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.

Sunday, December 23, 2012

ebselen - neuroprotective treatment?

Having seen that this was supposed to be a stroke drug. I decided to write about it since I had never heard about it. Ask your doctor whatever happened to this.

ebselen  - neuroprotective treatment?

 


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From 1998 so your doctor should be familiar with this  

Ebselen in Acute Ischemic Stroke A Placebo-Controlled, Double-blind Clinical Trial

treatment within 48 hours.
ConclusionsEarly treatment with ebselen improved the outcome of acute ischemic stroke. Ebselen may be a promising neuroprotective agent. 

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From 2001 

Ebselen Protects Both Gray and White Matter in a Rodent Model of Focal Cerebral Ischemia

Results Ebselen significantly reduced the volume of gray matter damage in the cerebral hemisphere (by 53.6% compared with vehicle, P less than 0.02). Axonal damage was reduced by 46.8% (P less than 0.002) and the volume of oligodendrocyte pathology was reduced by 60.9% (P less than 0.005). The neurological deficit score was reduced by 40.7% (P less than 0.05) and the volume of tissue immunopositive for 8-OHdG and 4-HNE was reduced by 65% (P less than 0.002) and 66% (P less than 0.001), respectively, in ebselen-treated animals.
Conclusions Delayed (2-hour) treatment with intravenous ebselen significantly reduced gray and white matter damage and neurological deficit associated with transient ischemia. The reduction in tissue displaying evidence of oxidative stress suggests that the major mechanism of action is attenuation of free radical damage. 
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From 2003

Ebselen, a Seleno-Organic Antioxidant, Is Neuroprotective After Embolic Strokes in Rabbits - Synergism With Low-Dose Tissue Plasminogen Activator

Conclusions— This study indicates that ebselen may be neuroprotective when administered shortly after an embolic stroke, but the time- and dose-response analyses suggest that it has a narrow therapeutic window. Nevertheless, ebselen may be beneficial if administered concomitantly with a thrombolytic because it significantly enhanced the neuroprotective activity of low-dose tPA.  

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From 1999 - 13 years - what happened to it?


Ebselen in Acute Middle Cerebral Artery Occlusion: A Placebo-Controlled, Double-Blind Clinical Trial

Abstract:
A randomized, double-blind, placebo-controlled trial of ebselen was conducted in patients with complete occlusion of the middle cerebral artery. Ebselen or placebo granules suspended in water (150 mg b.i.d.) were orally administered within 12 h of onset and continued for 2 weeks. The major end points were the maximum volume of cerebral infarct measured on follow-up computed tomography and the Glasgow Outcome Scale score at 1 month. One hundred and five patients were enrolled in this trial. Although the intent-to-treat analysis of 99 patients (43 given ebselen and 56 given placebo) did not reach statistical significance in reduction of the infarct volume (p = 0.099), the protocol-compatible analysis of 83 patients with complete occlusion of the middle cerebral artery (34 given ebselen and 49 given placebo) determined a significant reduction using ebselen treatment (p = 0.034). A good outcome was seen in approximately 15% more patients from the ebselen group, but the difference between the 2 groups was not significant (p = 0.129). There was a corresponding significant reduction in the volume of cerebral infarct and an improvement in the outcome of patients who started treatment within 6 h of onset. These findings may suggest that ebselen protected the brain from ischemic damage in the acute stage.


 

 

 

 

 

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