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, August 25, 2014

Association of Cognitive Functioning, Incident Stroke, and Mortality in Older Adults

I would never sponsor research that doesn't solve one of the problems in stroke, like this one. Man, we're wasting time and money doing these.
http://stroke.ahajournals.org/content/45/9/2563.abstract?etoc
  1. Denis A. Evans, MD
+ Author Affiliations
  1. From the Rush Institute for Healthy Aging, Department of Internal Medicine (K.B.R., D.A.E.), Rush Alzheimer’s Disease Center (N.T.A., R.S.W.), Department of Neurological Sciences (N.T.A., R.S.W.), and Department of Behavioral Sciences (R.S.W.), Rush University Medical Center, Chicago, IL; and Department of Medicine, University of Minnesota, Minneapolis (S.A.E.-R.).
  1. Correspondence to Kumar B. Rajan, PhD, Department of Internal Medicine, Rush University Medical Center, 1645 W Jackson Blvd, Suite 675, Chicago, IL 60612. E-mail kumar_rajan@rush.edu

Abstract

Background and Purpose—Stroke increases the risk of dementia; however, bidirectional association of incident stroke and cognitive decline below dementia threshold is not well established. Also, both cognitive decline and stroke increase mortality risk.
Methods—A longitudinal population-based cohort of 7217 older adults without a history of stroke from a biracial community was interviewed at 3-year intervals. Cognitive function was assessed using a standardized global cognitive score. Stroke was determined by linkage with Medicare claims, and mortality was ascertained via the National Death Index. We used a Cox model to assess the risk of incident stroke, a joint model with a piecewise linear mixed model with incident stroke as a change point for cognitive decline process, and a time-dependent relative risk regression model for mortality risk.
Results—During follow-up, 1187 (16%) subjects had incident stroke. After adjusting for known confounders, lower baseline cognitive function was associated with a higher risk of incident stroke (hazard ratio, 1.61; 95% confidence interval, 1.46–1.77). Cognitive function declined by 0.064 U per year before incident stroke occurrence and 0.122 U per year after stroke, a nearly 1.9-fold increase in cognitive decline (95% confidence interval, 1.78–2.03). Both stroke (hazard ratio, 1.17; 95% confidence interval, 1.08–1.26) and cognitive decline (hazard ratio, 1.90; 95% confidence interval, 1.81–1.98) increased mortality risk.
Conclusions—Baseline cognitive function was associated with incident stroke. Cognitive decline increased significantly after stroke relative to before stroke. Cognitive decline increased mortality risk independent of the risk attributable to stroke and should be followed as a marker for both stroke and mortality.

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