SPMLs & EtOH

SPMLIHGROwSEPFD Exasperating, but always what is asked of us (especially by surgeons) is ‘What is an SPML?’ and ‘Why do it that way and not the standard (aka proper) way?” Did you spot the conceptual error? Actually two. 1. ‘do it’ There is no “it”. SPML has half of the process name missing from the abbreviation. The only letter in ‘ SPML’ that is essential is the “S”. Selective . Selective isn’t a list of those muscles that have tissue contracture. It is selective of what functional abnormalities are to be dealt with – and – in more than one way, not just by cutting. Contracture is not a THING, singular. It is a salad of things only part of which is tissue contracture. That brings up another part of the ‘S’. The reactive contracture caused by high gain spreading reflexes is not there at all while under anesthesia. Anesthesia methods must be selected so as to not blind us to the abnormal reflexive abnormalities which we have found are worse in functional loss than obvious tissue contracture. Range of motion should NEVER be the measure of outcome. More is NOT better. Power loss and inability to control wide range are sources of treatment failure, failure to improve function. With treatment we want to: Still be able to do whatever functional things existed, as before, but longer. Do them better. Be able to do a more functional but different thing instead. Do it several ways depending on the situation – situational capability. Remove joint damaging muscular patterns & thus head off joint damage. Detect structure risks before x-ray visualized damage occurs.

2. Why do it “ that way?” We don’t do the surgery that others do this way or that way.

We are doing something else . It turns out, as luck would have it, that we CAN use this as a less invasive way to be very selective as to how much & where and note overall change as we proceed. In our original tracked series of 500 cases, close to half also had additional open surgery. Most of the open surgery could have been prevented had we known what we now know 30 years before we first started doing this. Patients treated as babies to 2 yo very seldom need the big open surgery. We do, sadly, a lot of really big repair surgery. Why? It is referred from places without a clue about prevention. Also fear figures in. Parents who dread intervention and resist EVERYTHING are a huge source of bad outcomes. Percs? We called them ‘percs’, not as a name but as a check box for the operating room who has to set up our surgical tables with an array of many tools all sterilized and ‘spore tested’. It is expensive to do that. With SPMLs, we don’t need all that equipment as we are only doing percutaneous things (tiny poke holes) – percs, now called SPMLs. Operating Room “Case Card” = Dr. Name______________ [ ] C-arm & radiology table [ ] #10 surgical blades & handles [ ] oscillating drill + 2 battery cartridges [ ] Midas Rex air drill with M10 side cutter, other________ [ ]

… many more things [x] only percs [ ] cast cutter

THAT is what ‘percs’ means – we don’t need all the big tools and will only use simple drapes and maybe a few small dressings (ordinarily kept in room anyway).

So about that abbreviation: You don’t has to call it SPMLIHGROwSEPFD. You can call it Johnny. You can call it Ronny. OK, sorry, no more burlesque. To truly understand what we are doing you should read the other books on our book shelf. These books are hugely redundant on purpose as we are essentially teaching a new CP language. Start with Mud. Then skim through the SACH-SAWCH book. It details why feet should never be our limitation. Absolute wildly extreme worse case: amputate & prosthesis. Prosthetics work fine. Seriously, that was done not that long ago. It was sought after by patients who didn’t want to be sidelined by feet that would not behave as feet should. Interesting but more importantly instructive. With misbehaving feet, we can attain prosthetic type (‘SACH’) foot function using ‘percs’ or SPML in high gain SPMLIHGROwSEPFDs even for – especially for – some of the nastiest situations you can imagine. These examples are as horrifying to the surgeon as they are to you – but even more so as complications with standard surgical methods are horrific.

This is a 12 yo girl who walked in staggering fashion unassisted, having athetoid CP – a nightmare for surgeons as athetoid patients respond to surgery unpredictably and badly. For no reason that we could pin down, her legs clamped together and she could no longer

stand, let alone walk. On the 12 th we see two adductor emg bars go full height as someone tries to coax her knees apart. No go. Next day, she had ethanol focal dysmyelination (we didn’t call it that back then) and three days later she could abduct & adduct with supple ease (& walk).

Spastic diplegia with extensive mesh skin graft for 3 rd degree burns from being plunged into extremely hot water. Not an accident. Full walking for first time after SPMLs We used SPMLs to also lengthen her skin to allow the range. No sutures.

Two examples of Wilson’s Disease: On the right a late teenager unable to even sit from extensive contracture, both tissue and reflexive. On right, lower: walking unassisted after SPMLs and SAWCH ankle/foot casts. On the left a 19

year old male who was chair only. Then after SPML showing off by running at the camera in the hallway. Another Wilson’s case was admitted (to Hematology) so that a severe platelet

deficiency (rare but known in Wilson’s) could be managed [120 volunteer fresh platelet donors] – took all day. Surgery was late evening once the

platelet count was satisfactory. Platelet protein load brought out rising ammonia. Got it done, though. Similar, but not as difficult, are sickle cell related cases and hemophilia contracture cases. All this is frightening if incisions are needed. Our first cases were CP as a result of Tetralogy of Fallot (& a few TF variations). Blue babies. The CP effort level was killing them before final staged cardiac repairs could be completed. Straight ‘local’ & ‘FFP’ and these kids looked far better than any CP kid post surgery treated the usual way. We were doing a ‘make do’. Open surgery was out of the question. Outcomes were jaw dropping. But, why??? <===

He was said to need tibial osteotomies (break shin bone and rotate lower half outward and metal plate or internally rod to hold the ‘correction’ until it heals. Long time off legs etc. A different diagnosis, not tibial torsion (= a twist in and of the tibia bone) but rather tibial rotation (which is still not in the books) [= tibia is fine, can manually unwind it but springs back inwardly through the knee joint] by spastic forces that were also thwarting his walking.

The tibia malrotation was gone before he got to recovery room. He walked on his own a few days later. There is always a wow case that compels rethinking what you think you know. That follows...

A 6 year old boy from New Zealand pops in because his mom was familiar with a family of a Tetralogy SPML patient. Essentially, do THAT to my kid. Nice kid, but, all energy. Pent up frustration trying but unable to walk. Then he did this:

In our suburb office, he ‘knee walked’ to the end of the hallway where we wanted him [also known as ‘tall crawl’ using no hands, on walls or floor]. We couldn’t say no to that, a really good indication of what is needed to walk unsupported. We were, then, only doing our cases of SPML under local anesthesia. Tetralogy kids knew to be still from all the stuff they have been through. Not this guy. It was a job holding him still and his medial hamstrings were like bow strings. They were the obvious target. The semitendinosus is a muscle that is relatively small with a really long tendon that sports and reconstructive surgeons remove without hesitation in order to replace knee ligaments and lots of other more needy things. It is not missed

(though later we hear that super high performance athletes have some high speed fine control issues with this missing). OK. Just release the semitendinosus contracture. That was all we could feel holding him back. Like popping a balloon, his surgery was over in a matter of seconds with nice supple range. You already know it went quite well. But, the degree of response was way more generalized than what we did. Now go read the Range vs Resist book and have your mind blown. Mine was. It wasn’t range contracture that was disabling. It was what the resistance was eliciting (afar) that was disabling! It isn’t the range, the arc stop point, but the tension applied to what was NOT contracted that was disabling. A super high speed muscle is functionally removed (still there but not doing much) and spasticity goes away – including in other places. Smaller ranges are quite functional if what is left is stable and supple.

THAT is what is selective. Where is the pesky reaction coming from? Go there. Luck has it that the high velocity stuff is always near the surface where high speed lives. <== That means rapid movement is needed to find and measure how much SPML is enough, it done awake or fully reactive though sedated.

This selects anesthesia methods. What does not suppress reflex abnormality? For example, sevofluorane, a terrific anesthesia (fast in, fast out) totally suppresses abnormal reflexes and reflex spread. We can’t find what to fix nor how much under ‘sevo’.

Abnormal reflex spread typically follows patterned forms. We know where to look. Why do SPML on the right leg when it is the left hip with the x-ray finding that got us here? Also denervated muscle units that undergo fibrosis run the whole muscle/tendon length. But they are hard to get at, in a minimal way, until they pass through the myofascia region, where the fibers spread out in a flat plane. Go there. It isn’t surgery to the myofascia or of the myofascia, but a convenient location to find and divide the bands that are making trouble as passing through. These dead bands constrain muscle elongation. Dividing these scar-like bands allows muscle range to be what it should be. Muscle might seem weak if the contracture has been taking the peak load. But with returned use, the muscle gets to do its own work and regains power. While we are talking about dead muscle units that degenerate in fibrosis, let’s discuss the ‘nerve block’ agents and why we use ethanol.

A closer look at that perfect wave: *Trying to make-do for small blue kids with cardiac related CP, *total frustration with experiments testing range of motion restriction not looking anything like CP, *some other serious complicating disorders with high risks etc. etc. and a *make-do operation does better than normal interventions. All that and then a Hollywood kid whose good operation made him slowly worse where a normally slow muscle got healed to a fast tendon. You have to rethink all of it and rethink past conclusions with new eyes.

Thought is a marble presented with infinite holes it can drop through, but only a few ring bells. Luck helps. Kids with holes in their hearts and misplaced artery plumbing have blood pump problems of low flow with low pressure. They squat to resist flow to the legs so their brains can get a turn. Low flow CP, especially if born early (they are) favors PVL over the other types of CP. And so THAT becomes the off ramp from a universally traveled wrongheaded intervention highway. Off the ramp we find mysterious new places and things to ponder

– and mull...

… to think and evolve.

I AM proof of evolution as I once did not believe in it. Let us evolve together.

Look at a child of cramped and staccato perambulation and envision Plato’s shadow on our cave wall lit of our own misunderstanding. Don’t confuse sailing stones with Sisyphus . What makes our struggling hero move? What is the true impediment over which, in a tortured manner, this youngster IS, somehow, PREVAILING? If reflexes generated by true effort are at the core of needing these movement alternatives, then go there. The level of intensity of compensatory effor t is highest at the point of success. It is not a measure of absent potential. Ask this of your own perceptions, as you examine. Is there a sense, here, that momentum can be controlled? Are there other things that functionally FLOW, in control, and expeditiously? Tall knee walking? Seamless and speedy creeping (on all 4’s)? When does the problem worsen? Sits well balanced (?) without losing upright control. Gestures meaningfully when telling stories or conveying complex ideas? Now rather than ask what will guarantee – absolutely – to maximize ranges of motion at every joint that when used had less than what we suppose is normal? Shark bite. OK. Long convalescence, big scars, considerable complications that are not infrequent, and maybe total loss of capability… sign here, nurse witness that.. or

What is the least thing I can do with the least risk of loss of anything which MIGHT improve function in a sustainable way? Something small, maybe even a bit short of our wishful mental dreams… but safe and quickly back to everything in life. Might need it again, but it is small enough that, even so, it is still less than above alternative, by a lot.

OK, we have things that attached to coated needles can find and stimulate nerve branches of our choosing. Then what? Injecting something that does something, and lasts, hopefully. Such as? Things that various people use include: Phenol = “an alcohol” Ethanol = “alcohol”

Cryo-ablation Radio-ablation Radiation - PHENOL

Take any carbon chain or molecule, from 1 carbon to however many, and stick a ‘hydroxyl’ [ -OH ] on one of the carbons and that molecule regardless of what else it is still also gets called “an alcohol”. Phenol is benzene with a single -OH stuck on. Xylol, for example, is benzene with two -OH s tacked on. Both phenol and xylol are ‘alcohol s ’ Phenol is used in medicine the way the military uses flame throwers. It KILLS! Anything & everything! Wipe down contaminated surfaces. Kill fungus. Kill viruses and anything else it touches. When used on nerves – it KILLS them. Dead. If a muscle is innervated by a dead nerve, the muscle also dies, slowly, in about a year, maybe two. That muscle as if gazing at Medusa is turned to biologic stone (fibrous scar). During those two years initial joy at the decrease of spastic reaction turns to horror. An even worse rigid contracture has replaced a lesser degree reactive contracture.

Kill fungus? OK. Tuberculosis goober on a surface. Phenol is good. Nerves? Noooooo. Why not? We don’t want what follows nerves made dead, even if by “an” alcohol. Something interesting about “ the alcohols”, they are mostly all poisons. Well, one major exception is “ alcohol ”. Only hydroxylated ==> ethane [ C-C-OH ] is called, simply, “alcohol”. It has many alternate names, though.

Including: Booze, vodka, ethyl alcohol, Cologne spirit, absolute alcohol, EtOH, methylcarbinol, hair of the dog (borrowed from a Rabies rx), spiritus fermenti, the -OH in hang-OH_ver, ...

What does ‘alcohol’ normally do? It is actually a food. It can be used the way sugar gets used as long as not in excessive amounts. Kept in bounds, it is an in-between or offshoot step in anaerobic metabolic cellular chemistry and consumed in the gut where hungry bacteria can drink it. Our use of ethanol (‘alcohol’) is much much simpler. Ethanol dissolves fatty greases (most alcohols do that – look on the Windex label). Myelin is a wrap of greasy fat around certain nerves (not all nerves) in order to give the myelinated nerves higher speeds. The body’s chosen high speed nerves are used to run ahead of other signals – up to 15 times faster. These are GREAT conduits of problems as well. They can deliver too many signals, too fast, and for too long. A tsunami of signals can release neurotransmitter faster than our nerve/muscle connections can remove, causing muscle to not let go, from twitch to unremitting clench. Terminology technicality is needed here: Signal ‘amplitude’ (voltage) of a nerve signal has very little meaning as voltage is only determined by the nerve’s diameter. Where and how many signals are the main things. Buggering myelin puts a slow spot (speed bump) in the nerve’s conduction where many fast flying signals pile up. They coalesce and come out the other

side as only one signal [= low pass filter]. A single intended signal that got swathed in noise (abnormal reflexive extra signals) returns to being just a single impulse. The nerve is not killed, so muscle does not see Medusa’s charming face. The injected 50% ethanol (1:1 with water) is not acting as a drug, something which acts as long as the drug hangs around. It is used as a solvent. It’s aftermath effect lasts until the nerve can get its myelin repaired. In a baby, that can take a year. At about five years old, such myelin repair can take five or more years. In an 8 year old it is likely, at least in part, for life. Neural systems remodel around function. This long effect means it is uncommon to need to repeat injection even after the expected repair time has lapsed. Cryo-ablation, radio-ablation, surgical division, segmental excision [neurectomy] & radiation are all nerve killers - read Phenol. Same outcomes. Ethanol nerve treatment seems lost in its origin as it seemed to sporadically popup with alternative ways to do neurectomy. Ethanol failed. It didn’t kill. But, still, it was not without effect though not the extreme of neurectomy (before the Medusa aftermath sets in). It was being used (but not often) in open surgery at the point where scissors would snip out a segment of nerve to assure the nerve didn’t grow back, maybe when the surgeon didn’t want a huge effect but just some effect. But others, who go after nerves, were also going through the list of potential injection choices. The physiatrists were in the lead on both phenol and sometimes ethanol. A huge problem – nobody saying it, but, it was out there hanging in the air – transverse myelitis. It is as if the spinal cord was cut across. Complete loss of everything in the lower body, paraplegia of spinal type. SENSATION & MOTOR – GONE! Nasty! This didn’t happen frequently, but it did happen. Wasn’t me! I was no where near the spinal cord! No. No where near it. It had to be (this became the established truth – though quite wrong) allergy. An immune triggered or focal allergic reaction to these substances which are quite safe to the vast majority of people. Like peanuts?

Who made this wrong – blameless – cause into discarded history? Mostly the Navy. The medical corps in the military are shared and the largest, most extensive, is the navy. The corpsmen – in war – were faced with narcotic dose risk to badly wounded. Safer, was local anesthesia & fast transport. By putting a needle right onto the femoral nerve (easy to find & confirm by rotating the needle to trigger the nerve) local anesthetic diluted in about 100 cc of saline was run. With that, numbness traveled upstream until BOTH legs and up to mid abdomen were pain free. Nerve surfaces do not bind to the surrounding fat and so that nerve/fat interface is a rather quick CONDUIT. Given enough VOLUME (the 100 cc) fluid can easily flow up and into the spinal canal traveling along pelvic plexus nerves. It is even reliable. When ethanol was used at surgery, this could not happen. It was hard enough to keep the drips on that small area. There are variations in internal anatomy as there are in faces. When done by blind injection, the practice was often to try a few spots and just use a lot – 30 cc here, 30cc there. Some of it has got to hit the nerve. And it did. But, if by LUCK (bad luck) – IF – that needle was dead on accurate, right where the doctor was wanting it, and 30cc went in, then distant leg burning, and occasional intraspinal effects followed (but not from local anesthetic which is safe even when injected directly into the intraspinal space (spinal anesthesia). Phenol or any alcohol can go intraspinal if used in volume. This war time field anesthesia was the main way all military lower limb surgery was done with great effect and low complication. Dentists who were also doubled as anesthesiologists (being by far the biggest medical section) were quite expert in this. Now, in a civilian setting, our own military background kept us from using the large volumes that we knew were being injected by others for nerve blocks. Our rule was 1cc or nothing. To make this a reliable method, we brought in an electrical engineer wizard Dr. Michael Polchaninoff, who also has a podiatry degree. He helped us use a spinal needle passed through a

plastic arterial ‘needle’ (flexible arterial line over the needle). With success, that became a new item, plastic coated needle (so only the needle tip metal conduction is exposed to the surrounds). That needle is attached by wire to electronics with which we can find a nerve, identify which it is by its ‘stim’ response, pulse over drive it to see what other body parts far away react to it… and then

inject the 1cc with absolute certainty of safety and an expectation of efficacy. Everybody doing this stuff knew everybody else so choices and methods spread very fast as to how, but not so much as what to inject. Hamstring innervation has huge variation. It is so easy to think you ‘got’ the hamstring branch when in reality there were 3 branches that divided off higher up. Those pushing volume to get it all, saw the up-flow consequences as chemical sciatica burns from their choice of what to inject. Phenol = bad. Podiatrists got quite good at this. Our own wizard, Dr. Toufic Boucherie, a pain anesthesiologist [who mostly treat pain – post op or cancer related] could find the smallest nerve in a flea. He was really talented, but died young. A great deal of our precision and localization tricks were perfected by him using our electrical approach and x-ray. It became our job when he died. On whom was ethanol used mostly? There were patients that surgeons wouldn’t touch with ten foot poles. Athetoid and dystonic patients were notorious for going ‘bonkers’ after surgical MUSCLE procedures. Somehow, this was not so with the limited volume ethanol perineural injections. Without surgical options this group became physiatry property until we figured the work around. An aside: All sorts of things were being used to kill nerves – you saw the partial list – and so a simple name for all of it was ‘blocks’ – blocking nerve pathways to downstream muscles that were chosen to be culled from the herd.

One exception, ethanol, was block-ish, though it did not denervate (we biopsied muscle in cases when we had later reconstructions to do and easy access to muscle that had ethanol nerve ‘ block’ (= no significant denervation was seen). Ethanol failed as a ‘block’ making it a success as its function sparing treatment of reactivity spread. But, alone, it could not create movement that was not there nor remove very severe spasticity as an isolated method. Already aware that – at least in the spastic diplegia kids – we were seeing “spasticity in parallel” [but didn’t, back then, know why] we applied the ethanol dysmyelination (selective & focal) to those nerve branches that when stimulated made other things jump. With the anesthesia insights from our departed colleague we have watched and appended our lists of what and how much to do and how to test what to do. As new anesthesia agents are introduced this remains critical. Prime example is sevofluorane. One whiff and you are gone. Count backward from one… ‘wuh---’, out. Great for scared kids. But, it makes nerve finding impossible as it kills the reaction we are hunting. So, often, when the child is crazy scared… “Have you ever smelled this?” asleep – start IVs etc. mask the trachea to protect against vomiting – rare but can happen … and switch to other anesthetics (‘Sevo’ is gone almost as fast as it came in). Intubation , demanded by anesthesia in many academic places, is generally terrible as curare type drugs are paired with it and a deeper level of anesthesia is required to not get wild reaction to the tube. Deep anesthesia makes us blind to the reactivity we are looking for.

Above, we see the obturator nerve looking down from above traveling to the left obturator canal where it passes from inside the pelvis to outside branching just before or as it passes through the canal. So, with slight placement change we can focally dysmyelinate the common branch, and coming off that the anterior branch and the posterior branch. There are pathways here for hip adductors AND hamstrings which are especially rich in those of the higher muscle speed types. It, in a way, is more representing speed sensitive musculature than muscles by name.

As SPMLs evolved we saw what those ‘layers’ of reactivity were actually all about. Variations in ethanol techniques have let us widen the scope. When we have anesthesia planned

for the legs, it is not uncommon that we will use that easy

availability to decrease upper extremity posturing problems that might, by themselves, not warrant a general anesthesia. But, as we already noted, to reduce our “missed opportunity score” (any patient having an anesthesia within one year of SPML for any reason ~7%) we have co-operated with ent, dentistry, general surgery, etc to handle outstanding pesky stuff in just the one anesthesia SPML session.

Mary Alexander, RPT supervised pre-op and post-op evaluations by our staff as well as tallying before and after evaluations by the independent PTs not privy to what exactly was done. All surgery was by a single surgeon. None of the outcomes were the word of that surgeon. The details that were reported (1997, see below) in Canada were, then given to a patient’s mother (a medical writer) to present in a meaningful but accurate way for general education of parents. That report was ‘trashed’ as ‘this is the crap we see on the web’ by a Canadian academic to a pediatric orthopedic session at an American meeting. 100% positive questionnaire response was dismissed as ‘placebo’. So, beware, this might be boogada boogada – all in everyone’s heads. Some placebo! That placebo follows:

This is our first thoroughly followed series which became the 2 nd & 3 rd etc. as we tacked on another year, each year for 8 years. From 1990 to 1994 we cut off the series at 500 patient surgical sessions – many being multiple sites per session and limited to patients having growth expectation clipping at 13 = 12yo or younger. You can see that SPMLs done alone (with ethanol as needed but no open incisions) was just under half of the cases. Exhaustive study

costs were financed by the Summit Area Public Foundation. This in depth study of cost and outcome was headed by Sheila Walsh, APN [advanced practice nurse, now Dr. Walsh] who was in charge of our team doing the pre-op and post-op data evaluations and documentation which had a 100% patient follow up, that is, none were lost. Cost to family and hospital, operating time,

convalescence duration and scope, with preop PT evaluation & postoperative PT reevaluation (in house AND independent) revealed a very high functional gain with extremely low, almost nil, complications from SPML. Cases done

open were not compromised by SPMLs also done at the same time – though that was not our thrust of interest. Basically, SPML never increased the larger open surgery time in any measurable way but it did reduce actual operating time frequently from preoperative projected time estimates. 100% of parents (of SPML) reported, by questionnaire, that they would do it again, knowing what they now knew, if sent back in time to re-decide. Over the following years that affirming opinion did not change. Aside from internal review and local orthopedic meeting presentations of specific aspects, the entirety was presented to the Canadian Orthopedic Research Society Annual Meeting, June 3, 1997 in Hamilton, Ontario, Canada by S. Walsh, APN. That session was overseen and the details reviewed by Dr. Robert Salter who stated that he liked the underlying concept and praised the depth of the study itself. It was thoroughly questioned and discussed by an audience of pediatric orthopedic attendees with overall positive regard. Since that time, adding oddball case observations and laboratory volunteer studies to try to pin down just what was happening, our methods evolved. What was small by necessity for cardiac patients became even smaller once we discovered ophthalmology tools. It became smaller not because we needed to be small anymore but because small was all that was needed once the underpinnings of success emerged – grudgingly. Range of motion isn’t it. Nice to have it, but that is not the target. This was not an easy belief to shed. Here is the important core of understanding: walking is a beautiful tune played on a masterfully built instrument. We tune that instrument in the way it can be played. Making the instrument taller, or straighter, or with more keys to press or holes to plug is irrelevant. The tune matters, only the tune. Know what is there, probe and test (stimulate) to see what makes what else spring forth - where and how much. THAT is the target. SPML is the overall gross tuning method, including focal ethanol to allow more precision and less REQUIREMENT to cut more places more extensively.

For those more complex but somehow mysteriously borderline walkers losing skill with growth, we actually prefer to do correction in two sessions though logistics drags us to single sessions. Why two? Zero loss of functional time post-op is a key target. Too much change, even for the better, theoretically, might be more than will allow unassisted quick relearning following surgery. Coming back for a second session, can be a good idea and not failure as functional gain from session 1 gets finer tuned allowing an easier session 2. Again, this is for the more complex walkers, the ones who were not just dampened by resisted movement but whose reading and transferal of the brain’s requests are being blinded by reflex noise. This is not just dampened effort as with elastics, but less able to react to unexpected change? Lost in a sea of noise, intent and feedback. Find the message: brumSwelouometh589ing fergyshhim123wertgfilar ounikjto etxtjkhismm. brumSwelouometh589ing fergyshhim123wertgfilar ounikjto etxtjkhismm. Something like this.

This youngster had open adductor ‘release’ [cut, divided, lengthened… = release of tension]. Upright, he kept scissoring. Under anesthesia as seen here, legs were easily spread wide manually by the assistant. Slowing the neural conduit with focal ethanol fixed it.

Now recall what elastics did to our athlete volunteers and ponder if noise driven reflexes spread to random other locations can dampen the pendulums used in walking. Of course. Do slow movements then repeat again fast, very obvious. Maybe that’s all you need to deal with. OK. If there is obvious contracture we can also quickly adjust that as well. But we do not want big ranges as more is not better. Loss of control can result from range that the patient can’t reign in or does not capture and redirect pendulum kinetic energy.. end swing dampening. Often after SPMLs in the legs, reduction of reflex overflow tone shows in the arms. We will accept that! But, especially in kids with dystonic aspects to the upper body, we can deal with arm dysfunctional posturing with ethanol ‘blocks’ aka ‘alcohol blocks’. And again the blocks are not actually “blocks”, they are … uh… mmm.. no no I’ll – oh: selective focal perineural ethanol dysmyelination -the term nobody uses for obvious reasons. In fact, it becomes a naming Rubik’s cube.

selective focal perineural ethanol dysmyelination focal perineural ethanol selective dysmyelination ethanol selective perineural focal dysmyelination... and so on.

TOXINS? It is confused with alcohol so often. We must include this although it does not belong in this topic – the most deadly toxin known to humanity.

<== This stuff costs us in the thousands of dollars per vial and often multiple vials are used (by non-surgeons). It has its place, but in leg use it is very short lived (measure in weeks) and has zero protective value. It does not prevent any of the damaging joint things that worry us in cerebral palsy. Effectiveness over time fades. Is this simply a gun that people without carry licenses can strap to their hips? Just asking.

So, we have beaten spasticity in parallel into the ground. Like elastics in normal volunteers, it is a layer, not a removal of anything. As a mechanical drag on the pendulum we just peel that away. But, in the more severe degrees of spasticity, it isn’t just the drag that must be dealt with. The reflex noise can be so severe that it interferes with decoding control messages that arrive ready to be sorted, interpreted, and delivered to the various muscles. We already mentioned it, but visually? Anything similar? Imagine a great video being watched on one computer (a good one) but you have to leave & so you obtain a copy of that video file to take with you. You put that file on your own (good) computer and … and … hmm mm, it won’t play! All you see is speckles and hear hiss. Bad file? Wasn’t it copied correctly to your ‘thumb drive’? A message pops up saying that you are missing a ‘codec’ [= coder decoder] for this kind of compacted file. It is a key used to unfold this KIND of very compressed file. There are many codecs for the many compressed file types. You download the mysteriously named codec and the movie plays fine.

See? If the circuit does not keep out extraneous signals then the unpacking fails. THE BRAIN SENDS FIELDS OF SIGNALS. If noise intermingles, then the message from the brain cannot be unpacked. A patient who shows control when in a relaxed (seated, floating, sedated) state but is worse in actual self controlled activity has a layered on ill effect. Function loss = blocked unpacking of a well sent message. This bridges parallel & serial defects. It represents the ‘maybe’ cases of group 1 patients – potentially able or able to use momentum – kind of? Group 2 – spasticity in series -includes some of the just mentioned noise cases. But, mostly the extra-pyramidal pathways to assist walking and movement requirements into a pattern for sending, are still there. These are the ones well used by cats. We don’t have as complex a set of pre-patterned total body postures and adjustments, so things done by this route by us look very thick and stereotypical. As group 2 also has much wider neural damage than PVL, the consequences are many. Walking might not even be on any one’s wish list. To swallow without choking, not arching getting into a chair, might be the wish list of the moment. But look at the introduction again. Not all of those no hope looking cases are to be just left alone. This is where clinical experience is irreplaceable.

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