Archive for month: August, 2015

This is the opening line from both Low Back Pain and Clinical anatomy of the lumbar spine circa 1979 and 1987. Grieves referred to LBP as an “epidemic” in 1983. Innumerable authors recognized it as the most common entrance complaint to family physicians (behind colds & flu) in the US (these studies being as early as the late 1960’s). So LBP is certainly like an epidemic accounting for some 45% of disability claims and recognized as the single most likely work-disabling condition worldwide. The question is when did it begin?? I am approaching 30 years in practice and my years at Palmer had a focus on LBP and its ubiquitous nature. The DC who sent me to Palmer, himself having been in practice for 35 years by 1983 always said: “bad low backs will keep you in cash!” Additionally he’d always refer to the “lazy” back i.e. folks who (now some 50 years ago) didn’t do enough “real work” to keep their back strong (and IF smoking is a contributor why didn’t our forefathers who all smoked continuously not necessarily suffer from it as much…?) So whether there is a “modern” epidemic of LBP depends on several things; the quality of reporting and diagnosis of it, the degree or tolerance the society allows you to complain about it and the assumptions that there are reputable treatments for it. Perhaps it’s our awareness and focus that has changed (at least in the last 75 years) not our backs. 

If you haven’t read David Seamen’s clinical synopsis: The chemistry of discogenic and disc herniation pain, I highly recommend you do…its available on this site. As Chiropractors we are of course just itching to “lay hands on” our patients to find and “cure” them of their pains, mechanically. However a potential reality of discogenic pain, herniation in particular is the undeniable chemical influences perhaps driving the pain. He discusses the concept of the herniation being “turned on” by inflammation in the diet. The difficulty we face given these chemical realities is at what point do we conclude “dietary inflammation” not necessarily a “heal-able” mechanical lesion is predominant? And if we are co-treating at what point do we conclude which protocol did the work or was enough to actually “work” given the high improbability patients will follow our instructions? Will diet modification definitively stop episodes in the future? There’s no simple answer in my opinion however its’ apparent that many mechanistic-methods have substantively been able to give long-term relief (without mention of diet) and cultures whose daily physical labor and lack of sitting (and soda?) simply have less LBP disability. I have not seen any studies to date where extensive and exclusive “diet modification”, in exclusion of mechanical interventions and/or dedicated Core control exercise, was shown to substantially end LBP or sciatic, however we do know type II diabetics show an increased expression of HNP.

Many of us tend to associate LBP with the disc, more specifically with a ‘herniated’ disc. However research which began in the mid 1970s’ and was described in depth in the 1987 text Clinical Anatomy of the Lumbar Spine (Bogduk & Twomey) explicated the most compelling source of acute LBP: internal disc disruption promulgating annular ‘tears’. Not coincidentally these “tears” create a pain profile mimicking a ligament sprain.

Sato et al (Eur Spine 2005) further delineates this  likely mechanism of acute (non-radicular) LBP; a “re-reputure of a previously repaired region in the posterior annulus of a moderately degenerated disc with an annular tear”.

Torsional injuries along-side degenerative changes create circumferential tears, these tears typically do not change the outer architecture of the disc so direction-preference is absent and an often “unendurable” (discogenic) pain persists until slowly healed with granulation tissue (type III collagen).

Only ~10% show ‘leakage’ thru the tear.

Sato found nearly 50% of patients developed the acute LBP with “casual” movements…further validating the “weakened” annular fiber theory and susceptibility to torsional strains; the disc’s weak link.

Sarno’s groundbreaking books beginning in the early 1980’s put a ‘non-organic/non-structural’ spin on the impending epidemic of LBP in western culture. Instead of adding more ‘mistaken structural causes’ to the fields of physical medicine (trying to “explain” why back pain disables so many) he opted to consider TMS (tension myofascial syndrome). The underlying cause is assumed to be personality issues which drive physical alterations which produce pain. Such traits include:

• Having a strong inner drive to succeed
• Having a great sense of responsibility
• Being self-motivated and disciplined
• Being their own severest critics
• Being perfectionistic and compulsive

Dr. Sarno’s theory is that these personality characteristics interact with stressful life situations to cause the back pain. He points out that the source of psychological and emotional tension is not always obvious. Dr. Sarno’s theory of TMS describes a mechanism whereby emotional tension is pushed out of awareness by the mind into the unconscious. This unconscious tension causes changes in the body’s nervous system. These changes include constriction in blood vessels and reduction of blood flow to the various soft tissues, including muscles, tendons, ligaments, and nerves in the back. This causes a decrease in oxygen to the area as well as a buildup of biochemical waste products in the muscles. In turn, this results in muscle tension, spasm and back pain experienced by the patient. He contends the majority of patients will improve with ‘counseling’….a small percent require physical interventions which have no “real” impact but foster the patients placebo effect.