ESOC 2024: “Cognition and Vascular Cognitive Impairment”

 Great research but useless for getting survivors recovered! The goal of stroke research is survivor recovery! DO YOU NOT UNDERSTAND?

What do survivors need to do to prevent this cognitive decline? That's the research needed!

ESOC 2024: “Cognition and Vascular Cognitive Impairment”

• Bastien Rioux, MD, MSc @B_Rioux

Originally published May 31, 2024 10.1161/blog.20240531.611984

European Stroke Organisation Conference
May 15–17, 2024

Session: Cognition and Vascular Cognitive Impairment

Seven researchers shared their work during this well-attended session on cognition and vascular cognitive impairment co-chaired by Sandra Billinger (University of Kansas Medical Center, Kansas City, United States) and Aleksandra M. Pavlovic (University of Belgrade, Belgrade, Serbia) at ESOC 2024. In this blog post, I comment on three take-home messages that are relevant to researchers and clinicians in stroke medicine.

Two researchers presented results that support a role for “strategic” white matter lesions in cognition using data from the Meta VCI Map consortium. Floor De Kort (UMC Utrecht, Utrecht, the Netherlands) first presented on the clinical relevance of white matter hyperintensity location in poststroke cognitive function. In this work integrating nine ischemic stroke cohorts and a total of 1,568 patients, De Kort identified certain locations, such as the left anterior thalamic radiation, which have differential associations with cognitive performance. Marvin Petersen (UMC Hamburg-Eppendorf, Hamburg, Germany) next presented a prediction model of cognitive performance using white matter hyperintensity dysconnectivity. In this study, Petersen used lesion network mapping in 3,485 individuals attending a memory clinic to improve the prediction of cognitive performance. Lesion network mapping was performed to quantify dysconnectivity, and Ridge regression was used to predict cognition across four cognitive domains. Lesion network mapping improved prediction of attention, processing speed, and verbal memory (but not language) over other available clinical variables. In summary, these two projects used large data sets of brain imaging and cognitive tests to demonstrate the clinical relevance of the location — and not just raw volume — of white matter lesions.

Marion Buckwalter (Stanford School of Medicine, Stanford, United States) next presented a coherent story on the effect of blocking the VCAM1-VLA4 axis on cognitive decline in a mouse model of infarct-induced neurodegeneration. Buckwalter presented data from a mouse model of infarct-induced neurodegeneration which is associated with lymphocytic infiltrates, blood-brain barrier leakiness, and loss of pericyte coverage. The use of VCAM1 and VLA4 blocking antibodies in this animal model prevented infarct-induced neurodegeneration, reduced blood-brain barrier leakiness, and improved pericyte coverage. These results support the promising role of blocking lymphocyte trafficking across the blood-brain barrier to prevent poststroke cognitive impairment,(Solve this problem, don't just tell us it exists!) and underline the need for additional studies in clinical trials after further exploration in translational studies.

Joanna Wardlaw (Centre for Clinical Brain Sciences, Edinburgh, United Kingdom) finally presented on the incidence, risk factors, and trajectories of cognitive impairment after stroke in the R4VaD study. Wardlaw summarized the R4VaD study, a UK-wide prospective longitudinal observational cohort of patients presenting at hospital stroke services within six weeks of stroke or transient ischemic attack. Participants were assessed through blinded central follow-up for up to two years, and cognition was rated on the Diagnostic and Statistical Manual of Mental Disorders (DSM)-V ordinal cognitive impairment scale. Age, pre-morbid modified Rankin Scale (mRS) score, baseline Montreal Cognitive Assessment (MoCA) score, and hypertension were among the top predictors of cognition at two years. These results are important as they may be used to stratify the risk of cognitive decline(Why aren't you solving this problem? Describing it does nothing.) after stroke in future interventional studies.