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‘Pain is not the only problem’: Sub-Threshold Micro-Trauma, Part 1

Sub-Threshold Micro-Trauma (STMT, Dean 2016) describes subclinical soft-tissue (voltage-gated tissues: muscle, fat, fascia, lymph, arteries-veins, and nerves) and hard-tissue (collagen-based tissues: bone, ligaments, tendons, cartilage) injuries, implying that the patient is asymptomatic and not seeking care, and is likely due to an abnormal movement pattern (faulty movement pattern; FMP) and associated with a symptomatic area of tissue, but not always at the symptomatic area.

The STMT Theory states that ‘A system of movement patterns employs muscles and joints that fire together on the same nerve network (Hilton’s Law), combined with other movement patterns employing muscles and joints that fire together by other nerve networks that are not synchronized sufficiently to produce a functional movement; therefore, these other movement patterns contribute to tissue damage within that system.’(Dean, 2016) Movement pattern synchronization employs ‘groups’ of actions, for example: walking. During a walking gait cycle the ankle extends, while the knee flexes, while the hip flexes, while the hip rotates, while the sacrum counter-nutates.… forming a synchronized ‘group’ action. STMT identifies any sub-set of the group as faulty, not the entire group. The faulty sub-set may have been self-learned, due to poor or wrong instruction, de facto, due to personal bias, or due to creep by fatigue (exaggeration patterns), and is never identified by one muscle, and certainly not a muscle described as ‘tight’, ‘short’, ‘turned-off’, ‘weak’, etc.

Sub-threshold implies sub-clinical tissue damage that does not have the attention of the patient/athlete; they have not sought care because there are no presenting symptoms that are annoying enough to cause intervention. The patient/athlete might notice minor changes in performance and brush them aside as episodic.

Micro-trauma implies non-traumatic, incidental tissue damage that does not evolve into the acute phase of healing; there is no noticeable soreness, redness, inflammation or tenderness. However, there is enough tissue damage to cause motor efficiency to change, such as: time under tension (strength), load-ability (plyometrics), total recruitment (load), active range of motion (mobility), capsular stress thresholds (stability), innervation (precision), metabolic delivery and waste removal (biochemical), and modality (novelty), for example.

Initially, the patient’s faulty movement patterns contribute to repeated temporal sub-clinical spikes of acute tissue damage that tend to resolve with the usual phases of healing, however, performance seems normal. Eventually, repeated FMPs overburden the usual phases of healing, and tissue repair is incomplete, insufficient or defective. Instead of restoring the motor and connective tissues to full function, they are replaced with scar tissue or incomplete tissues and altered motor mappings. Inflammation accumulates since clearance rates are encumbered by spikes of re-injury. Repeated FMP over time drive complete recovery to fail. Multiple phases of healing overlap and tissue repair becomes impossible… as the faulty movement pattern becomes an assault. Optimally, asymptomatic FMPs are identified and corrected into a productive and useful skill.

With enough repeated and unresolved acute spikes of tissue injury, the patient/athlete will begin to experience symptoms, and experience repeated failures to control the movement pattern. In many cases the early warning signs are disregarded, and the patient/athlete persists with the assaulting activity. Then one day, the patient will feel symptoms with movement, and experience the usual calor, dolor, rubor and functio laesa, and the patient seeks care due to symptoms. But I have not said all. In the background, the patient’s FMP has taken a detour in an attempt to remain functional at all costs… by diverting the demands of the FMP into an alternate FMP. The second-generation FMP employs different, unaffected muscles, and may even change whole-body gravity dynamics, shifting the weight, approaching the skill with more force or aggression (sometimes called ‘Plan B’). The patient seeks out care only after the second-generation FMP has failed, since now performance of any kind is impossible.

Patients with LBP in your office actually have 5 problems: (1) a complaint of back pain, (2) a faulty movement pattern, (3) a secondary faulty movement pattern, (4) repeated failed attempts at healing, (5) and emotionality related to unresolved LBP. A focus of pain resolution is a diluted attempt to case-manage LBP, because ‘pain is not the only problem.’

LBP Blog General information

Series Description

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

© Copyright 2021 SpineSync, Forester Dean, DC
Duplication with permission only
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