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, September 17, 2015

Phosphodiesterase inhibition as a therapeutic target for brain ischemia.

Another interesting piece of research needing followup. But that won't occur until we destroy the existing failures of stroke associations. What a great stroke association would look like.
 httpha://europepmc.org/abstract/med/26350339

Highlight Terms
Preclinical studies have shown that phosphodiesterase inhibitors (PDE-Is) represent a potential pharmacological strategy for the treatment of brain ischemia sequelea. PDE-Is 3, 4 and 5 have been tested in several brain ischemia models. All the three PDE-Is after acute or chronic treatment decreased the degree of neurodegeneration and most of them improved functional recovery after brain injury by specific cellular and molecular mechanisms mainly involving an anti-inflammatory and/or neuroprotection action. In contrast to the large number of investigations using PDE-Is in experimental brain ischemia research, the number of clinical studies is still limited. The purpose of this review is to summarize the data currently available on the effects of PDE-Is in experimental models of cerebral ischemia.

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