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| Digital ExclusiveWhy the Term "Mechanical Low Back Pain" Must Go
In my last article [June 3 issue], I made fun of the terms "bone-out-of-place" (BOOP) subluxation and mechanical low back pain (MLBP). Both terms are equally flawed; however, the latter term seems to be reasonable when taken at face value. Indeed, I regularly hear intelligent DCs talk about MLBP as if it is a documented reality - which it is not. Not one study has ever demonstrated the existence of MLBP.
We should realized that MLBP is a term that was made up and used to describe pain associated with the following:1
- Pain is usually cyclic.
- Low back pain is often referred to the buttocks and thighs.
- Morning stiffness or pain is common.
- Start pain is common.
- There is pain on forward flexion, and often, on returning to the erect position.
- Pain is often produced or aggravated by extension, lateral flexion, rotation or standing.
- Pain usually becomes worse over the course of the day.
- Pain is relieved by a change of position.
- Pain is relieved by lying down, especially in the fetal position.
These manifestations of MLBP suggest that mechanical nociceptors are irritated by these events; however, no study has ever shown that nociceptors are selectively "mechanically irritated" and thereby create mechanical low back pain.
Mechanical low back pain is just a term - and a bad one, as it causes one to think that pain is driven by solely mechanical events. This might be true if we were constructed like the Tin Man from "The Wizard of Oz," before he got his heart - except that the Tin Man, Dorothy, the Cowardly Lion, and even the Scarecrow recognized that the Tin Man's joints were of a mechanical and chemical nature; that is, they all needed to keep the Tin Man's joints oiled as they went "off to see the Wizard." Consider the fact that we can't separate mechanics from chemistry in inanimate objects like cars, but somehow, we try to do this with the human body.
It is a bit shocking to consider that our "straight chiro" colleagues have reduced human dysfunction to a BOOP, and our medical and "mixer" colleagues have reduced human spinal function to the equivalent of a robot made out of an Erector set. And we wonder why neck pain, head pain and back pain rage on - because pain is not caused by a BOOP or a solitary mechanical problem.
Why Mechanical Low Back Pain Is a Dumb Term
First, we should consider that it is completely inappropriate to condescend to "straight" chiros for "believing" in the BOOP subluxation, and then simultaneously turn around and promote MLBP, which also does not exist as a reality. Sooner or later, we are going to have to accept the fact that BOOP and MLBP are both goofy terms; they don't refer to anything that commonly occurs in the human system.
Thankfully, Kirkaldy-Willis did not name his book Managing Mechanical Low Back Pain. Such a title would massively contradict his statement about the mental aspect of back pain:2
"In the management of low back pain, the physician must determine how much of each of these four attributes influences a patient's response to illness (physical, mental, emotional, spiritual). It has been estimated that 75% to 90% of physical ills arise from emotional or spiritual problems. Each patient with a physical problem also has an emotional one. In some people, the emotional problem is by far the greater one."
Mechanical low back pain? I don't think so; what a dumb and poorly descriptive term. Should we maybe call it psychological low back pain? No, that would also be dumb. It's just "low back pain," and it is likely to be caused by physical and psychospiritual factors.
Does physical mean "related to structure" only? No, the physical body requires oxygen, food and water to run properly; in other words, we need proper biochemistry for the body to function - an obvious fact known by all (so don't interpret my apparent sarcasm as being patronizing); it's just that it is easy to forget biochemistry when one's sole clinical focus is to "treat mechanical low back with manipulation," or to magically "free the body of nerve interference by adjusting subluxations."
While we know that drugs do not represent the answer to back pain and often do not work adequately, which is the same for adjustment/manipulation, people do get relief with anti-inflammatories and muscle relaxants - and patients will routinely state that their head, neck, and back pain is afforded some relief by NSAIDs.3 In a review article about medical therapy for low back pain, we are told:4
"The combination of cyclobenzaprine (Flexoril, a muscle relaxant) and naproxen (a NSAID) was better than naproxen alone in reducing objective muscle spasm and tenderness, and increasing range of motion of the lumbosacral spine."
Spasm? Tenderness? Reduced range of motion? Sounds like mechanical low back pain. With this in mind, how is it that mechanical low back pain can respond to a chemical intervention like drug therapy? It doesn't make any sense.
Clearly, the term "mechanical low back pain" is inappropriate. If we use the term "mechanical," we think the problem is mechanical - and back pain is not a mechanical problem. Consider that the lion's share of nociceptors are of the polymodal variety, and each has numerous chemoreceptors on its membrane, such that a noxious chemical will bind to its respective receptor and induce action potentials in the nociceptive axon, which can ultimately lead to the experience of pain.
The following represents an updated list of chemicals that have receptors on polymodal nociceptor membranes: bradykinin, hydrogen ions, prostaglandin E2, leukotriene B4, serotonin, histamine, interleukin-1, interleukin-6, tumor necrosis factor, glutamate, GABA, acetylcholine, norepinephrine, adenosine, ATP, estrogen, glucocorticoids, corticotrophin releasing factor, substance P, neurokinin A, cholecystokinin, somatostatin, bombesin, angiotensin II, neuropeptide Y, endorphins, enkephalin, dynorphin, nerve growth factor, brain-derived neurotrophic factor, glial-derived neurotrophic factor, and fibroblast growth factor.5 So-called "silent nociceptors" are not responsive to any stimuli until the presence of inflammatory mediators "wake them up," after which they respond to mechanical stimuli. Pain is chemical and mechanical ... never just one.
Furthermore, it is known that the cells of injured discs and joint tissue release chemical mediators such as pro-inflammatory eicosanoids (prostaglandin-E2, leukotriene-B4, thromboxane A2) and pro-inflammatory cytokines, such as interleukin-1 and tumor necrosis factor.6,7 If injured discs and joints release chemical mediators, and these mediators can cause inflammation and pain, why would we ever choose to help advance the notion that back pain is mechanical? It does not make any sense.
Back pain is clearly driven by psychological, mechanical and biochemical issues. It is just back pain - and clinicians need to focus on reducing these causes of the pain, and avoid using labels that will impede appropriate thought processes related to the diverse factors that drive the generation of pain. Pain is never only psychological, mechanical or biochemical ... so terms such as "psychological pain," "mechanical pain" and "biochemical pain" are inaccurate and should be avoided.
I recently played golf with my good friend Dr. Leonard Faye. At one point, he tested my level of dogmatic attachment to nutrition by asking me the following question: "Which is more important in patient care for back pain: nutrition or adjustments?" Fortunately, I passed the test, because my answer was, "That depends on what is wrong with the patient; maybe exercise is most important." Then I hooked my drive into the woods, became depressed, and my back started hurting.
References
- Waddell G. The Back Pain Revolution. Churchill Livingstone: New York; 1998: p. 136.
- Kirkaldy-Willis W, Bernard TN. Managing Low Back Pain, 4th ed. Churchill Livingstone: New York; 1999: p. 103.
- Borenstein DG, Wiesel SW, Boden SD. Low Back and Neck Pain, 3rd ed. Saunders: Philadelphia; 2004: p.812.
- Borenstein DG. Medical therapy for low back pain. Drug Therapy 1992;22(10):93-102.
- Byers MR, Bonica JJ. Peripheral pain mechanisms and nociceptor plasticity. In: Loeser JD (ed.), Bonica's Management of Pain, 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001: p.26-72.
- Schmidt RF. The articular polymodal nociceptor in health and disease. Prog Brain Res 1996;113:53-81.
- Watkins LR, Maier SF. Beyond neurons: evidence that immune and glial cells contribute to pathological pain states. Physiol Rev 2002;82:981-1011.
David Seaman, DC, MS, DACBN
Port Orange, Florida