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, March 14, 2014

Muscle Atrophy, Voluntary Activation Disturbances, and Low Concentrations of IGF-1 and IGFBP-3 Are Associated With Weakness in People With Chronic Stroke

You've identified the problem,
What the hell is the solution?
Don't do things only halfway.

http://ptjournal.apta.org/content/early/2014/02/26/ptj.20130322.abstract
  1. Thiago Luiz Russo
+ Author Affiliations
  1. M.A. Silva-Couto, Department of Physical Therapy, Federal University of São Carlos, Rodovia Washington Luis, Km 235, Monjolinho, São Carlos, São Paulo, Brazil 13565-905.
  2. C.L. Prado-Medeiros, Department of Physical Therapy, Federal University of São Carlos.
  3. A.B. Oliveira, Department of Physical Therapy, Federal University of São Carlos.
  4. C.C. Alcântara, Department of Physical Therapy, Federal University of São Carlos.
  5. A.T. Guimarães, Department of Physical Therapy, Federal University of São Carlos.
  6. T.F. Salvini, Department of Physical Therapy, Federal University of São Carlos.
  7. R. Mattioli, Department of Physical Therapy, Federal University of São Carlos.
  8. T.L. Russo, Department of Physical Therapy, Federal University of São Carlos.

Abstract

Background and Purpose The muscle weakness that is exhibited post-stroke is due to a multifactorial etiology involving central nervous system and skeletal muscle changes. Insulin-like growth factor I (IGF-1) and IGF binding protein 3 (IGFBP-3) have been described as biomarkers of neuromuscular performance in many conditions. However, no information about these biomarkers is available for chronic hemiparetic subjects. Thus, the purpose of the present study was to investigate possible factors involved to muscle weakness in chronic post-stroke subjects, such as serum IGF-1 and IGFBP-3 concentrations, muscle volume and neuromuscular performance of knee flexors and extensors in chronic hemiparetic post-stroke subjects.
Methods A cross-sectional study was performed on 14 post-stroke subjects who were paired with healthy controls. Mobility, functionality, balance and quality of life were recorded as outcome measures. The knee flexor and extensor muscle volumes and neuromuscular performance were measured by nuclear magnetic resonance, dynamometry and electromyography. The serum concentrations of IGF-1 and IGFBP-3 were quantified by ELISA.
Results The hemiparetic group had low concentrations of serum IGF-1 (25%) and IGFBP-3 (40%); reduced muscle volume in the vastus medialis (32%), vastus intermedius (29%), biceps femoris (16%), semitendinosus and semimembranosus (12%); reduced peak torque, power and work of the knee flexors and extensors; and altered agonist and antagonist muscle activation compared to controls.
Conclusions Low serum IGF-1 and IGFBP-3 concentrations, deficits in neuromuscular performance, selective muscle atrophy, and decreased agonist muscle activation are presented in chronic post-stroke subjects.

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