ROM Resist & New Zealand

Range v Resist & The NewZealand Visitor This book will be a trip!! In fact MOST of the other books in this library are set up to get you here – to torment you out of what you think is real. BUT WHERE IS THE SCIENCE?? [long intro follows] Oh, you have no idea. Good science embraces failure. And we were so embraced - nonstop - for well over three YEARS with experimental failure after failure after... yaaah... well, sorry .

If you read the SACH / SAWCH book, then you would think that no matter how bad a foot is, structurally, we should be OK. Worst case, take a meat cleaver – WHACK – and on goes a nice shiny new prosthesis! That is something that is guaranteed to work! You don't need feet. You need what behaves as feet.

Once upon a time (these images from the 1920's) we had no way to FIX club feet. Aside from the many skin break down problems, the cosmetics were awful and severely shunned by women in particular. This was the humane remedy. She

didn't want feet. She wanted to mingle. She wanted what looked and acted like feet. This is a repeating theme in medicine, do something, anything that feels better, at least until a real fix comes along.

A congenital club foot is born clubbed and is a mechanical problem. But, not born that way, as a neurologically caused "club" foot (spastic or dystonic) is a neurofunctional imbalance problem that becomes clubbed. You would expect treatments to differ. They do, conceptually. But we look at a kid crouched & legs medially rotated, chugging, across the room (family cheering) and the question is do we get the butcher's cleaver to try

to merely STRAIGHTEN what we see? As with 1920s clubs the issue was somewhat cosmetic but even more so - FUNCTIONAL. Motion data? 99% is angles and distances. If there is 60 degrees of contracture [missing range of movement] then it is 60 degrees of bad, as it might seem. Less range is bad. More range is good. Even more range is good-er? Ahh. So much is said about mechanical (constraint) issues that NEUROLOGIC based abnormality gets this kind of short shrift. That the contracture (missing range) isn't a single thing like a nail or a screwdriver, it is a hodgepodge of things each adding to the overall loss of functional movement and to the perceived stoppage noted when put through range of motion exams. Mechanical concepts are so easy to visualize, whereas neurological mechanisms are so...so, so neurological! The brain! Trillions of synapses. It even allows a person with a small focal brain injury to not recognize half of their own body? Really? Like that. Off putting. Seeking answers we tend to dwell on what we can mentally visualize. Consider that everything real about you, that YOU SEE, is mentally seen. It is in your head – neural stuff representing what is out there. Not to beat a dead horse, but getting a grip on how the brain conjures woe or happiness can send you in so many wrong directions. And indeed it has. We are here to erase what we thought we learned from experience (somebody else’s) looking at cerebral palsy and to revisualize it better with new observations, with tight control on what is being seen. The idea was simple. Use normals and layer on things that would make the normals look and act like cerebralpalsy. Really. How hard could THAT be?

You, grasshopper, are here to be set on the righteous path. But, first, you must suffer (as we did) before enlightenment brings you a nice cold beer. We begin with constraint . A hallmark of CP. Limitation of motion. Loss of range of motion is the disability! Everybody knows that! Just a matter of how much range loss does how much functional loss? Look in the texts. A thick and heavy CP book becomes a flyer if you remove all instances of “strength” and “range of motion” from the chapters. Bring on the engineers. This is going to be an easy paper.

Thousands of measurements. Angles, distances, lengths, speeds, velocitty and acceleration analysis … harmonic analysis… pressure plots…

on & on

& on ?

Nothing obvious yet? & on & on..

We will study what happens when you RESTRICT range of motion in a neurologically and structurally normal person. Some adults. We will start with teens, 6 boys and 6 girls from a nearby gymnastics school. We will restrict knee extension as our first series. From full extension (0 deg) to 60 degrees of loss of knee extension. A 60 degree 'contracture', so to speak. Our lab is a basketball court and the planned walk was around the court edge at whatever pace was 'comfortable and sustainable’. Typically a 30 degree contracture gets nearly 100% recommendation for surgery as being unsustainable. We have that scope of loss well covered. [Big thanks to Dr. Langrana from Rutgers engineering, the aeronautic engineering department as well as IEEE engineering members from Rutgers for help in getting these contraptions perfected. Jack Jolly MS (Rutgers engineering) thesis work was massive and perfect. ] At first, only one leg gets constrained. Study what both legs do when only one has constraint. We have already beaten ankle/foot constraint into the dust, (SACH SAWCH) so now the more important knee joint should be really disabling with more and more loss of allowed range. It wasn't. Test is too easy? OK, instead of walking around the big room, go down the several flights of stairs, around the hospital back up the stairs and then recircle the room. No problem? They are not even sweating! Ordering way more pizzas and cola than was anticipated but the only request we got from our subjects was "What next?" A week of this and our plan to simulate CP was going up in smoke. On to constraint of flexion, knee can only bend so far... Same. Keep adding other constraints, one leg, two legs, ankle with two legs etc etc etc. And NOTHING TO SHOW for it!!

The engineers were quite happy. Their contraptions were working well and the actual measured constraints vs the device settings were also of great engineering interest – but – smiling kids wanting more? This was not the plan. More than 400 pages of SUMMARY!! (The wide perforated computer print out pages single spaced and small print!) Jack's thesis was 4" thick! A splinter of information from those trials was published but it was completely irrelevant to CP. Or was it? Three years pouring through the numeric data and the wide range of visuals... The one thing they all did, if given an asymmetrical impairment, was to mirror it. Maintaining continuous function seeks symmetry. Why? No matter what was restrained, the parts found a way to time everything else to the most restricted pendulum. Pendulum symmetry. An inkling at 2.75 years of blood shot eyes... pendulum symmetry??... is it about passing energy from one side back to the other... conservation of MOMENTUM and ENERGY no matter what? A thought... what if - instead of attacking motion we instead attack MOMENTUM? Nothing gets range restricted.

OK. Our new lab. Dr. Michael Polchaninoff, an electrical engineer and podiatrist, is interested and will handle the engineering issues (which turned out to be all electrical – right up his alley). We will create a well fitted sticky suit (won't shift on skin) that blocks no

joints. It will be an anchor for elastics that will be applied so as to dampen movement. Subjects should be healthy. First, test on adults who can tell us what they are experiencing medically (resident doctors). First subject is a young Seton Hall resident in orthopedics who ‘jogs religiously’ (a Seton Hall joke – get it?).

Room was a large teaching room. About 30 x 40 ft. Infrared beams track the subject and turn on the emg data dump to the computers as the subject enters and then passes out of the camera viewing part of the walkway – about 12 feet of viewed walking. Also testing optimum backdrop color with paper backdrops (before painting the place). We'll try an easy one first. Semitendinosus. Elastic from ishium to pes on upper anteromedial tibia. The elastic is marked incrementally to use pre walk stretching measurement of the resist properties. By feel we are seeking what feels similar to kids walking with CP.

As we use emg live as we test CP slow & fast passive motion we have, we think, a pretty good idea of how that stretch should feel.

It is set up to go from minimal to quite resisted.

Straighten knee from flexion (start at 90 degrees) to straight. Do this with thigh held vertical. 3 levels of extension in this triad called 'severe'. Straighten knee similarly with thigh held flexed 45 degrees. This triad was called 'moderate'. [hah] Straighten knee with thigh held horizontal. This triad was called 'mild' tension as this tension still allows near full knee extension even with the thigh flexed. Tension levels are labeled as 1 through 9.

There are two preresist levels. 00 = only wearing bathing suit.

0 = rig is on but no elastic tension is set. 0 equaled 00 so all was well. After testing with elastic resistance then we retest walking free as in 00. Pressure sensors on the soles of the feet had no detectable effect on walking at all. Good.

So how did we do?

Well the emg (all 8 channels on a pen plot strip writer) created a sea of black ink. The paper, a total mess of black, dripped ink. A nasty mess to clean up !! Our healthy jogger was having trouble, before level 3, just getting all the way around the room even once, thus making the infra red beam triggers useless. So we triggered by hand. Our subject related that walking

was most difficult. He was having all sorts of symptoms. Something he ate? We were not up to our planned best stress level yet. And so after just a few passes and attempts to dial down the emg signals to a range that could be read we came to this.

He could not make the full room circle ending with the 12 foot path through the camera zone. So we had him start at the video edge. No room circle. By level 5, he could only crawl across the field and then wound up sitting in the middle of the room panting "..can't.. no more.." waving us off.

Obvious conclusion? He didn't know he had cardiovascular disease. Stop and go straight to medical exam and have the cardiologist call us. The result? He was as cardiac fit as any man his age and more so. All tests were fine. We suspected that opinion that came several days later, after we redid the trial with a die hard marathon runner. Same result and same words "..can't.. no more.." waving us off. Less ink with the emg rewired with a battery of swappable resistors – but still not enough. A lot of emg – looked nonstop but impossible to know when on & when off were all still drippy. No cardiologist this time. Next pass, find a human being not capable of fatigue? Be sure that the emg can be dialed down in an astronomy kind of way. We moved our lab into a borrowed existing lab in Hershey Penn. Thanks U Pen. With our emg diverted into their system that had industrial potentiometers with three embedded levels meant to measure stuff that was beyond human – their engineers and Dr. Polchaninoff guessed maybe 1/1000 signal reduction? Maybe more? Our subject was a 9 yo international championship Irish step dancing

competitor accompanied by her aunt. <==Yes, she was pleading for a rest at a point past that of the prior adults. But her aunt was shouting “You CAN do it! Do it for the CHILDREN!! Do it for IRELAND!!” We offered her $100/hour to keep going.”

And? ?

She finished. All of it. Her “after” walk had similarities to hypotonia (Prader-Willi etc.) with knee locking to reduce weakness collapse. A true normal was had two days later. The emg was easily read. Summed up – massive cocontraction. This was even in the muscles that you would think out to take a free ride as the elastics were doing their job too far. Why add to it?

From this alone we had the key to it all... The disability is energy insufficiency. Energy demand exceeds delivery.

Cardiac output is peaked. Circulation through sustained muscle tension is delayed waiting for off periods which are few and very brief. Typically any leg muscle in walking is very briefly on.

You push a swing, briefly and it goes away... then comes back. After the big first push the ones that follow are minimal – replace for wind resistance and friction at the top.

The 'failed' constraint trials done much earlier were screaming this. But inertia – of perception – hid it. People with excellent nervous systems and healthy fit bodies seek to create symmetrical pendulums that can pass their energy back & forth … or energy gets lost. Disability isn't about what the person can do. It is about what they can sustain. In the constraint studies we saw that even in a well fitted nearly unpadded cylinder cast from groin to ankle we still get about 10 degrees of flexion in stance phase. The knee flexion of stance is driven strongly by inertia which is only only guided or deflected but not produced (except by the ileopsoas which is in the body – outside the leg like the mom, not in the swing, pushing the kid on the swing. Wheeeeeeeeee. But looking closer at what this young dancer did was mind blowing. There was NOTHING in or on the feet except sensors which had zero ill effect when tested. Medial rotation crouch gait? Really? With toe walking??

Who asked for toe walking? This is a phenomenal athlete. Whatever she is doing she is doing for a GOOD reason! By definition. She succeeded in doing what turned out to be a most difficult feat.

Time to geek out. Fourier analysis of the gait in the constraint experiments found that 5 (occasionally 6) 'harmonics' [think gears] if well picked for relative size and linked together can reproduce human walking even when abnormal. That means abnormality also has limits. We can only do well or do badly with the parts we have built in.

We were on to the symmetrical pendulums trick... but, here, we defeated the pendulums – didn't we? The Joe Paluka punching gizmo is a vertical pendulum. Punch Joe in the nose – he goes down then returns back and bumps you. Notice anything weird in her stance phase?

We see that swing phase knee flexion, which is normally supple and inertial, is of strikingly low change in both stance and swing. Cocontraction (emg) is maintaining a new structure (harmonic #6). It is a long vertical mechanically stiff rod (ignoring the structural contours). Gait has become a wheel with the axle on the ground. It uses only a very short arc centered on that spoke being vertical. A big wheel using a short arc so that the rise is minimal and the fall past midstance is minimal. Another solution to this:

Go from hither to thither with least energy. Straight line – a wheel – but wheels need roads or flat surfaces to be worthwhile. Man in the wild? Not a best choice. Low amplitude travel of the center of mass en route – least work against gravity. Inman's 6 determinants got that done. But his subjects were not self damping (nor elasticized to be so). They had amputations but not CP. OK. Use a BIG wheel as plan B. You see this everywhere in articles – something or other is amiss and it [the amiss part] CAUSES short stride length .

Ooooo, the horror of it all! Short stride length. It causes this! Right? Have you been asleep? Short stride length is a CHOICE, a solution, to keep going by using yet another way to reduce energy loss. We saw in the early elastic trial levels (1 through 3) that initially the only 'abnormality' was crouch. It was enough to remove the elastic tension and that is then it is just a shorter person walking normally [chart has increased

flexion baseline as only abnormality – here at 14 degrees]. Normal is close to zero. But as the elastics get ‘worse’ the dampening can't be dodged anymore. A ' plan B ' emerges.

Plan B. Create a very long spoke for a very big wheel, but crouch enough to get some of the dampening down. Medially rotate to further diminish the elastic pull on the tibia (at the 'pes'). And . . . toe walk ! ?? Huh? W W Why? Because a wheel needs its axis at the center. A forefoot rollover makes a 'cam' – a valve LIFTER (we are avoiding lifting). Plantar flexion is adds more length without more tension and, more importantly, it moves the roll center to wheel center. Gotta hold that wheel spoke intact without wobble.

Co-contraction. Now about this time we were already into doing lengthening with minimal exposure as it was designed to handle congenital cardiac based CP (tetralogy and such). The children turned blue with walking. It was life threatening as back then the cardiac repairs were staged over time as they

had not figured how to make the needed cardiac repairs grow with the patient. The patients were to be operated under local anesthetic with some plasma to offset anti coagulation. It was not to cure, but just make less so that they did not force too early a next cardiac repair. These kids did spectacularly well with so little done and frightening the tar out of us doing it! Then came a visitor from New Zealand whose parents had wind of this from a common (cardiac) patient at same rehab facility. Please. Six years of solid PT and no trace of walking. Mmmm... OK.

Preop on left. EMG is bouncing bar type (inset is a scribble equivalent for single frame discourse). He could not walk and needed to be held aloft. He collapsed after only a few highly assisted steps. At surgery, he didn't hold still the way cardiac patients always do. So, the obvious finding of bow-stringing semitendinosus was addressed first and that was all that that was needed to then emulate a supple swing phase (supine), our goal. Done. Like popping a balloon. We included our

ethanol perineural nerve injections which we had refined over many years long before our 'percs'. In fact some of our nerve injections were done open until we found a way to track the nerve with a needle through a teflon catheter and got even better efect with nearly no ill aftermath. The right side of the image is him one week later. I don't know about what 'p' value this would be but we were singing hallelujah.

We now know that we have two main groups of patients which are not even hinted at by GMFS anything. 1. Those with sensibility that allows quick – spontaneous – correction in whatever they are doing (crawling?). 2. Those with sluggish responses to exam changing or interfering with their objectives. So, those 'with the moves' and those without. The without cases typically are anoxic or chem toxic based neurological injury rather than low focal flow or contained focus bleeding. Group 1 can detect situational change that needs correction. Group 2 is more impervious to changes that need attention. 1 & 2 have potential control improvement that differs.

If you graph distance traveled (d) against time (t) then we see that walkers have even progression (straight line). Those who cannot manage the side to side well timed energy transfers stop with each step and their graph looks like steps. These are steppers. Steppers need to be intermittently stabilized with each step. They seek islands of stance stability. Walkers need to keep the flow rolling and so

stabilizing things (toe plates in AFOs, wrong pitch etc.) disables walkers by thwarting the smooth TRANSITIONS required for energy passage. <==Two point transition.

Spindles

Let's discuss spindles. Starting at 'C' (above) the short yellow bits represent spindles (named for their shape). Spindles are made of muscle & sensory tissue. When muscles elongate and have tension the pull includes the spindles which get elongated by the action. Think banana. The spindle outer peel is of longitudinal muscle. If these muscles are being stimulated then the spindle wants to get shorter and fatter. If not stimulated, then it stretches easier. Within that peel (the banana) is a lengthwise rod of three sections, of muscle<=sensor=>muscle. When the end muscles are stimulated, they tug on the central sensor which let's fly a scope of signals that vary with the stretch of this central rod. That output goes to the spinal cord with many connections to complex reflex arcs that are both local and widely distributed depending on the intensity. THIS IS WHERE SPASTICITY LIVES. If the gain (base tension) of the inner core muscle is set too high (as in spastic diplegia) then any tension added elicits a return response and that response may be in excess if the gain is set too high.

Response gain set too high, results in a gush of response. The flood of

neurotransmitters exceed the volume which the normal mechanisms can immediately clear, so the effect is even more and more sustained and goes into too many out paths. Signal that isn't helpful is called 'NOISE'. Try having a conversation when people around you are shouting. Also when the signal recycles as if an echo.

A signal is sent from the brain to a muscle. The brain has an intention of what this should do. Preceding this, it actually sends what the tension should be if it goes as it was hoped. With the spindles reset and the muscles signaled, the spindles should be happy :-) and thus have nothing to add. There is no reflex. Happy happy spindles.

But if the incoming setting does not match, the spindles are empowered to send signals to adjust muscles to match the intention. This mechanism is very fast, and, very patterned, and thus cat-like. In fact nature has cats giving the main signal only to the spindles which then elicit the main muscle action and adjust on the fly. Can't teach old dogs new tricks? Can't teach cats any tricks. They have more than enough of them (survival wise) built in, but you won't see any complex new stuff.

If the reflex mechanisms don't allow sustained success, people don't just give up. They, unlike cats, find alternative things to get the job done.

When it comes to sustaining a plan it is about energy. Hold on to the pendulum or make new ones THAT MATCH. Like putting your fingers in your ears for loud noise, w-sit to turn off lower leg spindle chatter.

Re-purpose other inherent skills.

If momentum is irretrievably impossible, then, go 'concentric'. Rather than having muscles do the opposite of their names (flexors stabilize and limit ongoing extension, while extensors stabilize and limit ongoing flexion). Repurposed, flexors flex. Extensors extend. Concentric is energy-wise not as thrifty as eccentric. But, we all go concentric when we are going up steep stairs as momentum is thereby hard to come by. Take another look at that mild to moderate spastic diplegia kid and ask isn't what she is doing a lot like climbing stairs? Is that form we are seeing THE abnormality or a 'Plan B' repurposed for 'getting it done?' For most, we don't call it crouch gait. We call it 'stair climbing’ gait or 'concentric’ gait.

The Case of the Very Unusual Case I know, single cases don't prove anything. Yes, but, we never said that we wish to prove anything. We seek a lack of current vision to widen our field of questioning! Probe. Explore. You can't ' boldly go ' where everybody already is. Odd cases take you into new fractals of questioning. This one is a dilly: In our CP clinic, a mother comes in from afar... some place called Hollywood. Her husband was one of those oddball camera operators – the ones that swoop on big metal arms to get the perfect perspective (sounds like us in a way). Relevant? Yes. He owned more cameras than I have teeth. His child from birth was 'shot' [poor word. Today we say videoed, but back then it was film] from birth to present. It was as tight and good a visual record as you will ever see. Ever. Mom had prearranged for us to have a projector to show the edited life of this child. It was a prime time edited sequence of events. The movie: Healthy looking preemie youngster evolves mild spastic diplegia over a two year span. He is running all over the place, but with an obvious mild medial rotation and mild crouch and does so on toe. His heels don't touch the ground when walking. I know – you are shouting cut the elastics! We didn't have that insight back then. Very functional kid, plays soccer (OK for age) and swims, pretty good at what we now call “T ball”; there was sleigh riding – everything. Somebody says he NEEDS surgery or in the future nasty whatever will happen. He had hamstring lengthening (Z lengthening of semitendinosus and semimembranosus) we read from the op note. Thankfully they stopped there. No 'Achilles' lengthening was done as was also planned as there was no contracture to lengthen. Odd, they thought.

The result? He did great! After a few months of healing & P.T., everything he did before he could now still do, but prettier, less crowd displeasing crouch. Two more years, and slowly that crouch was showing itself. Increase P.T. Another year and he was not back to where he was before surgery, he was worse – a lot worse. He didn't even look 'class 1' anymore... kind of 2 ish. He preferred to not [the above long list goes here – soccer etc] as fatigue and always needing to quit was embarrassing, becoming a sitter. Big city genetics diagnostics follows. CP doesn't get worse with time. Obviously a genetic progressive thing was earlier confused with CP (happens a lot). Genetics result? No. It is CP. Neurologists? Same. It was ordinary mild CP that is somehow was really slow to fully manifest the neurological basis that it had (in the head where mystery lives). Palpating (feeling & probing) the surgical area, just felt thick, thick and indistinct. Fast or slow movement didn't seem to favor how it felt where. My suggestion: “I think we need to do an exploratory operation.”& NEVER ever had that been suggested by me for CP! Something local was amiss in that old surgery . He didn't look like CP at all when he was sitting relaxed. We only saw the grimacing and arm stiffness when he was working hard to walk our corridor circuit which he could not complete. To this suggestion, & mother's horror? “I was hoping you would say that.” My husband? has been saying this for the last year!”

So, what did we find? You have been shown enough experimental stuff to figure it out.

The semitendinosus (ST) which well above the knee thins to a narrow tendon, had, at the surgery area, blended into a thick rope most of which was added to by the now conjoined semimembranosus (SM). ST is a smaller muscle with comparatively more tendon than muscle. It's tendon attaches far below the knee joint in a forward area called the 'pes'. Sports surgeons don't hesitate to steal the tendon (of the ST) to repair knee ligaments. Although some high speed control issues my be experienced in those that opt (bad <==Because of where it attaches (pes) any knee movement, at all, has a very long ST excursion. A lot of distance for any angular change. That = 'high velocity'. The SM is a huge muscle – very choice) to continue high performance competition.

powerful – which does the bulk of the work. It attaches right at the joint edge, nearly into the joint. Because it attaches so close to the knee joint, it has a really short length change with even full knee flexion. That = 'low velocity muscle'. ST and SM have the same muscle biology, but fast/slow relates to the attachment effect on distance traveled in a given arc and thus velocity. Rather than saying that muscles living 'in this place and that place' are more spastic, we can say that about muscles which have velocities that top out the spindle sensors (which is where spasticity actually lives) that are preset at too high gain (volume turned up too high).

In this place and that place' the high gain thresholds are crossed by the local high velocities. [THAT is one long sentence stream!]. Short version: Speed kills. If true, then, changing the attachment such that low velocity becomes high velocity will make that BIG muscle BECOME fast & more spastic. Likewise, a uselessly nasty fast spastic muscle can be reclaimed to better function by shortening it's excursion. The two are not flip sides of the same coin as the natural high velocity muscles are typically small. Giving them a short lever attachment reduces both the spasticity and useful power.

The semitendinosus & gracilis have very long paths to insertion in the pes, well below knee center. These are ‘high speed ‘ muscles (distance/time) but small in actual muscle mass. They are, perhaps, more functional as sensory than as power sources. Thus they are both huge

sources of abnormal reflex when their spindles are allowed to run at top sensitivity undampened (as in spastic CP). The larger powerfulmuscles of small excursion, react less primarily but are recruited by the signal blast from the undampened spindles in the high speed muscles.

Should the semimembranosus become attached to the pes via cross

attachment to the semitendinosus tendon, then the huge semimembranosus becomes a ‘high speed’ muscle whode spindles become ‘screamers’. When open lengthening surgery uses a common incision toboth tendons, and thus removes the fat barrier between them then this possibility becomes very real. We would EXPECT, given a huge conversion to high speed spindles from the slower ones, that spasticity would become worse. It does. The sartorious path is different in that flexion makes it looser. Interestingly, sports surgeons have noticed seemingly less control at high speed in athletes who have

had the semitendinosus harvested to rebuild their knee ligaments. This is a musing not proven but it does [now] make sense. So is the ST muscle an evolutionary muscle we don’t need. Maybe. But it may have found another employment after time as a super speed component of the spindle control system.

Now, in this context, let’s consider how the extraparamidal system operates. The brain has a specific thing it wants to do and tends to it. As thet is happening the associative movement mechanism is reflexly keeping the body in the attitude to allow this intent. As that requires very high speed adjustment it is local and uses well EVOLVED templates of movement (patterns) in gradations of extent as the associtive portion of the act. We do not think about swinging our arms when we walk, but the rotational momentum of the lower body with each step needs to be countered with a counter rotation (arm swing/shoulder to shoulder rotation). So what have we learned? We do not want big muscles to get attached to high velocity tendons or that muscle becomes suddenly very spastic crossing the stretch reflex threshold that we see as spastic CP. Yet, low velocity muscles seem to be spastic. ?? Yes, because they respond to the spinal cord level reflex of their partner high velocity muscles. Interesting warped idea … CP kids donating their semitendinosus tendons to wounded athletes with knee ligament damage. Athletes who seem to always get the $ $$, pays for both. OK. BAD idea. But now hard to forget what is going on. Remedial surgery for our Hollywood kid removed the semitendinosus tendon as far as able (to the pes) and closed the space with fat. Then attaching the common conjoined muscles (ST&SM) to the stump of the semimembranosus (right at joint edge and advancing fat to disallow any healing wandering. At the core of what had gone wrong? A single incision for two functional KINDS of muscle broke the fat barrier between them. Healing married them. Nature also chose the tendon traveling the most (doing the most?) to be the common target to which to adapt healing ('Wolf's law).

?? What?

Huge improvement. [Happily ever after.]

You have suffered enough. Go get another book.