Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, May 4, 2012

reciprocal inhibition - Why should we care?

If we know how this works we might be able to apply it to reduce our spasticity.
From
http://www.cmcrossroads.com/bradapp/docs/rec/stretching/stretching_2.html

Stretching and Flexibility - Physiology of Stretching

by Brad Appleton
When an agonist contracts, in order to cause the desired motion, it usually forces the antagonists to relax (see section Cooperating Muscle Groups). This phenomenon is called reciprocal inhibition because the antagonists are inhibited from contracting. This is sometimes called reciprocal innervation but that term is really a misnomer since it is the agonists which inhibit (relax) the antagonists. The antagonists do not actually innervate (cause the contraction of) the agonists.
Such inhibition of the antagonistic muscles is not necessarily required. In fact, co-contraction can occur. When you perform a sit-up, one would normally assume that the stomach muscles inhibit the contraction of the muscles in the lumbar, or lower, region of the back. In this particular instance however, the back muscles (spinal erectors) also contract. This is one reason why sit-ups are good for strengthening the back as well as the stomach.
When stretching, it is easier to stretch a muscle that is relaxed than to stretch a muscle that is contracting. By taking advantage of the situations when reciprocal inhibition does occur, you can get a more effective stretch by inducing the antagonists to relax during the stretch due to the contraction of the agonists. You also want to relax any muscles used as synergists by the muscle you are trying to stretch. For example, when you stretch your calf, you want to contract the shin muscles (the antagonists of the calf) by flexing your foot. However, the hamstrings use the calf as a synergist so you want to also relax the hamstrings by contracting the quadricep (i.e., keeping your leg straight).

It still does not answer the question as to how the agonists inhibit (relax) the antagonists.

Until that is understood I don't see how we are going to figure out how to stop spasticity. Researchers anyone? Whats your theory?