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.

Monday, June 25, 2012

Intensive insulin may backfire in acute stroke

Another question for your doctor. Its going to be hard to remember everything you need to tell your doctor right after your stroke so you better hope they are up-to-date.
http://www.news-medical.net/news/20120625/Intensive-insulin-may-backfire-in-acute-stroke.aspx
Intensive control of glucose levels in patients with hyperacute stroke may do more harm than good, results of the randomized INSULINFARCT trial suggest.
The researchers found that infarcts expanded more in patients given intravenous insulin treatment than in those given subcutaneous insulin, despite the intensive regimen providing enhanced glucose control.
Charlotte Rosso (Pitié-Salpêtrière Hospital, Paris, France) and co-workers call the results "disappointing," in view of previous data from animal studies indicating that hyperglycemia contributes to infarct growth.
"We have no explanation for this discrepancy between preclinical and clinical data but they clearly indicate the need for a reappraisal of the pathophysiological models of glucose energy metabolism alterations in the early phase of focal cerebral ischemia," the team writes in Stroke.
Intensive insulin treatment (IIT), delivered intravenously from within 6 hours of stroke symptom onset, resulted in excellent glucose control. In all, 95.4% of 87 patients in the IIT group had average insulin levels below 7 mmol/L over the first 24 hours of treatment, compared with 67.4% of 89 patients who received subcutaneous glucose.
Yet the average infarct growth on diffusion-weighted magnetic resonance imaging (DWI) between baseline and days 1-3 was more than twice that in the than IIT glucose group, at 27.9 versus 10.8 cm3, from similar initial volumes of 11.4 and 10.5 cm3, respectively. The time to initial DWI was nonsignificantly shorter in the IIT than the subcutaneous glucose group, at 132 versus 157 minutes.
Patients' longer-term outcomes were unaffected by insulin treatment, however. At 3 months after stroke, 45.6% of each group had good functional outcomes, defined as a modified Rankin Scale score of 0-2. In addition, 15.6% and 10.0% of the IIT and subcutaneous insulin groups died, respectively, and 38.9% and 35.6%, respectively, had a serious adverse event, defined as symptomatic intracerebral hemorrhage, neurologic worsening, and any event that was life-threatening or extended hospital stay.

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