Traumatic LBP aside, there are (6) possible categories to organize LBP contributors. Classical orthopedic exams would likely not rule out these:
(#3) Chemical & (#4) Immune contributors:
When clinicians think of LBP and chemical contributors, they should be thinking ‘inflammation.’ Inflammation is simply the natural immune reaction to acute tissue damage (a fall to the hip, or lower seat belt impingement due to MVA), and is designed to mediate further tissue damage or infection, and to restore the normal tissue repair processes. This process typically takes 4-5 days in heathy persons without co-morbidities to healing, such as prior metabolic diagnosis (DM, NA), lowered immunity (arthritides), and poor diet (high histamines, poor gut biotics, alcohol use.)
When inflammation is unresolved and tissue repair is unsuccessful, chronic infiltration of inflammatory chemistry persists and destroys the LBP joints (synovosis, panniculosis, athrosis), and joint function. Instability and pain follow. The lumbar spine is particularly unique, since it in chronically loaded (axially; gravity) with the articulations being compressed, and commonly mal-positioned due to PoLR.
Without resolution, the onset prevalence of inflammatory mediators stimulates the sympathetic nervous system to amplify adrenal function and cortisol production, known as Sympathetic Syndrome. This cascade of sympathetic amplification adds to the state of chronic pain since GABA is interrupted, and inflammatory chemistry persists unmediated.
Nociceptive modulation (top-down) becomes insufficient to deal with escalating sympathetic amplification, and soon the patient is experiencing low back spasms (trigger points) due to oxygen starved hyper-tonal low back muscles (erector muscles) known as Sympatheticotonia. Trigger points are oxygen-starved bundles of isolated muscle that are not contributing the natural “contract-relax’ motor cycle, instead they remain contracted in a negative oxygen-starved coma, unable to provide important proprioceptive feedback (gamma gain, stretch, tone), or follow central control. Motor control attempts to fire ‘around’ the damaged tissue leading to SCAD (symptomatic compensation to associated dysfunction.)
Chemical changes begin to occur within the joints, ligaments and tendons as calcific or ionic salt deposits interfering with joint function range-of-motion (aROM) and comfort. Chemical changes can occur at the cortex of the vertebrae. These changes are attempts to stabilize an unstable, weak spine because the patient does not sequence Core Neutral prior to distal motor patterns. I do not agree with the terminology “degenerative changes.” This language suggests that the spine is degenerating, falling apart, ageing, crumbling, moving away from that pristine perfect spine model (that no one has.) I would prefer to term it “responsive changes”, since the spine is reacting to usual loads (however useful/unuseful or incidental), and whatever movement the spine does most days. The clinician can’t just point to osseous changes on an X-Ray with a pencil eraser, and blame the observed changes for the problem. Osseous changes respond to patterns of use (casual and forceful), and the spine’s total ‘clock-time’ spent with GFR, and prevailing chemical health (inflammation, diet, etc.) and… how many times the spine’s ‘job’ has changed. What does this mean? A ‘job’ is a chunk of time that the spine’s primary experience is the same; years of standing at a job, for example. Then, the ‘job’ changes when the spine is seated for years; the spine is primarily experiencing a change in loading. Degenerative change is a slow, methodical evolution of the chemistry of the bone to adapt to loading ‘jobs.’
I have a patient that was a landscape contractor for 12 years, he was primarily in a half-squat position and dug holes with his arms all day. Due to chronic carpal tunnel, he switched careers to be a personal trainer for 12 years, then sat in grad school classes for 4 years, then became a tennis player. The patient’s spine had to change 4 times to adapt to completely different loading and use pattern periods. How many times can the spine change ‘jobs’ until it just can’t skeletally adapt anymore? Osseous changes seen on plain film and advanced imaging are chemical changes; bone re-modelling is a chemical process. How would a surgeon expect to physically case manage a spine when the process is chemical?
Chemistry has an important contribution in LBP diagnosing and case management. I would venture to say every attempt to case manage LBP without looking closely at patient diet, gut health, blood labs, spinal loading habits, patient awareness of Core Neutral, and how many times the patient’s spinal job has changed over a lifetime is futile, or possibly neglect. The #1 co-morbidity to LBP is smoking… think on that chemistry. ‘Pain is not the only problem.’
LBP Blog General information
These articles intend to (1) re-evaluate the prevailing clinical practices thought to manage low back ‘pain’, (2) submit and debate novel low back ‘pain’ contributors and mechanisms, (3) meet patient expectations & satisfaction and clinically meaningful results, (4) recommend a conservative non-surgical course of care to over-ride ‘pain’ instantly, and (5) restore ADLs and patient confidence on the first visit at low cost. This article has a companion podcast.
Dr. Dean Bio
Forester Dean is a chiropractic and physiotherapy sports medicine doctor practicing in Los Angeles, California. Dr. Dean is a lifetime athlete, and currently teaches tennis, track, boxing, yoga. The Core X System™ Campus flagship location was opened by Dr. Dean in 2020. www.preformancecxs.org
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