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.

Showing posts with label Reciprocal inhibition. Show all posts
Showing posts with label Reciprocal inhibition. Show all posts

Monday, March 14, 2016

Practicing movements at different speeds enhances certain nerve functions after stroke or spine injury

How are your stroke protocols going to change based on this?
http://www.news-medical.net/news/20160310/Practicing-movements-at-different-speeds-enhances-certain-nerve-functions-after-stroke-or-spine-injury.aspx
Changes in one circuit of nerves, but not another, in the spinal cord depend on how quickly muscles must move to complete a task, according to results from the Human Motor Control Laboratory of Professor Kozo Funase, PhD, at Hiroshima University. The results could influence physical therapy routines for patients struggling to control their bodies after a stroke or spine injury.
Multiple different types of circuits of nerves control the communication between motor and sensory nerves in the spine. One, called presynaptic inhibition, works like a gate to control incoming sensory information and prevents muscle spasms. Another, called reciprocal Ia inhibition, coordinates pairs of muscles by making one set relax so another can contract, like when your triceps stretches out so you can flex to show off your biceps.
Several studies showed that motor skill training influences these neural circuits, but scientists had not considered the speed of the training.
"We wanted to investigate if practicing a particular movement when moving slowly could change the nerves more or less than practicing the same movement at full speed," said Mr. Shinji Kubota, a former physical therapist and current PhD student in Prof Funase's lab.
The results suggest that different circuits of nerves respond differently to movement speed. The presynaptic inhibition circuit becomes more sensitive to signals telling muscles to contract after repetitive movements of any speed. The reciprocal Ia inhibition circuit becomes more active after repetitive fast movements, but is unchanged after repetitive slow movements. More inhibition of the nerves means the muscles will be less active.
"During physical rehabilitation after a stroke or a spinal cord injury, a common problem for patients' is that their muscles are spastic -- they contract and become stiff or cause uncontrollable shaking. Spasticity is speed dependent, so the spastic symptoms can get worse when patients try to move quickly, but slow movements are usually easier," said Kubota.
Motor skill rehabilitation may be more effective if therapy routines reflect which type of neural circuit controls the physical movement.
Skillful movements, like moving the arm to reach for a cup, are controlled by the presynaptic inhibition circuit which is unaffected by movement speed, so practicing at a slower-than-normal speed that avoids spasticity could still produce positive changes. In contrast, walking relies on the reciprocal Ia inhibition circuit to repeatedly switch muscle activity from contracting to relaxing and this circuit is improved only after practice sessions of fast movements.
Advocating for scientific rigor, Kubota is cautious about claims for immediate clinical applications of the results.
"Injuries to the brain or spine present all kinds of challenges for therapists to consider. Understanding the mechanisms underlying changes in neural circuits will probably be a key element in developing effective rehabilitation approaches for people with central nervous systems disorders. My next goal is to create an animal model of stroke injuries and investigate if there is any link between changed nerve function and improved physical performance," said Kubota.
Source:
Hiroshima University

Tuesday, September 2, 2014

Reciprocal Inhibition

Thanks to Amy for finding this for me . This was me trying to understand how muscles are told to relax. My OT used to command me to relax my spastic muscles, it never worked. Somebody out there has to be brilliant enough that they can write up a stroke protocol to fix the fucking spasticity. And since that won't occur for 50 years you had better start figuring out how to treat spasticity on your own. You're screwed until then.

Reciprocal Inhibition

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?

Sunday, April 10, 2011

Reciprocal Inhibition

Something that would be good for you to understand for a better idea of what your spasticity is.
http://www.physiobob.com/forum/neuro-physiotherapy/1040-neuro-inhibitory-facillatory-technique.html#post3785

Reciprocal inhibition is the term used to describe a muscle's automatic response to the contraction of its opposite. When the Muscle Control Center (MCC) requests a muscle to contract, that muscle is facilitated, and the opposite, or reciprocal, muscle is required to relax, or become inhibited. The smooth facilitation of the contracting muscle depends upon the smooth release of its functional opposite. Though this is how we tend to explain this we should note that the decerebrate posture is one of flexion or rigidity. Therefore a flaccid arm is really an arm with a lot of input from the brain to relax the flexor tendency. To move say the biceps to flex the elbow would therefore to reduce that dampening on the biceps, whilst perhaps at the same time maybe even increasing it's "relaxation" of the triceps (or not as I am not sure on the reseach here). This concept makes working with head injury and stroke most interesting in deed.

Reciprocal inhibition is a built-in, automatic neurological function, designed to provide for optimum joint function and longevity. It is a fundamental function in proper body movement.

When all the neurological connections between the MCC and muscle are clear, the muscle will be able to respond smoothly and easily to the MCC's signals to work or relax. If one muscle becomes permanently facilitated, as in a cramp, spasm, or chronic tension, the opposite becomes correspondingly inhibited. This disables normal joint function, and results in stress that can lead to deterioration of the muscle, tendon, and joint tissues. In this case, if the client has spasms in their biceps and you test the triceps, you will find it weak.


Another simple example:


To get an idea of reciprocal inhibition in action, hold a heavy book in one hand, palm up. With your other hand feel the front of your upper arm. It's contracted and hard. Then, feel the back of your upper arm. It's relaxed, and flaccid. Include this as a flexibility technique to improve your active and PNF stretching.

Thanks to the Physiobob PT forum.