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.

Tuesday, May 5, 2020

Cognition in the First Year After a Minor Stroke, Transient Ischemic Attack, or Mimic Event and the Role of Vascular Risk Factors

As far as I can tell this is totally useless. Describes a problem, offers no solution. So after this type of event you are completely on your own to figure out your own treatment. And yet you still will have to pay your doctor for nothing.  THIS IS WHY SURVIVORS NEED TO BE IN CHARGE, they wouldn't allow such research to continue unless it provided solutions. 

Cognition in the First Year After a Minor Stroke, Transient Ischemic Attack, or Mimic Event and the Role of Vascular Risk Factors

Korinne Nicolas1,2,3, Christopher Levi2,3,4,5, Tiffany-Jane Evans1, Patricia T. Michie1,2, Parker Magin1,2,3, Debbie Quain1,2, Andrew Bivard3,6 and Frini Karayanidis1,2,3*
  • 1Functional Neuroimaging Laboratory, School of Psychology, University of Newcastle, Newcastle, NSW, Australia
  • 2Brain and Mental Program, Hunter Medical Research Institute, Newcastle, NSW, Australia
  • 3Priority Research Centre for Stroke and Brain Injury, University of Newcastle, Newcastle, NSW, Australia
  • 4University of New South Wales, Sydney, NSW, Australia
  • 5Sydney Partnership for Health, Education, Research and Enterprise, Sydney, NSW, Australia
  • 6Melbourne Brain Center, Royal Melbourne Hospital, University of Melbourne, Melbourne, VIC, Australia
Background: Cognitive impairment following a minor stroke or transient ischemic attack (TIA) is common; however, due to diagnostic difficulties, the prevalence and underlying cause of impairment remain poorly defined. We compared cognition in patients after a minor stroke, TIA, or mimic event at three time points in the first year following the event. We examine whether cognitive impairment occurs following these events and whether this impairment differs based on the event type. Further, we measure whether these findings persist after controlling for age, education, and the presence of vascular risk factors and whether the presence of vascular risk factors, independent of event etiology, is associated with cognitive impairment. Lastly, we investigate whether increased stroke risk, as assessed by the ABCD2, is associated with reduced cognition.
Methods: Medical information, a cognitive screening test, and a measure of executive functioning were collected from 613 patients (123 minor stroke, 175 TIA, and 315 mimics) using phone interviews at three time points in the first year following the event. Linear mixed models were used to determine the effect of event type, vascular risk factors, and predicted stroke risk on cognitive performance while controlling for confounders.
Results: There was no relationship between event type and performance on either cognitive measure. When all confounders are controlled for, performance on the cognitive screening test was uniquely accounted for by the presence of heart failure, myocardial infarction, angina, and hypertension (all p < 0.047), whereas the measure of executive functioning was uniquely accounted for by the presence of hypertension and angina (all p < 0.032). Increased stroke risk also predicted performance on the cognitive screening test and the measure of executive functioning (all p < 0.002).
Conclusions: Our findings indicate that cognitive impairment following a minor stroke or TIA may be attributed to the high prevalence of chronic vascular risk factors in these patients. This highlights the importance of long-term management of vascular risk factors beyond event recovery to reduce the risk of cognitive impairment. Increased stroke risk (i.e., ABCD2 score) was also associated with reduced cognition, suggesting that it may be helpful in signaling the need for further cognitive evaluation and intervention post-event.

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