Deans' stroke musings: Early Shortening of Wrist Flexor Muscles Coincides With Poor Recovery After Stroke

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.

Thursday, July 19, 2018

Early Shortening of Wrist Flexor Muscles Coincides With Poor Recovery After Stroke

What the hell prevents this from occurring? That is what survivors want to know. On my own I started wearing these, wore out three sets in 4 years. They start to smell after a while.

Seems to have worked, my wrist is somewhat loose but very little movement because of dead area in brain.

http://journals.sagepub.com/doi/abs/10.1177/1545968318779731

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Karin L. de Gooijer-van de Groep, MSc, Jurriaan H. de Groot, PhD, Hanneke van der Krogt, MD, , , ...

First Published June 25, 2018 Research Article

Abstract

Background. The mechanism and time course of increased wrist joint stiffness poststroke and clinically observed wrist flexion deformity is still not well understood. The components contributing to increased joint stiffness are of neural reflexive and peripheral tissue origin and quantified by reflexive torque and muscle slack length and stiffness coefficient parameters.
Objective. To investigate the time course of the components contributing to wrist joint stiffness during the first 26 weeks poststroke in a group of patients, stratified by prognosis and functional recovery of the upper extremity.
Methods. A total of 36 stroke patients were measured on 8 occasions within the first 26 weeks poststroke using ramp-and-hold rotations applied to the wrist joint by a robot manipulator. Neural reflexive and peripheral tissue components were estimated using an electromyography-driven antagonistic wrist model. Outcome was compared between groups cross-sectionally at 26 weeks poststroke and development over time was analyzed longitudinally.
Results. At 26 weeks poststroke, patients with poor recovery (Action Research Arm Test [ARAT] ≤9 points) showed a higher predicted reflexive torque of the flexors (P < .001) and reduced predicted slack length (P < .001) indicating shortened muscles contributing to higher peripheral tissue stiffness (P < .001), compared with patients with good recovery (ARAT ≥10 points). Significant differences in peripheral tissue stiffness between groups could be identified around weeks 4 and 5; for neural reflexive stiffness, this was the case around week 12.
Conclusions. We found onset of peripheral tissue stiffness to precede neural reflexive stiffness. Temporal identification of components contributing to joint stiffness after stroke may prompt longitudinal interventional studies to further evaluate and eventually prevent these phenomena.