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

Spastic cocontraction in Hemiparesis. Effects of Botulinum Toxin

I really don't care about their use of botox. But they did come up with an objective way to measure spasticity.  Which needs to be utilized when testing spasticity protocols, the manual testing of when your muscle 'catches' has got to stop.
http://onlinelibrary.wiley.com/doi/10.1002/mus.23427/abstract

Abstract

Introduction:

In this study of spastic hemiparesis we evaluated cocontraction during sustained agonist/antagonist efforts, before and after botulinum toxin (BoNT) injection in one agonist.

Methods:

Nineteen hemiparetic subjects performed maximal isometric elbow flexion/extension efforts with the elbow at 100° (extensors stretched). Using flexor and extensor surface electromyography we calculated Agonist Recruitment/Cocontraction Indices from the 500ms peak voluntary agonist recruitment, before and one month after onabotulinumtoxinA injection (160U) into biceps brachii.

Results:

Before injection, Agonist Recruitment and Cocontraction Indices were higher in extensors than flexors (resp. 0.74±0.15 vs 0.59±0.10, p<0.01; 0.43±0.25 vs 0.25±0.13, p<0.05). Biceps injection decreased extensor cocontraction index (-35%, p<0.05) while increasing flexor agonist recruitment and cocontraction indices.

Discussion:

In spastic hemiparesis, stretch may facilitate agonist recruitment and spastic cocontraction. In the non-injected antagonist, cocontraction may be reduced by enhanced reciprocal inhibition from a more relaxed and therefore stretched agonist or through decreased recurrent inhibition from the injected muscle.

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