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, December 22, 2022

Association of Carotid Plaque and Flow Velocity With White Matter Integrity in a Middle-aged to Elderly Population

I can't tell what this means. I had 80% carotid blockage that completely closed up post stroke(glad that occurred).

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.

 

Association of Carotid Plaque and Flow Velocity With White Matter Integrity in a Middle-aged to Elderly Population

David Leander Rimmele, Elina Larissa Petersen, Eckhard Schlemm, Simon S. Kessner, Marvin Petersen, Carola Mayer, Bastian Cheng, Tanja Zeller, Christoph Waldeyer, Christian-Alexander Behrendt, Christian Gerloff, Götz Thomalla

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Abstract

Background and Objectives It is uncertain whether there is an association of carotid plaques (CPs) and flow velocities with peak width mean diffusivity (PSMD) and white matter hyperintensities (WMH) independent of shared risk factors. We aimed to study this association controlling for biomarkers of inflammation and cardiac dysfunction and typical cardiovascular risk factors and spatial distribution.

Methods We included participants from the population-based Hamburg City Health Study, recruiting citizens between 45 and 74 years of age. Medical history was obtained from structured interviews and extended laboratory tests, physical examinations, MRI of the head, echocardiography, and abdominal and carotid ultrasound were performed. We performed multivariable regression analysis with PSMD and periventricular, deep, and total volume of WMH (pWMH, dWMH, tWMH) as dependent variables. PSMD was calculated as the difference between the 95th and 5th percentiles of MD values on the white skeleton in standard space. Volumes of WMH were determined by the application of a manually trained k-nearest neighbor segmentation algorithm. WMH measured within a distance of 1 cm from the surface of the lateral ventricles were defined as pWMH and above 1 cm as dWMH.

Results Two thousand six hundred twenty-three participants were included. The median age was 65 years, and 56% were women. Their median tWMH was 946 mm3(IQR:419, 2,164), PSMD 2.24 mm2/s × 10−4 (IQR: 2.04, 2.47), peak systolic velocity (PSV) of internal carotid arteries 0.70m/second (IQR:0.60, 0.81), and 35% had CPs. Adjusted for age, sex, high-sensitive CRP, NT-proBNP, and commonly measured cardiovascular risk and systemic hemodynamic factors, both CPs (B = 0.15; CI: 0.04, 0.26; p = 0.006) and low PSV (B = −0.49; CI: −0.87, −0.11; p = 0.012) were significantly associated with a higher tWMH and PSMD. Low PSV (B = −0.48; CI: −0.87, −0.1; p = 0.013) was associated with pWMH and the presence of CP with pWMH (B = 0.15; CI: 0.04, 0.26; p = 0.008) and dWMH (B = 0.42; CI: 0.11, 0.74; p < 0.009).

Discussion Low PSV and CP are associated with WMH and PSMD independent of cardiovascular risk factors and biomarkers of inflammation and cardiac dysfunction. This points toward pathophysiologic pathways underlying both large and small vessel disease beyond the common cardiovascular risk profile.

Trial Registration Information The trial was submitted at clinicaltrials.gov, under NCT03934957 on January 4, 2019. The first participant was enrolled in February 2016.

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