Anatomy Trains

Not every day of these conferences can equal or best the previous, and this day was a bit weaker than the others, and Christoph was intuitively right to stay with Riccarda and head for the sauna and a restful day.

One frustration of delving into the science of myo- and fascia and stretch and healing is that the best-laid conclusion of rats and men are frequently contradicted by some expert I meet just outside the hall right after such nice conclusions are presented so cleanly and forcefully.

Yesterday morning a surgeon was talking about fascial force transmission in CP spasticity (mostly in kids) where they do a tendon transfer to turn a wrist flexor into a wrist extensor to counter the tendency of the flexors to overcome the extensors, a spasticity that leaves kids with chronically and strongly flexed and pronated wrists.

After describing the effects on the fascia of the surgery, the surgeon expressed his hope for being able to simply transfer the nerve, which would automatically reduce the spasticity by sending the flexion signaling to the extensors. This seemed like a great idea, but a neurological surgeon from Italy looked me up during the break because of his interest in Anatomy Trains and mentioned in passing that what the orthopaedic surgeon had mentioned would never work neurologically (they don’t know how to transfer a nerve and hook it up to the amazingly complicated and delicate architecture of motor end plates (which immediately made sense also - what do I know about all this?)

This conference, after a couple of 45 minute keynotes followed by a staccato round of 15 minute presentations of research. Everyone runs over, leaving no time for questions. And after every one I find a competing researcher in the hall, railing about how those results are skewed, or a competent clinician saying that the implications of that research are contradicted every day in her practice.

All the research suffers from limitation in that to pas muster as research design, the question asked must be very narrow, and the hunger from the clinicians is for the very broad. Too much TGF-Beta in a wound and it will go pathological and have too much fibrosis, but someone else says that can be solved by a 20-30% stretch for 10 min/day as part of the treatment plan, and then someone else says that only works on patients who …

One is left with a frustrating sense of circularity that should produce the excitement of being in a young field, but instead leave me grumpily saying, “Go away and figure this out, and come back and talk to us when you’ve got something definite to say!” Conferences like this, of course, are how that process happens.

How ‘normal’ is the inflammation process, the source of much structural pain? Are the NSAI’s commonly prescribed helping or hurting? Or more to the point, who do they help and who do they hurt? Many of these scientists never touch and look as though they are never touched. (There are exceptions - Willie Fourie, for instance, is ice-breaking for the rest of us: (http://www.csp.org.uk/director/members/newsandanalysis/frontlinemagazine/archiveissues.cfm?item_id=8FE96D74E465397197C9CD9CC90DDDD8&article=)

But ok, having expressed my frustration, here are few highlights from the day:

Filiz Ale found that stretching a muscle (of a rat) to its full length for a while left it weaker when it returned to resting length. suggesting (but not proving) to me what I had long thought: that sustained yoga would be a bad preparation for an American football game.

Robert Schleip was at pains to take myofibroblasts (MFB’s) down from the Superman status so many have given them since the first FRC. Even where they are prolific, as in the thoracolumber fascia (TLF - everyone loves their three-letter acronyms, or TLA’s), they generate only 1/100th of the power that the erector spinae can generate in a second - and these cells take 20 minutes to turn on and an hour to turn off.

A panel set up to allow clinicians to show scientists what they are doing for the scientists to comment on what research says about it went very badly, with the clinicians shoving each other out of the way to present only their successes (failures are so much more instructive), and the bewildered scientists commenting as they could on such incomplete and badly presented ‘case studies’. Bum-scrunchingly embarrassing.

Carmen Sacrista, an orthpaedic surgeon from Madrid, claimed in the pre-conference material to be healing (strong word!) fully separated ACL’s without surgery. I skipped out on Willie Fourie’s excellent second presentation to go hear this joker. First, she was in an untucked track suit and sneakers - ok, scientists are individualistic, but then she spoke in a monotone face down into the mike with a thick Spanish accent, presenting MRI’s that were inconclusive to me (but I’m not an experienced MRI reader - but the ACL only looked completely separated in one of the befores, and only looked completely healed in one of the afters. And she simply refused to be forthcoming about what treatment they were using.

She stated that the ACL had a number of elastic fibers and was a visco-elastic non-Newtonian fluid (a dubious statement about ligaments i the first place, ore true of the GAGs in between the fibers, but the ACL is pretty fibrous in my book), but then failed to address convincingly how what they did from the outside of the joint (and we learned only that it was ‘aimed at the back of the joint capsule to affect the synovium’) could overcome the tendency of the broken ACL to retract away from its
distal end. How could they bridge that gap without surgery?

My day ended with Chris Stein who spoke on the Typaldos’ Fascial Distortion model. (Stephen Typaldos was a DO who lived in Bangor Maine. I was always going to go up and meet him soometime, and then he upped and died before I took the chance. He has a lot of followers among the osteopaths of Germany, where he taught.) The system asks us to believe that patients the world over will indicate their exact diagnosis by the way they point to the pain, and treatment proceeds on that basis - do they rub, point, or sweep the area? Each points to a different type of facial distortion, and each requires heavy, old-Rolfing type pressure to resolve and restore. www.fdm-europe.com

It was quite a day for heavy pressure - the cupping that pulls the skin into bruising, the girl who received treatment with the Graston tools Warren Hammer is touting came to dinner with skin on the treated area that was bruised and broken out with the strength of the treatment. Some of you who have been treated by me are saying, “Tom’s complaining about heavy pain and pressure?” - but some of this stuff is just out there in terms of ‘destroy an area and it will normalize’. Sometimes it works, I suppose, but it seems a haphazard method of treatment, and I hope the pain I dish out has more meaning than that.

Here are some highlights from Day 2, though the coup de grace on the old anatomy was delivered by Jaap van der Wal, but more on him in the previous post.

The theme of the day was the sideways connections of the fascia within the muscle. Jst how does the muscle convey its force to the fascia and vice versa?

Carla Stecco of the famous Stecco family started the day by tracing the ‘trellis’ (I would say onion bag) arrangement of the fascia at rest, with additional ‘crimping’ in the tissue. Dense irregular tissue is not ‘irregular’ at all, but has a variety of directions at very precise angles for dealing with the forces. What slides, and what is fixed?

How much is the thoracolumbar fascia a sense organ and how much a force transmitter? asks Jonas Tesarz.

Jean-Paul Delage, working with Guimberteau, shows the cells in the paratendon (what we used to think of as the sheath).

Peter Purslow showed great pictures of the honeycomb of the endomysium, showing the same angle of fibers Stecco described, which go longitudinal when the muscle is stretched, and go circumferential when the muscle is contracted. Interestingly, while the endomysium is well-equiped to transmit force, the perimysium - which is continuous with the epimysium - is poorly constructed to transmit force - so what it is for?

I am hoping for an interview with this extraordinary man, whose prophetic voice 20 years ago (well before I wrote Anatomy Trains) was judged too radical and ignored, only to be brought back for this conference by the FRC organizer, Peter Huijing, who now recognizes how important Jaap’s work is.

Jaap did dissections way back then with new eyes and realized that the pictures in the anatomy books were 1) impossible, and 2) what the anatomists wanted to find. Recognizing way back then that muscles do not attach to bones, he dissected fasciae in way to show how the muscle fibers attach into the septa that eventually attach to bone, but that the ligaments are linked in series with the muscles.

We have long thought that muscles provide an outer, contractile force and (in eccentric) resistance to force, but that ligaments were local to the joint and acted passively and only at the extreme end of range of motion.

While there are a few true ligaments that act in this way; the cruciate ligaments, imbedded within the knee capsule, really joint bone without being in series with a muscle, but most of the rest, including the sacrotuberous (familiar to most readers as part of the Superficial Back Line), pubofemoral, and the epicondylar ligaments are in series with the muscles, and therefore can be engaged in any position of the joint (which makes much more sense).

At the other end of the muscle is the sliding tendon (n the case of the forearm or leg muscles, say) and the link into the periosteum of the distal bone, sometimes including other ligaments.

The point being - and here’s the revolutionary thought - that almost every muscle is set up as what van der Wal calls a ‘dynament’: a ligamentous strip, then a muscle, then another ligamentous strip, i.e. fascia-muscle-fasia. All the hamstrings are obviously set up this way: long strip of fascia, intervening muscle, long strip of fascia. This needs a diagram and expansion, so stay tuned for the references, but this is major and will change our thinking about how the body works and thus how to treat it when it doesn’t.

Van der Wal’s other major discovery is that there is no fundamental difference between muscle and fascial receptors: spindles, GTO’s, specialized endings and free nerve endings are all fundamentally fascial stretch receptors - just being stuck into differing types of fascia for different types of readings. That simplifies things, but I am not as sure of this conclusion yet. But the ‘dynament’ concept is radical, sensible, and sure-footed.

Although the conference will need to develop over the few days and I am majorly jet-lagged, here are a few highlights from the first day:

Helene Langevin has found an interesting puzzle in the areolar tissue where the cells, small but rich in lamellopodia (they are start-shaped) depolymerize (disassemble) their microtubules (cytoskeleton) and organize actin microfilaments (cytomuscle) to flatten outward like a pancake, collapsing vertically to help the fascil medium spread out. There is still viscoelasticity in the matrix, but it is helped by fibroblasts pancakizing in the subcutaenous tissue (but hindered, as we learned last time, by the myofibroblasts in the denser fascial sheets. My conclusion: the mesodermal cells are more a spectrum of a single cell type than than distinctly muscle or connective tissue.

More evidence from Hicks: Muscle cells are syncitia, each muscle fiber is originally many cells that blend, so each muscle fiber is multinucleated into a myotubule - at which point it starts becoming responive to acetylcholine and therefore conractile. No strain is needed to form a glom of muscle cells into a functioning myotubule, the presence of fibroblasts is enough. More evidence of the guiding role of the fascia in movement morphogenesis.

Lots of new evidence supporting Huijing’s contention of stress and strain being carried across muscle boundaries, and even how the intra-muscular stress is acrried by the endomysium.

Tomorrow the coup de grace to the concept of ‘muscle’ - stay tuned for the iconoclast Jaap van der Woll.

Google any of these names to follow the work, but I will publish full references when I get sorted.