Ther. 1999; 22:458-72.
5. Ross E. Moving towards a rational pharmacological management ofpain with an improved classification system of pain. Expert Opin Pharmacother. 2001;2:1529-30.
6. Bove GM, Seaman DR. Subclassification of radicular pain using neurophysiology and embryology. Proceedings of the 7th Interdisciplinary World Congress on Low Back & Pelvic Pain. November 9-12, 2010. Los Angeles, p.155-159.
7. Bove GM et al. Inflammation induces ectopic mechanical sensitivity in axons of nociceptors innervating deep tissues. J Neurophysiol. 2003;90(3): 1949-55.
8. Hebert JJ et al. Subgrouping patients with low back pain: a treatment-based approach to classification. Sports Health. 2011;3:534-42.
9. Murphy DR. Clinical reasoning in spine pain. Volume 1. Primary management of low back disorders using the CRISP protocols. CRISP Education Research; Pawtucket, RI. 2013.
10. Murphy DR. Clinical reasoning in spine pain. Volume 2. Primary management of cervical disorders using the CRISP protocols. CRISP Education Research; Pawtucket, RI. 2016.
11. Seaman DR. Body mass index and musculoskeletal pain: is there a connection? Chiropractic Man Ther. 2013;21:15.
12. Seaman DR. The DeFlame Diet. Wilm, NC; Shadow Panther Press; 2016.
13. Seaman DR, Palombo AD. An overview of the identification and management of the metabolic syndrome in chiropractic practice. J Chiropr Med. 2014; 13(3) :210-19.
14. Seaman DR. Weight gain as a consequence of living a modern lifestyle: a discussion of barriers to effective weight control and how to overcome them. J Chiro Humanities. 2013;20(l):27-35.
David Seaman, DC, is consultant for Anabolic Laboratories and has designed several nutritional supplements. He has authored many articles on the topic of diet, inflammation, and pain. His most recent book written for laypeople is entitled The DeFlame Diet. He posts regular DeFlame nutrition updates at DeFlame Nutrition on YouTube andFacebook.
