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, February 24, 2022

White matter hyperintensities 1 year after stroke linked to cognitive scores

My doctor told me I had a bunch of white matter hyperintensities but never showed me them on any scan, so I don't know the size, location or any intervention needed, because my doctor knew nothing and did nothing. I have zero cognitive impairment.

 

White matter hyperintensities 1 year after stroke linked to cognitive scores

 

White matter hyperintensity volumes at 1 year strongly correlated with contemporaneous cognitive scores after stroke, according to study results published in Neurology.

“Although numerous studies have assessed baseline [white matter hyperintensities (WMH)] and [modified Rankin Score (mRS)] change after stroke, we are not aware of any studies that have assessed WMH progression and mRS change after stroke, or if WMH progression or severity at specific time-points affects variation between both mRS and cognition post-stroke, despite these measures being collected increasingly by ongoing studies,” Una Clancy, MB, BAO, BCh, of Edinburgh Imaging and the U.K. Dementia Research Institute at the University of Edinburgh, and colleagues wrote. “The present in-depth analysis builds on previous work from the Mild Stroke Study-2 on 1- and 3-year outcomes after stroke, which included predictors of cognition and cognition-mRS relationships but did not assess longitudinal change incorporating all three elements of cognition, mRS and WMH.”

multiple images of a brain scan
Source: Adobe Stock

Clancy and colleagues recruited 264 patients (mean age, 66.9 years; 41.7% women; median mRS = 1) within 3 months of a minor ischemic stroke, defined as NIHSS score less than eight and not expected to lead to an mRS greater than two. Repeat MRI occurred at 1 year and cognitive and mRS assessments at 1 and 3 years. Researchers used longitudinal mixed-effects models to examine change in Addenbrooke’s Cognitive Examination-Revised (ACE-R) and mRS.

At 1 year after stroke, results showed a stronger association between normalized WMH volumes and 1-year ACE-R (beta = –0.259; 95% CI, –0.407 to –0.111 more WMH per 1-point ACE-R decrease) compared with subacute WMH volumes and ACE-R (beta = 0.105; 95% CI, –0.265 to 0.054). Researchers noted an association between 3-year mRS and 3-year ACE-R (beta = –0.272; 95% CI, –0.429 to –0.115), as well as between combined change in baseline-1-year jointly assessed ACE-R/mRS and fluctuating WMH volumes.

“We need to closely track the natural history of dementia post-stroke and determine whether clinically and radiologically distinct dementia subtypes emerge over time,” Clancy and colleagues wrote. “Identifying subgroups will allow future triage of clinical presentations to appropriate services, the development of disease-specific management strategies and targeted entry into future research trials.”

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