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.
Many patients have spondylolisthesis and it’s a concern as to when and how to best decompress them. Slippage on flexion/extension films can certainly indicate the “stability” of the segments but can be impractical and mercurial. By simply elevating the prone patients’ legs bilaterally from the ankles (creating a shear at L5) pain provocation becomes obvious. Upwards of 10% of the population may have this anomaly but most aren’t necessarily in pain from it directly, and degeneration typically stabilizes the motion segments at that level in a large percent. This simple procedure (from McGill) can help us recognize if a patient presents with: 1. a shear-instability or 2. an active spondylolisthesis generating the shear-instability. When uncovered positioning should minimize the shear (extension) and thus supine or prone with slight flexion or an abdominal roll are most appropriate. Since our exam already involves checking for extension/recumbent extension tolerance or intolerance the awareness of these issues should already be apparent and this additional check a pertinent verification. Proper use of the McGill shear-instability test (palpation of the lumbar spine half-lying on the table) along with these other procedures should capture most patients’ conditions and lead us to the best possible outcomes.
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.
“Just a few words about my experience of working with Travis.
From the initial contact, he went above and beyond with answering my many questions about a chiropractic table I was considering purchasing. After the purchase, he made sure to personally deliver the table to my office in Canton, Ohio. He has always availed himself to me, even long after the purchase of the equipment.
Then just recently, he proved his value once again by reaching out and helping me with some marketing materials.
He is a class act all around. I give Travis a huge thumbs-up. I know you will be in good hands with Travis Buffy on your side.
Joseph Medina, D.C.
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.
Intradiscal pressure research
In 1994 a study published in the Journal of neurosurgery (Ramos & Martin) demonstrated the disc-pressure effects of prone traction.
It’s important to note 3 particular findings which are relevant to our daily practice protocols.
1. There is an apparent “threshold” distraction tension at (and above) which rapid intradiscal decompression (negative IDP) occurs.
2. Above a certain level of distraction an apparent “inverse-reaction” occurs i.e. the intradiscal pressure begins to rise.
This was approx. 80-100 pounds.
3. The “threshold” distraction-tension that initiated the negative IDP in the patients tested was between 35-40 pounds.
The implications should be obvious;
when recumbent only a minimal tension is needed to create negative IDP.
IF signs/symptoms fail to improve with a minimal force (50-75) but the patient is fully tolerant of traction more force is likely worth a try. However by the time ~80 pounds (~10 sessions) is reached without positive improvement it may be likely “decompression” will not eliminate the pain.
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.
Global spine J 2014 Dec;4(4):279-86.
Alentado VJ et al
Conclusions: There are limited studies supporting any optimal duration of conservative treatment prior to surgery for cervical and lumbar radiculopathy. Therefore, evidence-based conclusions cannot be made. Based on the available literature, we suggest that an optimal timing for surgery following cervical radiculopathy is within 8 weeks of onset of symptoms. A shorter period of 4 weeks may be appropriate based on natural history studies. Additionally, we found that optimal timing for surgery following lumbar radiculopathy is between 4 and 8 weeks. A prospective study is needed to explicitly identify the optimal duration of conservative therapy prior to surgery.
Comment: Many of us prevaricate as to when to refer…and often IF it is in the patients’ best interest. Though the latter question is always open to argument the decision in the population of “surgical-likely” patients does appear to be about 8 weeks. UPMC in 2012 adopted a 12 week conservative-failure prior to referral to expensive imaging or invasive options. Clearly some patients have ominous symptoms requiring an earlier (4 week) referral.