ROM Resist & New Zealand

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).