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 5, 2013

Brain Imaging and Cognitive Predictors of Stroke and Alzheimer Disease in the Framingham Heart Study

You'll need to have your doctor analyze this and tell you what  needs to be done to prevent another stroke and dementia. You do expect your doctor to know about this before you bring it up? Don't you? Or are you giving them another pass like the non-knowledge they imparted about your stroke recovery?
http://stroke.ahajournals.org/content/early/2013/08/06/STROKEAHA.113.000947.abstract

  1. Sudha Seshadri, MD, DM
+ Author Affiliations
  1. From the Department of Neurology, Boston University School of Medicine, Boston, MA (G.W., A.S.B., R.A., P.A.W., S.S.); The Framingham Heart Study, Boston, MA (G.W., A.S.B., R.A., P.A.W., S.S.); Department of Biostatistics, Boston University School of Public Health, Boston, MA (A.S.B.); and the Department of Neurology, University of California at Davis, Sacramento, CA (C.D.).
  1. Correspondence to Sudha Seshadri, MD, DM, Department of Neurology, Boston University School of Medicine, B602, 72 East Concord St, Boston, MA 02118. E-mail suseshad@bu.edu

Abstract

Background and Purpose—Exposure to vascular risk factors has a gradual deleterious effect on brain MRI and cognitive measures. We explored whether a pattern of these measures exists that predicts stroke and Alzheimer disease (AD) risk.
Methods—A cognitive battery was administered to 1679 dementia and stroke-free Framingham offspring (age, >55 years; mean, 65.7±7.0) between 1999 and 2004; participants were also free of other neurological conditions that could affect cognition and >90% also had brain MRI examination. We related cognitive and MRI measures to risks of incident stroke and AD ≤10 years of follow-up. As a secondary analysis, we explored these associations in The Framingham Heart Study original cohort (mean age, 67.5±7.3 and 84.8±3.3 years at the cognitive assessment and MRI examination, respectively).
Results—A total of 55 Offspring participants sustained strokes and 31 developed AD. Offspring who scored <1.5 SD below predicted mean scores, for age and education, on an executive function test, had a higher risk of future stroke (hazard ratio [HR], 2.27; 95% confidence interval [CI], 1.06–4.85) and AD (HR, 3.60; 95% CI, 1.52–8.52); additional cognitive tests also predicted AD. Participants with low (<20 percentile) total brain volume and high (>20 percentile) white matter hyperintensity volume had a higher risk of stroke (HR, 1.97; 95% CI, 1.03–3.77 and HR, 2.74; 95% CI, 1.51–5.00, respectively) but not AD. Hippocampal volume at the bottom quintile predicted AD in the offspring and original cohorts (HR, 4.41; 95% CI, 2.00–9.72 and HR, 2.37; 95% CI, 1.12–5.00, respectively). A stepwise increase in stroke risk was apparent with increasing numbers of these cognitive and imaging markers.
Conclusions—Specific patterns of cognitive and brain structural measures observed even in early aging predict stroke risk and may serve as biomarkers for risk prediction.

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