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.

Wednesday, May 13, 2026

Arterial widening emerges as key driver of small vessel stroke

 How will this change your competent? doctors' protocols on treating stroke? Oh, nothing will happen because there are NO protocols, since your doctor is guessing every step of the way, Hope the guesses are correct because your doctor gets paid regardless!

Arterial widening emerges as key driver of small vessel stroke

A prospective study of 229 patients with lacunar or mild non-lacunar stroke found that large-artery stenosis was not associated with cerebral small-vessel disease (cSVD) or incident infarcts, whereas arterial widening and basilar artery dolichoectasia were strongly linked to lacunar stroke, higher cSVD burden, and progression of brain lesions over 1 year.

The findings, published in Circulation, challenge traditional atherosclerotic paradigms and suggest that intrinsic microvascular pathology plays a central role in cSVD, underscoring the need for mechanism-specific diagnostic and therapeutic strategies in stroke care.

“This study provides strong evidence that lacunar stroke is not caused by fatty blockage of larger arteries, but by disease of the small vessels within the brain itself,” said Joanna Wardlaw, University of Edinburgh’s Institute for Neuroscience and Cardiovascular Disease, Edinburgh, United Kingdom. “Recognising this distinction is crucial, because it explains why conventional treatments like antiplatelet drugs are not as effective for this type of stroke and highlights the urgent need to develop new therapies that target the underlying microvascular damage.”

For the study, the researchers followed 229 patients (mean age, 65.9 years; 57% with lacunar stroke) with serial clinical and MRI assessments over 1 year to evaluate the impact of large-artery stenosis and arterial widening on stroke subtype and cSVD. Large-artery stenosis (≥50%) was present in 20.5% of patients and basilar artery dolichoectasia in 15.7%, with multivariable analyses adjusting for demographic and vascular risk factors.

Results showed that large-artery stenosis was not associated with cSVD markers or incident infarcts and was instead linked to lower odds of lacunar versus non-lacunar stroke (odds ratio [OR] = 0.49), whereas basilar artery dolichoectasia was strongly associated with lacunar stroke (OR = 4.67), higher small-vessel disease burden (OR = 2.57), increased risk of incident infarcts (OR = 2.29; 75% subcortical), and greater progression of white matter hyperintensities over 1 year (β 0.15 per log10 volume increase).

The researchers said that future treatments should target the underlying small vessel damage. Trials such as LACI-3 are now testing whether existing drugs, including cilostazol and isosorbide mononitrate, can protect the brain, reduce further strokes, and help prevent problems with memory, mobility, and dementia after lacunar stroke.

Reference: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.126.079493

SOURCE: University of Edinburgh

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