It was classic RTM.

Read the manual?

Yup. In this case, the manual was any chapter on patterns of muscle innervation as described in the physiology books. We knew this stuff, but it was all disconnected factomania. Basic science, not practical working knowledge.

But it WAS.

Yeah. The body has all sorts of neat and curious ways to get tough jobs done. Seldom is anything ever just A-B-C. That's why simple deduction fails. We think linearly. Yet, nature is quixotic, chaotic, nonlinear and ever surprising. Nature finds and takes all sorts of shortcuts or makes one part serve umpteen uses.

One mechanism in particular was acting up. It is called the "gamma efferent system". In muscle there are scattered sensors. They report back their readings of what is going on. The various nerve fibers are named like coaxial wires, by their gauge and coverings. The naming is just a bunch of letters, Greek in this case. Those sensors in the muscles which detect acceleration report back over gamma type nerve fibers.

Those fibers sending information upstream feed into a spinal circuitry which shares afferent, that is, incoming information. The underpinning effect or purpose of that shared information seems to be to set up or favor certain precomputed or built-in gross patterns of complex movement. Favor certain patterns, given certain input, over others. Last moment, this orchestration score can be activated and modified on the fly - especially when speed of action selection is called for. Its a built in box of tricks, so to speak. Pulling away a hand when a finger is burned is not an array of discrete actions thought up in response to pain in the brain. An entire body responds to a local stimulus well before burning is felt as an ouch.

Less dramatically, our acceleration sensors help to keep us from being knocked over from sudden loss of floor support and help us maintain direction or strength of push during unexpected walking surface changes without our actually thinking through all the many details. Who really thinks about walking - except those who can't do it?

We learn to take conscious advantage of these basics. Like the percussionist poised with cymbals just before the conductor's cue. Poised and ready to go.

I don't see that? Like what?

Like all that ants in the pants dancing about a tennis player does waiting for a serve. Those left right jitters keep the left right circuit patterns primed and in the cue to be acted on. That cuts the time required between perceived need and correct response.

Oh. Yeah. I wondered about that. Cool.

Many kinds of gross movement are precipitated by data coming in from the periphery by way of the spinal patterns, what-ifs set up before the head gives one of them the go-ahead, with certain modifications of scope or degree of direction. In spasticity, that confirmation or specific selection go-ahead isn't always actually waited for and confirmed. Spinal contingency plans may well execute as they are brought to the fore. We have an in place dampening mechanism.

Brakes. We rev the engine with the brakes on.

Yes. Simple informational impulses from the acceleration detection thingies can cause entire patterns of muscle tension to actually occur if the brakes are not being used. In nasty cases, resultant abrupt changes caused by reaction can elicit further reaction to reaction. Then reaction to that reaction.

It is exactly like a microphone which feeds back making everybody cover their ears. Sound detected by the microphone gets amplified and the detected loud amplified sound gets detected again by the microphone and then amplified to even louder level which gets picked up and amplified on and on until it is shrieking and sustained. High amplification, called high gain by science folks, without a dampening mechanism runs away.

Gamma efferent fibers carry signals from the acceleration detectors. That is step number one. Then, step two happens.

Rocky would have said step B.

I'm off Rocky. That Rambo thing has me confused. Step two is that a spinal cord mediated barage of signals gets flows out as a barrage of direct undampened output to assorted muscles - many muscles - resulting from the elicited pattern response to the initial signal. Think of it as fireworks. A thin glow, like our gamma signal, goes up and then boom, a wide bloom of sparks showers out and down broadly.

So, a muscle peculiarly set up for detection of fast movement sends up a flair signal and an entire limb or even half a body is showered with muscular activity. That is what that big onslaught of muscle activity is - a step two reaction. Undampened over reaction. If you can bag that initial signal before it triggers all that broad reaction then maybe things might behave better?

Spasticity is DEFINED as over reaction to detected velocity. Bingo. We are talking about spasticity., not just tightness, or "tone", or rigidity, or stiffness, or coarseness or firmness or frigidity or immobility or inflexibility or rigor or.. or.. or.. uh..

Preservation?

OK! If you can cut the offending signal, you may see gross reduction of muscular over reaction broadly. That is what we saw.

That trick ought to work many ways, it is so elemental. Indeed, that is the case. We can just snip certain incoming nerve fibers that carry that signal - or at least the ones which are going nuts with nonstop activity. That is what is called selective dorsal rhizotomy. The neurosurgeons put in a stimulus then watch a bunch of fibers for nonstop buzzing. Those fibers that do not settle down after the stimulus is stopped, the ones that behave like the runaway microphone, get cut - the ones which won't quit.

We can identify which muscles or portions of muscles are most likely to send that signal and disconnect the tension to that portion of the muscle - and only that portion. The effect ought to be the same. Geometry also matters. Certain muscles attach far from joints and therefore have to travel further for any given movement than other muscles that attach closer to the joint. The long travel requires accelerations above a threshold that causes the neurologic fireworks. Simply moving such a muscle's attachment closer to the joint makes the new slower speed not trigger the previously seen over reaction.

Indeed, the muscle that seems to be "more involved", neurologically worse, seems so not because it is more neurologically involved in that muscle's representation in the brain, but because that muscle's speed characteristics cross a threshold in the feedback mechanism which triggers the fireworks. A muscle that is poorly controlled may become well controlled and actually useful by merely getting it to go slower, mechanically, or by buggering portions within the muscle which over excite the acceleration receptors.

How?

If you can slow the speed by which the nerve loops conduct, then the input will probably fall below the fireworks threshold. Fast conducting nerves have a fatty covering which allows a certain chemistry to speed conduction. Without that fatty covering, the exposed section slows transmission.

We defat nerves using alcohol injection to create a speed bump which slows conduction. That strips the speed related secondary fireworks out of the loop of innervation and muscle response. What was gross all-or-none muscle reaction becomes more precise individualized muscle action without the screaming chorus. One muscle will act without always getting a bunch of recruited tag ons.

It is further complicated by another aspect of anatomic geometry. Muscles commonly share tendons. The quadriceps "muscle" is actually four muscles which at one end share a common tendon. Like the FourTops singing group which share a single stage, four part harmony. The calf is three muscles, a trio, which share a single (Achilles) tendon at the far end. Yet, the three portions have very individual kinds of action, reactions and SPEED.

The speed of each portion is in part also dictated by the other end of each unit. So, even though attached by a single tendon at one end, the speeds vary because the other ends alter how far each part travels, when, and how fast. One portion acting above the fireworks threshold triggers a mess in the entire group. Conversely, slow or calm just that one portion and you calm the entire group.

If the shortening is in the fastest component, and it usually is, then a big problem follows. If you lengthen the common tendon by the amount that the long traveling part needs, you may well exceed the length that the other portions can contract to do their job. If the medial gastroc needs one inch of length to get the full range but the soleus only travels half an inch when it is working, then a common tendon lengthening of one inch will disable the soleus - the actual power house of the group. Power5 muscles use short arcs of motion.

When a tendon is tight, the tug can elicit the nasty response. Think of the tendon as a tree trunk. The myofascia is something like the branches if the leaves are the muscle. However, the myofascia covers the muscle the way the casing covers a sausage. The muscle units connect to this casing which fibers eventually dive into the muscle. Often the contractures attributed to the tendon (the trunk part) are really in the myofascia and only portions of the myofascia. Typically, in a muscle with contracture, a strip of myofascia is thickened and short and not the whole thing.

THAT was the big observation. We had always assumed that the shortening pathology is muscle by muscle and talking about tendons. In fact, while physiologic action may be muscle wide, scar-like contracture is spotty.

Interestingly, when selective dorsal rhizotomies are done, the initial response looks good. Then later, most to nearly all, will get some fibrosis in the myofascia of some muscles and especially so in those muscles of long excursion (the high velocity muscles). That fibrosis, in turn, makes the kids look spastic again as if the SDR is failing.

Yet, very careful exam shows that a slowly performed exam of joint range is not unlike that same exam done fast. That is, it isn't speed related. It isn't spastic. It is true fibrosis. Given an underlying predisposition to spastic reaction, such fibrosis magnifies the trigger. It makes nonspastic muscle send high signals and elicits group response. We demonstrated this in experiments on normal kids who we rigged with nasty devices. We could make them behave quite like spasticity, electrical muscle activity (EMG) and all.

So, we attack primarily and disproportionately, muscles of long excursion (or their sub portions) first and then take out any clear residual shortening in the others that will definitely impair function just by way of constraint alone.

There was an even more dramatic realization which came as a result of parents keeping good records and also taking videos. We discovered how open lengthening could at first improve a child, clearly and without argument, to not only recur but then eventually have them look more spastic than before - way more spastic than before. Those videos made it very clear. It looked more NEUROLOGICALLY worsened, not just tighter. How could that be?

Fortunately, back then, we were still doing open surgery for the ones with big scars from prior open tendon lengthening. The finding was that the very large muscles - the power muscles - the big beefy muscles which give you your muscular shape and which do the big work (and which are the slow muscles of short excursion attaching close to the joints) those muscles had their tendons confused.

Confused? How?

A common surgical incision and exposure of both fast and slow tendons. The tendons, via scar and remodeling of tissue in surgical planes which involved the deeper muscles, became intermingled. Deep tendons got cross connected to more superficial tendons (those sitting above them toward the surface - the HIGH SPEED ones). Large slow muscles become high speed by way of cross attachment. High speed muscles are low volume skinny but long affairs. You could toss them out altogether and not miss them all that much. Surgeons take entire hunks or the totality of these skinny ones to rebuild knee ligaments and such. We can toss them if they behave badly enough. But the big ones do the big work and seldom have speed reactions which cross the fireworks threshold - UNLESS - they get connected to the fast tendons through a common scar. That scar results from a common surgical exposure of both tendons. The plane of fat between them may get lost. It does more than glue. It reorganizes according to muscle tension and can even cross attach the muscles.

In a sense you can describe spasticity by the pound. How many pounds of muscle have high speed connection. If the volume of muscle connected for high speed goes up, then the sensors within them which report high accelerations also goes up.

I am certain this is why our percutaneous lengthening data is so good on the long range end. We don't have this complication.

Gee. So, did everybody understand this?

No. Two physiologists actually came to a lecture, they confessed later, to ridicule me publicly for my faith healing no scar bull crap. They were husband and wife, as I recall.

Ooooo.

Yeah. Oooooo.

Did he?

Fortunately, they listened first then had the lights go on. They were from Johns Hopkins. One of them suggested that the problem was the name. Percutaneous implies a different hole to do the same surgery. This was not the same surgery at all. We should have named it better. Hold on - I have to plan this - it doesn't just flow - uh - Selective Percutaneous Myofascial Lengthenings in Velocity Dependant Neuromuscular Gamma-efferent High Gain Feedback Oscillation Syndromes. Did I get it right?

I didn't get it all, repeat that.

I can't.

Come on.

I can't. I twy and twy but thpit jutht compth thout thpraying aphther the firpflst attempt. I spthart thpraying and sthpoiling my schptheech. Justh tpthikging about it turnspth me into Sylvespther the cat.

Percs.

Yeah.

What about the spine?

Oooo, that's a whole nother thing again.