Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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.
My back ground story is here:

Saturday, September 1, 2018

Using priming to promote neuroplasticity and motor learning post-stroke

In your Aim 1 you already have a high functioning survivor selected, high intensity walking is not normally possible. It took me years to get to that point.

Author: Li, Xin
Citable URI:
Advisor: Morton, Susanne M.; Reisman, Darcy S.
Publisher: University of Delaware
Date Issued: 2018
Abstract: The majority of stroke survivors experience persistent motor impairments even with rehabilitation treatments. An underlying mechanism for this is the decreased motor cortical excitability in the lesioned hemisphere after stroke. Priming techniques, such as acute exercise and transcranial direct current stimulation (tDCS), can increase motor cortical excitability and enhance motor learning in healthy individuals. But whether they have the same effects in people with stroke is unclear. Selective serotonin-reuptake inhibitors, a type of antidepressant medication, can change motor cortical excitability in healthy individuals and in acute stroke survivors. Moreover, they can interact with tDCS, changing the effects of tDCS in healthy individuals. Given that up to 30% of stroke survivors take antidepressant medications, this is an important factor to consider when evaluating the effects of tDCS in stroke. The overall purpose of this dissertation was to investigate the neurophysiological effects of exercise priming and tDCS (with chronic antidepressant intake as a factor), and to investigate the effects of tDCS on locomotor learning in people with chronic stroke. ☐ In Aim 1, we showed that exercise priming, in the form of 5 minutes of high-intensity walking, induced increased motor cortical excitability in the lesioned hemisphere, as measured in a resting upper extremity muscle. This finding is significant because it provides evidence on the effectiveness of a clinically feasible exercise priming paradigm to induce broad excitability changes in the brain. ☐ In Aim 2, we showed that stroke survivors taking antidepressant medications had higher motor cortical excitability in the non-lesioned hemisphere compared to those not on antidepressants. We also found that application of anodal tDCS as a primer over the lesioned hemisphere produced differential effects on excitability in the unstimulated, non-lesioned hemisphere, depending on antidepressant-taking status. In antidepressant-takers, motor cortical excitability in the non-lesioned hemisphere increased, while it decreased compared to sham in those not taking antidepressants. These findings draw attention to the fact that stroke survivors may not respond in the same way to tDCS as healthy individuals, and that antidepressants, and potentially other medications and stroke-related factors, must be considered and their effects investigated before providing tDCS as a clinical treatment. ☐ Finally,
in Aim 3, we showed that anodal tDCS over the lesioned hemisphere did not have any effect on split-belt treadmill locomotor learning and retention in chronic stroke survivors. We speculate that split-belt adaptation may not be sensitive to modulation by tDCS. Future studies should investigate whether tDCS affects other types of locomotor learning. ☐ Overall, this work demonstrates the potential of exercise priming for stroke recovery, and highlights the complexity of tDCS usage in people with chronic stroke. Future studies should focus on how individual differences affect priming in stroke.

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