Deans' stroke musings: White matter hyperintensity burden in acute stroke patients differs by ischemic stroke subtype

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, July 8, 2020

White matter hyperintensity burden in acute stroke patients differs by ischemic stroke subtype

Survivors most certainly don't care about this. They want to know what the fuck their doctor is doing to cure this. Useless. THIS is precisely why survivors need to be in charge. They wouldn't approve useless research like this with no intervention to solve the problem.

White matter hyperintensity burden in acute stroke patients differs by ischemic stroke subtype

View ORCID ProfileAnne-Katrin Giese, , Adrian V. Dalca, , Kathleen L. Donahue, Marco Nardin, Robert Irie, Elissa C. McIntosh, Steven J.T. Mocking, Huichun Xu, John W. Cole, Eva Giralt-Steinhauer, , , , Robin Lemmens, View ORCID ProfileJohan Wasselius, Arne Lindgren, View ORCID ProfileTatjana Rundek, Ralph L. Sacco, Reinhold Schmidt, Pankaj Sharma, Agnieszka Slowik, , , Daniel Woo, Steven J. Kittner, Patrick F. McArdle, Braxton D. Mitchell, Jonathan Rosand, View ORCID ProfileJames F. Meschia, Ona Wu, Polina Golland,

First published June 3, 2020, DOI: https://doi.org/10.1212/WNL.0000000000009728

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Abstract

Objective To examine etiologic stroke subtypes and vascular risk factor profiles and their association with white matter hyperintensity (WMH) burden in patients hospitalized for acute ischemic stroke (AIS).

Methods For the MRI Genetics Interface Exploration (MRI-GENIE) study, we systematically assembled brain imaging and phenotypic data for 3,301 patients with AIS. All cases underwent standardized web tool–based stroke subtyping with the Causative Classification of Ischemic Stroke (CCS). WMH volume (WMHv) was measured on T2 brain MRI scans of 2,529 patients with a fully automated deep-learning trained algorithm. Univariable and multivariable linear mixed-effects modeling was carried out to investigate the relationship of vascular risk factors with WMHv and CCS subtypes.

Results Patients with AIS with large artery atherosclerosis, major cardioembolic stroke, small artery occlusion (SAO), other, and undetermined causes of AIS differed significantly in their vascular risk factor profile (all p < 0.001). Median WMHv in all patients with AIS was 5.86 cm³ (interquartile range 2.18–14.61 cm³) and differed significantly across CCS subtypes (p < 0.0001). In multivariable analysis, age, hypertension, prior stroke, smoking (all p < 0.001), and diabetes mellitus (p = 0.041) were independent predictors of WMHv. When adjusted for confounders, patients with SAO had significantly higher WMHv compared to those with all other stroke subtypes (p < 0.001).

Conclusion In this international multicenter, hospital-based cohort of patients with AIS, we demonstrate that vascular risk factor profiles and extent of WMH burden differ by CCS subtype, with the highest lesion burden detected in patients with SAO. These findings further support the small vessel hypothesis of WMH lesions detected on brain MRI of patients with ischemic stroke.