SACROILIAC JOINT SUBLUXATION is a dramatic sign that many women with hypermobility can demonstrate. While standing, they rotate one hip to elicit a bony shift that generates a clunking sound. In medicine our name for this is crepitation.
Crepitation are sounds elicited by shifting of one bone over another or of a soft tissue, like a ligament, over a bony prominence. Sometimes the phenomenon can be palpated as a vibration but not grossly heard.
During crepitation, as one theory has it, gas that normally resides in the joint is caused to suddenly collapse and expand. I speculate that ligaments are suddenly twanged like guitar strings by the “guitar-pick” configuration of bony prominences.
One phenomenon that led me to my theory is what I have termed the “Levator snap”. The Levator scapularis muscle connects the upper-posterior neck/skull region to the top of the scapula prominence called the Superior Scapula Spine, which is shaped like a guitar pick.
Levator scapularis is long thin muscle, which indicates that it has a long draw, but weak pulling power. Short & wide muscles are the strongest; like Masseter muscle, the chewing muscle, which is strongest in the body & complicit in TMJ disorder (see my thread reader unroll).
Levator scapularis (LS) functions to “drive & steer” scapula during shoulder rotation; by contacting to pull & lossen Superior Scapula Spine. Scapula (shoulder blade) dips & rotates CW & CCW during shoulder rotation depending on pull vector of LS working in concert with Rhomboids
Point of insertion of LS upon Superior Scapula Spine (SSS) is where a snapping sound emanates when a spastic LS creates a taught “guitar string” that snaps when picked by the SSS “guitar pick”. This point of insertion is called an enthesis; an infamous enthesis in Fibromyalgia.
The “Levator snap” & LS muscle spasm are oft caused by a unilateral low-riding shoulder, which is common in Fibromyalgia, which is attendant with one sacroiliac joint being loose & droopy plus an associated overlying functional scoliosis (both common in those with hypermobility).
Circumstance of one shoulder lower conscripts LS muscle, as a compensatory effort, to provide lifting power to assist Superior trapezius to hold up the lower shoulder. In this activity, LS becomes chronically stressed, spastic, & elicits snap when it impinges & overrides SSS.
Sacroiliac joint disorder, functional scoliosis, & Levator snap of LS tendon on SSS are common in those with Fibromyalgia. But so is pain at the enthesis point of insertion of the LS tendon upon the SSS. Very common.
Pain in upper region of the shoulder blade is so common in Fibromyalgia to be a signature of the disorder. I have been collecting pharmaceutical ad illustrations for Fibromyalgia medication ads for more than ~8 years; nearly every ad portrays this pain locus in illustration.
Chronic shoulder pain & Thoracic Outlet Syndrome (TOS) are common concomitants of Fibromyalgia. In other thread reader unrolls, I have discussed physiologically dynamics of these disorders.
Several years ago, I attended a national conference on chronic pain. Dr. Shah, physician researcher at NIH, presented his study of painful trigger points within the Superior trapezium (ST), infamous for the presence of these tender nodes in ST of people with Fibromyalgia.
Presence of painful knots in shoulder muscles of people with Fibromyalgia is my assertion, not Dr. Shah’s. These are points that people who claim benefits with myofascia trigger point injection are favored of injecting (dry needles, procaine, lidocaine, cortisone, etc.).
I won’t dispute temporary benefits of these injections; cortisone dampens natural healing inflammation. What Dr. Shah found at microscopic level, via sensitive ultrasound & micro-pipettes to extract tissue juices: foci were anoxic, ischemic, inflammatory (reactive substances).
My consideration was his findings represented evolutionary tissue responses to chronic muscle fiber contraction/spasm. After lecture, I asked Dr. Shah if he had discovered peripheral etiology of Fibromyalgia pain generation. What he discovered can’t be seen in dead tissue preps.
Remember, by this time I asked Dr. Shah my question (even today) the THEORY of “Central Sensitization” had been adopted as dogma in Fibromyalgia. After I asked him, Dr. Shah looked at me with a deadpan stare & then walked away. Why did he not comment?
I have often thought Dr. Shah was reticent to comment & thereby compromise future NIH grants. Who can say? IMO, pain generation of Fibromyalgia (FM) is a peripheral event & brain regions lit up on f(MRI) of brain tissue of pwFM represents myriad pain messages hitting the brain.
In recent years, neurology researchers have been reporting small fiber neuropathology in peripheral tissues of pwFM. Does this represent neural tissue burnout from chronic inflammation & mast cell overactivation at the cellular level? Who can say?
Who can assert with scientific accuracy that the pain of Fibromyalgia does not occur exactly where patients report it - in the periphery? No one can disprove this hypothesis at this time.
My theory of peripheral generation of FM pain is as worthy as conclusions of studies where rats told researchers they were generating excessive body pain via shameful exaggeration of overreactive/overthinking brains; an idea at variance with laws of survival & natural evolution.
Back to data that suggests peripheral pain generators in Fibromyalgia. At the 10th Interdisciplinary World Congress on Low Back and Pelvic Pain, Belgium (Antwerp), October 2019, I presented eight papers on this subject (on-line).
Inception of my studies was a two year project in a general practice clinical setting. Within several hundreds of patients new to me (<1,000), I kept an eye out for patients with Fibromyalgia & Hypermobility & then studied them. I found over 200.
My efforts were not funded, but required thousands of hours of my after-hours compilation of data & sophisticated clinical reports. Efforts were to guide these patients through a forethought protocol; a maze of orthodox clinical studies & time consuming authorization processes.
End point was to bring as many patients as possible across finish line in time allotted to me by the gods. I was able to gather data on N=50. They were ones I reported. In effect study was not flawed by selective culling of patients based on outcomes. Chips landed where they fell
The outcomes of my Study of Fibromyalgia & Sacroiliac Joint Subluxation Chronic Pain Disorder Syndrome (my diagnostic term) were as follows:
The alternative theories & novel findings I have recorded above are mostly my own. This thread is becoming too long & likely unable to sustain audience attention at this point. I will initiate a new thread to encompass the findings of my studies. It will be my next essay. Aloha.
@threadreaderapp unroll
