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Notes from the 4th Fascia Research Congress, part 2

In September of 2015 I had the great pleasure to attend the Fourth International Fascia Research Congress (FRC 4) in Reston, VA. Partly to help me process information, and partly to invite those who could not attend to feel at least peripherally involved, I took notes and posted them on my FB profile page in real time, marked by #FRC4


Later I pulled them all together, cleaned up the type-os and blatant misspellings, and added some additional information about the speakers.


Here then are my FRC 4 field notes, with the disclaimer that I didn’t understand everything that I heard, and I may have gotten things wrong. (Hey, you get what you pay for.)


A complete copy of the congress proceedings can be found for sale here:



FRC 5 will be in 2018, probably in Europe. Time to start saving those pennies.





The Functional Coupling of the Deep Abdominals and Spinal Muscles, Andre Vleeming, PhD.


We need stability in lower spine. Load is transferred to low spine and pelvis. Hard to explain how this works without understanding loading and unloading systems.


To use big levers– legs– we need the lumbodorsal fascia (LDF) to be strong. From L4 to S1 the LDF acts as a sling with the abdominal obliques with a crossover pattern. (This changed how hernia surgeries are done now, btw)


Functional relationships show complete interconnection. The film of the dissection is astonishing. This also shows L-R connections that we often don’t think about.


LDF can be divided into layers with different muscular attachments. How does this affect connected muscles?


The space between T10 and S1 is important for mobility, but needs support. Transversus turns out to be much bigger and more complex than we thought.


So the trunk stacks up as bony rings. Top to bottom: rib cage; muscular ring– obliques, LDF, etc; bony ring — pelvis. Vleeming wants to find out how force load works with these containers.


(Confession, I don’t really know what force load means here.)


Is the LDF container a pressure chamber? Maybe not, but in testing it they found a hollow, vertically aligned triangular structure at the spinal aspect of the LDF (think of a Toblerone box on end—like that). At lateral raphe—this is a densification of ct.


Main takeaway, I think, is that the LDF layers are completely functionally reliant on abdominal muscles through the common tendon: it is not 2 systems.


So deep abdominal muscles actually girdle posterior trunk. Many chronic low back pain patients have very weak and dysfunctional paraspinals and abdominals. This is stuff we probably assume, but he demonstrated with pressure sensors. This can change the way we teach about load transmission. (If we teach that.)



Hyaluronan (Preeti Raghavan, MD)

Looking at issues in spasticity.

No correlation of degree of spasticity (not carefully measured) to reduced reciprocal inhibition.

If you change the viscosity of extracellular matrix (ECM), can you interrupt the development of spasticity? She asks through looking at hyaluronan (hyaluronic acid, HA). HA helps sliding. If it becomes too viscous and thick, movement is reduced, and pain is increased.

Viscosity increases because of increased concentration in tissues, or a decreased outflow from lack of movement. This pattern of course penetrates into muscle depth, leading to muscle stiffness.

30% of muscle force is transferred thru fascia, so stiffness is a real problem in efficient movement.

So maybe spasticity could be redefined, changes in soft tissue, stiffness, contracture, etc. if we treat the fascia.

Massage appears to help in short term. She asks if hyularonidase (HA destroyer) might help for stiffness, spasticity. Injections in stroke patient led to increased ROM in 1 week.


Even for a 7-year stroke, passive finger ROM was increased, then active movement improved. She suggests that changing consistency of CT reduces resistance to movement. She has done this with 30 people so far. Risks: injecting the right spots, hypersensitivity. Fewer risks than Botox.

Spasticity comes from CNS problem, hyperexcitability of the stretch reflex. Spindles are “culprit”. We also see stiffness, inability to control movement, hypertonia, all leading to contracture of connective tissues. Her starting thought was that lack of movement causes lack of ability to move. (I have been saying this every since I learned about neuroplasticity, btw)

Time for post stroke recovery is highly variable. Spasticity appears to arise later in the recovery process. Raises the question of whether it is a primary or secondary result of stroke. This. Is. So. Cool.


Cell Micromechanics (Boris Hinz, PhD)

He works mostly with fibrosis and wound healing. Myofibroblasts behave as the cell repair police. They pull on matrix, may help contract to heal wounds. Alpha sma is a marker for a special type of actin. Examples of this process include dupuytren contracture, burns, fibrotic organs.

So in this paradigm, myofibroblasts are bad guys, associated with fibrosis. What makes fibroblast become a myofibroblast? Mechanical stress and a chemical change. It would be good to control this change in cases with risk of pathology. It all partly depends on stiffness of local tissue. When fibrosis builds in soft organs it’s stiff and interferes with function.

Myofibroblasts pull, pull, pull, create more and more distortion in CTs. Needs to be interrupted.

He wanted to measure stiffness of different areas of the skin.

He used a type of cantilever to measure force and stiffness at a very tiny level. Can provide a cellular picture of skin, even collagen fibers in almost-living fibers (still well-hydrated). He scanned various points each 3 times, ended with 100k data points.

Skin has variable stiffness regions, and it gets stiffer with age. It ranges from 1-5 on this scale.

They put cell cultures in plastic dishes, infinitely stiff (this can distort cells, make them act weird). They added a softer substrate so cells behave more normally.

The more you extend tissues, the stiffer they get; not elastic.

TGf (growth factor) is a latent factor in extracellular matrix, ECM.

Integrin in can activate growth factor (TGf), leads to pulling vicious circle. Like loading a spring. Think of a candy wrapper. If you pull (with integrin) on only 1 side of a peppermint wrapper, nothing happens. Pull on both sides, get candy. The wrapper stands for ECM.

Watching wound healing on rats, when the wound is externally supported, the wound healing is less disorganized. (This is counter-intuitive to me. We learn that weight-bearing stress is important in wound healing. This now makes me think that the processes within damaged muscle, tendon, ligament must look really different than in skin and loose CT.)

Strained matrix releases growth factor, which induces fibroblasts to become potentially pathological myofibroblasts.




Sports Medicine (Michael Kjaer, MD, DMSc)

Speaking on athletics and tendon overuse… things work great until an injury happens. Focus is long standing pain and loss of function in tendons in sports.

A comparison of normal v. pathologic tissue in Achilles tendons show clear cellular changes. Electronmicroscopy show aligned fibrils in healthy area, and disorganized arrangement in localized, injured area of same tendon.

In elongated fibroblast cells the nucleus is also elongated. It appears that the damaged part of the tendon is not load-bearing. Lots of explanations, no consensus on over-healing response in tendinopathy.

Kjaer suggests that injury initiates t-pathy. So he rejects the “rupture healing” theory.

Another explanation is overload that can lead to changes. Maybe tendons can share loads in different fascicles, like muscles do– shear forces may be distributed.

In bovine models changes accrue in interfascicular space. Nerves and capilllaries can be found there. (Eek, metabolic activity in this space is different in day v. nighttime, I find that really strange.)

How much change happens in tendons? Exercise shows collagen turnover, but we don’t know how much. Horse research says nothing turns over.

We can track tissue turnover by looking for C-14 from atomic testing in tissues. (There’s a nice thought.)

Tendinopathy history of treatment strategies
Muscle strength training
Eccentric exercise, explosive
Eccentric exercise, slow (has robust evidence)
He is not convinced that is always better than resistance training; tendon probably doesn’t care.
Eccentrics are easier to do at high intensity, which makes a difference. Controlled, slow resistance is related to stiffer, stronger tendons (as opposed to jumping). (In this context I am taking “stiff” as a good thing in tendons.)

Conclusion: high load for 3 seconds seems fine for treatment.



Fascia from an embryologic and genetic perspective (Mark Schuenke, PhD)

Continuity as demonstrated through photos. Why is fascia continuous? Because of embryology. (He says).

Starting at 3rd week of development we have cells for the ectoderm, endoderm, mesoderm. Our muscles and CT arise from part of the mesoderm.

At day 32 the limb buds are developing with various -tomes, feeding back to spinal cord. This is when myoblasts enter limb buds.

About day 37 some mesenchymal cells are organizing into chondroblasts and future bones. Future myoblasts are also present.

At day 50 muscles and CT are differentiating, muscle packets divide into individual muscles.

Nerves develop on the scaffolding of new blood vessels.

Tcf4 is a precursor signaling the development of CT. It lays down in a predictable pattern, even without muscles as scaffolding (!)

It could be that these signallers direct muscle formation (rather than other way around).

Tcf4, hox11 are 2 signals that direct muscle and CT development through different pathways in early weeks.

By 9 weeks a new chemical signal, cd34 is present. Tcf4 is still here, muscles develop inside the CT.

By 22 weeks fascial layers are evident and begin to become compartments.

In fascicles, there’s probably not a lot of turnover. It is easy to show that tendons get stiffer with only 12 weeks of training. Deconditioning also leads to less stiff tendons. Rest leads to breakdown of tendon. (Here again, “stiff” seems to mean “good” or “strong”.)

Tendinopathy shows lots more chemicals than healthy tendons. Could be a sign of insufficient loading.

Cross-links. This is going over me, sorry. Non-enzymatic cross links are irreversible. Exercise seems to reduce them.



Fascia and Surgery, J-C Guimberteau, MD

Surgeons and manual therapists are similar because we are both in direct contact with tissues. Our responsibility is clear, but we can’t promise good results every time.

We must treat each patient as a completely unique being. We observe nonlinear, random behavior.

Anatomical components are formed in an irregular, in fractal manner. (Pictures of many types and locations of skin in polyhedrons that move.)



Surgery and Fascia Therapy, Thomas Hausner, MD.

Orthopedic surgeon in trauma surgery, top to toe

Here to share experiences with fascia from a surgeon’s POV.

He agrees with J-CG that manual therapists and surgeons would serve patients better by working together.

Fascia can be a problem or a solution in surgery.

CASE: A sailor had rope burn on leg, leg was hard and swollen ( compartment syndrome). Happens a lot with lower leg fractures, can lead to nerve damage, deformities. (This is right out of my book, makes me happy!!)

Fasciotomy into all 4 leg compartments, needs to be widely tied together, may need graft. (Picture showed laces crossing an open wound to gradually pull together the skin on the edges.)

When compartment syndrome is in the foot, requires opening all 9 compartments.

Now we’re on pathophysiology, this is my home base.


CASE: Carpal tunnel syndrome

Nice images of median nerve.
Causes can be anatomical or systemic disease.

Normal nerve is surrounded by soft perineurium. Compression leads to blood-nerve barrier resistance, CT layers get thick, impermeable.

He doesn’t do steroid injections; he sends patients to manual therapists. If there is no improvement, he operates, cuts the retinacular ligament. He prefers open surgery; studies that compare endoscopic v. open surgery show no benefit for closed surgery after 1st 2 days.

CASE: Femoral nerve compression after hip replacement.

In 6 months, major atrophy of quads developed. A band of post surgical scar was compressing nerve. 3 days after release, patient can move leg; at 8 weeks he had full ROM. Scar problem was related to post surgical inflammation.


CASE: Hernia repair and post-op pain.

Nerve damage from scarring, adhesions, compression of peripheral nerves. OMG that hernia is huge.
Literature suggests 30% have post op pain due to adhesions. Adhesions and scars can catch up, entrap nerves too. Requires several options for reparative surgeries.


CASE: Dupuytren contracture.

Dupuytren patient with previous surgery has chronic pain in an isolated area of the hand. It doesn’t spread or change color (like CRPS would). He tried a new incision from the medial side, gave more room for nerve, had final success.


His own ACL ruptured in karate tournament. His friends the knee surgeons laughed… It has healed well, no surgery. J


Stay tuned for Part 3! 

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