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, December 19, 2013

Shining a Light on Stroke

This should be continued as a test for the next week so the neuronal cascade of death could be observed and maybe figure out how long it lasts.
Shining a Light on Stroke

  1. Michael J. Minzenberg
  1. Department of Psychiatry, University of California School Of Medicine, Sacramento, CA 95817, USA. Email: michael.minzenberg{at}ucdmc.ucdavis.edu
Stroke remains a common and serious consequence of numerous underlying illnesses and risk factors, such as hypertension and diabetes. Understanding how the brain changes after stroke may help to advance treatments for this illness. To this end, Barth and Mody have developed an improved in vivo model of the anatomy and physiology of ischemic stroke that uses photothrombosis—occlusion of a blood vessel through injection of a dye followed by irradiation—combined with stereotaxic localization (the use of a three-dimensional coordinate system to place the optic fiber) to monitor neurological changes before and after ischemic stroke.
The researchers inserted the optic fiber into the hippocampal artery of mice to isolate blood flow to the hippocampus, a brain region that is important in learning and memory and is particularly vulnerable to ischemic stroke. Blood flow was then selectively blocked in the artery through light activation of a photosensitive dye, rose bengal, which induced blood clot formation. Measuring neuron population activity in the hippocampus before and after this procedure, the authors observed a massive, brief high-frequency epileptiform discharge (HFD) in affected neurons, followed by a negative shift in the baseline electrical potential, which is consistent with neuronal depolarization due to hypoxia (inadequate oxygen). This was followed by a long-lasting decrease in neuron oscillatory activity in the gamma range (30 to 119 Hz), which is generally important to complex cognitive processes such as memory. Interestingly, only the initial HFD was also observed in the contralateral hippocampus, which is often affected by the spread of seizure activity from the other side of the brain.
This work elegantly characterizes the neurophysiological changes that unfold in the wake of stroke, thus setting the stage for elaboration of the biochemical basis and time course of these changes. These findings also suggest that events, such as the HFD and subsequent negative electrical potential, might provide specific targets for therapeutic intervention aimed at attenuating epileptiform activity or other disturbances in electrical activity, ultimately to mitigate the deleterious effects of these processes on the brain. Such knowledge should aid in the development of new therapies designed to restore brain function in stroke survivors.

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