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.

Showing posts with label cerebral small vessel disease. Show all posts
Showing posts with label cerebral small vessel disease. Show all posts

Saturday, May 31, 2025

Too much time in bed may harm brain health after TIA, mild stroke

 It it your doctor's COMPLETE RESPONSIBILITY TO GET YOU RECOVERED so you don't do this. You doctor needs to solve the problem instead of just telling you not to lie in bed. That would be a sign of an incompetent doctor! NO solutions!

Too much time in bed may harm brain health after TIA, mild stroke

After a mild stroke or transient ischaemic attack (TIA), longer in-bed time and sleep duration were linked to greater small vessel disease burden and poorer cognitive performance, underscoring the potential role of sleep patterns as modifiable risk factors for brain health after a stroke, according to a study published in the journal Neurology.

“These results show that disturbed sleep may be a marker of adverse brain health, even for people with mild strokes or TIAs,” said Joanna M. Wardlaw, MD, University of Edinburgh, Edinburgh, United Kingdom. “While many people know that a lack of sleep can lead to health issues, less is known about the effects of sleeping longer at night or spending a long time in bed trying to make up for having trouble sleeping --whether people are doing this consciously or not.”

The study involved 422 people (65.6 ± 11.8 years; 67% male) from Edinburgh and Hong Kong with an average age of 66 years who had a mild stroke or a TIA (NIHSS <7). Within 1 to 3 months after the stroke, cerebral small vessel disease was assessed on MRI, cognitive performance was assessed using Montreal Cognitive Assessment (MoCA), and sleep quality was analysed using a structured sleep questionnaire at baseline visit.

Longer in-bed time was independently associated with greater global small vessel disease and Fazekas periventricular white matter hyperintensity burden, and with lower total MoCA score after covariate adjustment. Longer sleep duration was independently associated with presence of cerebral microbleeds.

“More research is needed to confirm these findings and also to look at whether prolonged sleep has negative effects on people who have never had a stroke or TIA,” Dr. Wardlaw said. “Of course, research is also needed on whether improving people’s sleep patterns after stroke could ward off some of these possible detrimental effects.”

The researchers noted that their results should be interpreted with caution because they only examined baseline cross-sectional data, which cannot establish causal relationships.

“Some relationships between sleep, small vessel disease, and cognition may differ in a longitudinal context and at different time points after stroke,” they stated.

Reference: https://www.neurology.org/doi/10.1212/WNL.0000000000213734

SOURCE: American Academy of Neurology

Monday, February 3, 2025

Cerebral small vessel disease linked to cognitive deficits in older adults

 Your competent? doctor needs to address and fix this problem before it causes another stroke.
Cerebral small vessel disease includes various conditions in which small blood vessels in the brain are damaged, often causing stroke.

Cerebral small vessel disease linked to cognitive deficits in older adults

Key takeaways:

  • Differences in neuropsychological testing were not significant at a 4-year follow up.
  • Logical memory function in all participants increased over the full 8-year follow-up interval.

In a small cohort of adults in South Korea, the presence of cerebral small vessel disease was associated with color reading and visual deficits, but not memory, across an 8-year follow-up interval, according to new research.

“Although [the] majority of [cerebral small vessel disease (cSVD)] manifests sub-clinically, it is a major source of cognitive impairment during aging process leading to mild cognitive impairment and dementia,” Ali Tanweer Siddiquee, MPH, of the Institute of Human Genomic Study and College of Medicine at Korea University Ansan Hospital, and colleagues wrote in The Lancet Regional Health. “Cognitive dysfunction caused by cSVD may account for two-thirds of all vascular dementia.”Brain illustration

According to new research from South Korea, cerebral small vessel disease was associated with a decline in certain cognitive functions across an 8-year follow up for individuals aged 49 to 79 years. Image: Adobe Stock

Siddiquee and colleagues examined the longitudinal relationship between cSVD and cognitive decline in adults from their middle age to their elderly years.

Their population-based, prospective cohort study collected data from the Korean Genome and Epidemiology Study, commenced in South Korea in 2001.

The study included 2,454 individuals aged 40 to 79 years, free of dementia and other cerebrovascular conditions. Participants underwent both MRI and a comprehensive neuropsychological battery at baseline between 2011 and 2014. All participants were subjected to the same testing in two separate 4-year cycles (2015–2018 and 2019–2022), during which cognitive function testing analysis was also conducted. The neuropsychological battery included verbal and visual memory, verbal fluency, Digit Symbol–coding, Trail Making Test–A, and Stroop Tests.

Small vessel disease was defined by the presence of age-related white matter change, lacunes and cerebral microbleeds on MRI at baseline, with the main outcomes defined as adjusted mean differences of cognitive test performances by cSVD groups over time.

Covariates that were likely to exert influence over both cSVD and cognition, measured at baseline, included lifestyle, health, exercise, substance use habits, BMI and blood pressure.

Out of 2,454 participants, 908 registered signs of cSVD via MRI at baseline. These participants were aged approximately 3 years older than those who did not have cSVD.

Scores were not significantly different among the cognitive test battery, save for Trail Making Test–A, at baseline among cSVD groups.

By the 8-year follow-up, participants without cSVD performed significantly better than their cSVD counterparts in Stroop–color reading (mean difference = 1.19; 95% CI, 0.02–2.36) and visual reproduction-recognition (mean difference = 0.11; 95% CI, 0.01–0.21)].

Siddiquee and colleagues noted, however, that significant worsening between the groups was not observed at a 4-year follow up.

While no differential changes were recorded among cognitive testing by cSVD groups, the researchers observed a decrease over time in logical memory (Story Recall Tests) and decrease in Stroop-word reading in both cSVD groups, which were nearly identical.

Data additionally showed that the presence of cSVD within the brain was mostly in the frontal lobe followed by basal ganglia area.

“The presence of cSVD may be an important risk factor of cognitive decline, especially executive functioning, and thus, early prevention of cSVD would help preserving cognitive function in a normal aging population,” Siddiquee and colleagues wrote.

Monday, April 8, 2024

Covert Cerebrovascular Changes in People With Heart Disease

Now if we had any brains at all in the stroke medical world this research would trigger more research to find ways to prevent silent brain infarction (SBI) and cerebral small vessel disease (CSVD). But there is NO leadership in stroke.

Covert Cerebrovascular Changes in People With Heart Disease


A Systematic Review and Meta-Analysis


  • Abstract

    Background and Objectives

    To determine the prevalence of silent brain infarction (SBI) and cerebral small vessel disease (CSVD) in adults with atrial fibrillation (AF), coronary artery disease, heart failure or cardiomyopathy, heart valve disease, and patent foramen ovale (PFO), with comparisons between those with and without recent stroke and an exploration of associations between heart disease and SBI/CSVD.

    Methods

    Medline, Embase, and Cochrane Library were systematically searched for hospital-based or community-based studies reporting SBI/CSVD in people with heart disease. Data were extracted from eligible studies. Outcomes were SBI (primary) and individual CSVD subtypes. Summary prevalence (95% confidence intervals [CIs]) were obtained using random-effects meta-analysis. Pooled prevalence ratios (PRs) (95% CI) were calculated to compare those with heart disease with available control participants without heart disease from studies.

    Results

    A total of 221 observational studies were included. In those with AF, the prevalence was 36% (31%–41%) for SBI (70 studies, N = 13,589), 25% (19%–31%) for lacune (26 studies, N = 7,172), 62% (49%–74%) for white matter hyperintensity/hypoattenuation (WMH) (34 studies, N = 7,229), and 27% (24%–30%) for microbleed (44 studies, N = 13,654). Stratification by studies where participants with recent stroke were recruited identified no differences in the prevalence of SBI across subgroups (phomogeneity = 0.495). Results were comparable across participants with different heart diseases except for those with PFO, in whom there was a lower prevalence of SBI [21% (13%–30%), 11 studies, N = 1,053] and CSVD. Meta-regressions after pooling those with any heart disease identified associations of increased (study level) age and hypertensives with more SBIs and WMH (pregression <0.05). There was no evidence of a difference in the prevalence of microbleed between those with and without heart disease (PR [95% CI] 1.1 [0.7–1.7]), but a difference was seen in the prevalence of SBI and WMH (PR [95% CI] 2.3 [1.6–3.1] and 1.7 [1.1–2.6], respectively).

    Discussion

    People with heart disease have a high prevalence of SBI (and CSVD), which is similar in those with vs without recent stroke. More research is required to assess causal links and implications for management.

    Trial Registration Information

    PROSPERO CRD42022378272 (crd.york.ac.uk/PROSPERO/).

    Get full access to this article

    Wednesday, March 13, 2024

    Cardiovascular Management in Asymptomatic (Silent) Cerebral Microbleeds and Suspected Cerebral Amyloid Angiopathy

    FYI, for your doctor to understand and implement.

    Cardiovascular Management in Asymptomatic (Silent) Cerebral Microbleeds and Suspected Cerebral Amyloid Angiopathy

    Originally publishedhttps://doi.org/10.1161/STROKEAHA.123.044167Stroke. 2024;0

    Cerebral microbleeds (CMBs) detected on blood-sensitive magnetic resonance imaging sequences are usually a sign of an underlying cerebral small vessel disease such as sporadic cerebral amyloid angiopathy or sporadic nonamyloid small vessel pathology (eg, arteriolosclerosis). Much of the enduring interest in CMBs relates to their high prevalence (partly due to the widespread use of magnetic resonance imaging) in the context of stroke, cognitive impairment and in healthy individuals, and the clinical uncertainties created about the safety of antithrombotic medications due to their association with both future hemorrhagic and ischemic stroke. Historically, the research literature overwhelmingly emphasized the future hemorrhagic risk associated with CMBs, potentially leading to unnecessary withholding of treatments proven effective at preventing thrombosis, such as anticoagulants in patients with atrial fibrillation who happened to have some microbleeds. The lack of strong guidelines in this area contributes to wide variation in clinical practice. In this article, we critically review and discuss the implications of silent CMBs and cortical superficial siderosis (ie, without symptomatic intracerebral hemorrhage) in different clinical settings: the general population, patients with ischemic stroke, and the memory clinic. Emerging evidence, albeit not from randomized controlled trials, suggests that in most patients, CMBs alone should not prevent the use of antithrombotics or anticoagulants for stroke prevention, when they are otherwise indicated. Where possible, we provide specific suggestions for clinical care grounded in both the limited available literature and our personal clinical practice.

    Tuesday, March 12, 2024

    Relationship of Perivascular Space Markers With Incident Dementia in Cerebral Small Vessel Disease

    Telling us of a problem with no suggested solution doesn't help stroke survivors one bit! What will your competent? doctor do to prevent this problem from happening?

    Or don't you have a functioning stroke doctor? RUN AWAY!

     

    Relationship of Perivascular Space Markers With Incident Dementia in Cerebral Small Vessel Disease

    Originally publishedhttps://doi.org/10.1161/STROKEAHA.123.045857Stroke. 2024;0

    BACKGROUND:

    Recent studies, using diffusion tensor image analysis along the perivascular space (DTI-ALPS), suggest impaired perivascular space (PVS) function in cerebral small vessel disease, but they were cross-sectional, making inferences on causality difficult. We determined associations between impaired PVS, measured using DTI-ALPS and PVS volume, and cognition and incident dementia.

    METHODS:

    In patients with lacunar stroke and confluent white matter hyperintensities, without dementia at baseline, recruited prospectively in a single center, magnetic resonance imaging was performed annually for 3 years, and cognitive assessments, including global, memory, executive function, and processing speed, were performed annually for 5 years. We determined associations between DTI-ALPS and PVS volume with cerebral small vessel disease imaging markers (white matter hyperintensity volume, lacunes, and microbleeds) at baseline and with changes in imaging markers. We determined whether DTI-ALPS and PVS volume at baseline and change over 3 years predicted incident dementia. Analyses were controlled for conventional diffusion tensor image metrics using 2 markers (median mean diffusivity [MD] and peak width of skeletonized MD) and adjusted for age, sex, and vascular risk factors.

    RESULTS:

    A total of 120 patients, mean age 70.0 years and 65.0% male, were included. DTI-ALPS declined over 3 years, while no change in PVS volume was found. Neither DTI-ALPS nor PVS volume was associated with cerebral small vessel disease imaging marker progression. Baseline DTI-ALPS was associated with changes in global cognition (β=0.142, P=0.032), executive function (β=0.287, P=0.027), and long-term memory (β=0.228, P=0.027). Higher DTI-ALPS at baseline predicted a lower risk of dementia (hazard ratio, 0.328 [0.183–0.588]; P<0.001), and this remained significant after including median MD as a covariate (hazard ratio, 0.290 [0.139–0.602]; P<0.001). Change in DTI-ALPS predicted dementia conversion (hazard ratio, 0.630 [0.428–0.964]; P=0.048), but when peak width of skeletonized MD and median MD were entered as covariates, the association was not significant. There was no association between baseline PVS volume, or PVS change over 3 years, and conversion to dementia.

    CONCLUSIONS:

    DTI-ALPS predicts future dementia risk in patients with lacunar strokes and confluent white matter hyperintensities. However, the weakening of the association between change in DTI-ALPS and incident dementia after controlling for peak width of skeletonized MD and median MD suggests part of the signal may represent conventional diffusion tensor image metrics. PVS volume is not a predictor of future dementia risk.

    Saturday, March 9, 2024

    High‐Sensitivity Cardiac Troponin T and Cognitive Function Over 12 Months After Stroke—Results of the DEMDAS Study

     I got nothing out of this. What meaning is there to this? Should doctors be doing something based on this? The mentors and senior researchers completely failed at their job of making sure research is useful.

    High‐Sensitivity Cardiac Troponin T and Cognitive Function Over 12 Months After Stroke—Results of the DEMDAS Study

    and for the DEMDAS investigators *
    Originally publishedhttps://doi.org/10.1161/JAHA.123.033439Journal of the American Heart Association. 2024;0:e033439

    Abstract

    Background

    Subclinical myocardial injury in form of hs‐cTn (high‐sensitivity cardiac troponin)  levels has been associated with cognitive impairment and imaging markers of cerebral small vessel disease (SVD) in population‐based and cardiovascular cohorts. Whether hs‐cTn is associated with domain‐specific cognitive decline and SVD burden in patients with stroke remains unknown.

    Methods and Results

    We analyzed patients with acute stroke without premorbid dementia from the prospective multicenter DEMDAS (DZNE [German Center for Neurodegenerative Disease]‐Mechanisms of Dementia after Stroke) study. Patients underwent neuropsychological testing 6 and 12 months after the index event. Test results were classified into 5 cognitive domains (language, memory, executive function, attention, and visuospatial function). SVD markers (lacunes, cerebral microbleeds, white matter hyperintensities, and enlarged perivascular spaces) were assessed on cranial magnetic resonance imaging to constitute a global SVD score. We examined the association between hs‐cTnT (hs‐cTn T levels) and cognitive domains as well as the global SVD score and individual SVD markers, respectively. Measurement of cognitive and SVD‐marker analyses were performed in 385 and 466 patients with available hs‐cTnT levels, respectively. In analyses adjusted for demographic characteristics, cardiovascular risk factors, and cognitive status at baseline, higher hs‐cTnT was negatively associated with the cognitive domains “attention” up to 12 months of follow‐up (beta‐coefficient, −0.273 [95% CI, −0.436 to −0.109]) and “executive function” after 12 months. Higher hs‐cTnT was associated with the global SVD score (adjusted odds ratio, 1.95 [95% CI, 1.27–3.00]) and the white matter hyperintensities and lacune subscores.

    Conclusions

    In patients with stroke, hs‐cTnT is associated with a higher burden of SVD markers and cognitive function in domains linked to vascular cognitive impairment.

    Registration

    URL: https://www.clinicaltrials.gov; Unique identifier: NCT01334749.

    Thursday, October 26, 2023

    Relationship of arterial stiffness and baseline vascular burden with new lacunes and microbleeds: A longitudinal cohort study

    I bet your doctor doesn't have a protocol for testing your arterial stiffness and certainly not one for  reducing it. 

    So if you have arterial stiffness what the fuck is your doctor's protocol to address the problem? Maybe something in one of these?

    Or does your doctor incompetently not even know about testing for and correcting this problem?

     

    Relationship of arterial stiffness and baseline vascular burden with new lacunes and microbleeds: A longitudinal cohort study

    Abstract

    Introduction:

    Arterial stiffness may have a significant impact on the development of cerebral small vessel disease (cSVD).

    Patients and methods:

    We obtained pulse wave velocity (24-h PWV) by means of ambulatory blood pressure monitoring (ABPM) in patients with a recent small subcortical infarct (RSSI). Patients with known cardiac or arterial embolic sources were excluded. Lacunes, microbleeds, white matter hyperintensities and enlarged perivascular spaces at baseline were assessed in a brain MRI and included in a cSVD score. A follow-up MRI was obtained 2 years later and assessed for the appearance of new lacunes or microbleeds. We constructed both unadjusted and adjusted models, and subsequently selected the optimal models based on the area under the curve (AUC) of the predicted probabilities.

    Results:

    Ninety-two patients (mean age 67.04 years, 69.6% men) were evaluated and 25 had new lacunes or microbleeds during follow-up. There was a strong correlation between 24-h PWV and age (r = 0.942, p < 0.001). cSVD was associated with new lacunes or microbleeds when adjusted by age, 24-h PWV, NT-proBNP and hypercholesterolemia (OR 2.453, CI95% 1.381–4.358). The models exhibiting the highest discrimination, as indicated by their area under the curve (AUC) values, were as follows: 1 (AUC 0.854) – Age, cSVD score, 24-h PWV, Hypercholesterolemia; 2 (AUC 0.852) – cSVD score, 24-h PWV, Hypercholesterolemia; and 3 (AUC 0.843) – Age, cSVD score, Hypercholesterolemia.

    Conclusions:

    cSVD score is a stronger predictor for cSVD progression than age or hemodynamic parameters in patients with a RSSI.

    Tuesday, May 30, 2023

    Examining first treatment for strokes linked to dementia

    Since you already have dementia when you get this stroke you'll have to hope like hell that your doctors are up-to-date on this treatment because you won't be able to inform them of this. Or better yet ask your doctor now to follow this since results are not expected for 5 years.

    Examining first treatment for strokes linked to dementia

    People who experience a type of stroke linked with nearly half of all dementias could be treated for the first time by repurposing two cheap and common drugs, a trial shows.

    Researchers found that isosorbide mononitrate and cilostazol, which are already used to treat other heart and circulatory diseases, can safely improve the debilitating outcomes people experience after lacunar stroke.

    The two drugs, which were found to be even more effective when used in combination, could be available as a treatment for lacunar strokes within five years, if the results are confirmed in further trials, experts say.

    Lacunar strokes affect at least 35,000 people in the UK each year. They are caused by cerebral small vessel disease, where small blood vessels deep within the brain become damaged and stop working properly. Small vessel disease is also a common cause of cognitive impairment and dementia.

    The strokes can be distressing as people may develop problems with their thinking and memory, movement, and even dementia. There are currently no specific effective treatments.

    The trial, led by the Universities of Edinburgh and Nottingham and the UK Dementia Research Institute, involved 363 people who had experienced a lacunar stroke.

    As well as their standard stroke prevention treatment, for one year participants took either isosorbide mononitrate or cilostazol individually, both drugs together, or neither.

    The trial, funded by the British Heart Foundation, investigated cilostazol and isosorbide mononitrate as they possibly improve the function of the inner lining of blood vessels, which researchers believe play a role in small vessel disease.

    Participants that took both drugs were nearly 20 per cent less likely to have problems with their thinking and memory compared to the group that did not take either drug. They were also more independent and reported a better quality of life.

    In addition, those who took isosorbide mononitrate were less likely to have had further strokes at one year than those who did not take the drug.

    Taken on their own, isosorbide mononitrate also improved thinking and memory skills, and quality of life, while cilostazol improved independence and mood. These effects were strengthened when the two drugs were taken together, researchers say.

    The team is now planning to test these drugs in a larger four-year clinical trial, which they hope to start by the end of 2023. They are also looking to test whether the drugs are effective in different conditions linked to small vessel disease, such as vascular cognitive impairment and dementia.

    Now we understand more about what is triggering these small vessel strokes to attack the brain, we've been able to focus our efforts on treatments that can put a halt to this damage. We need to confirm these results in larger trials before either drug can be recommended as a treatment. However, as these drugs are already widely available for other circulatory disorders, and inexpensive, it shouldn't take too long to move our findings from research into everyday clinical practice."

    Joanna Wardlaw, Professor and Chair, Applied Neuroimaging, University of Edinburgh

    Professor Sir Nilesh Samani, Medical Director at the British Heart Foundation, said: "These promising findings provide a long-awaited positive step towards the first treatments becoming available for lacunar strokes, offering much needed hope for thousands of people. Lacunar strokes are not the only way that cerebral small vessel disease can affect someone. These findings also open new avenues of research into other conditions related to small vessel disease, such as vascular dementia."

    Source:
    Journal reference:

    Wardlaw, J. M., et al. (2023) The Lacunar Intervention Trial-2 (LACI-2) Randomized Clinical Trial. JAMA. doi.org/10.1001/jamaneurol.2023.1526.

    Thursday, March 30, 2023

    Echocardiographic correlates of MRI imaging markers of cerebral small-vessel disease in patients with atrial-fibrillation-related ischemic stroke

     

    I see nothing here that is going to get survivors recovered or EXACTLY prevent dementia. So I would fire everyone involved. Solve the problems of stroke survivors, not just tell us they exist.

    Echocardiographic correlates of MRI imaging markers of cerebral small-vessel disease in patients with atrial-fibrillation-related ischemic stroke

    Kaili Ye1, Wendan Tao1, Zhetao Wang2, Dayan Li3, Mangmang Xu1, Junfeng Liu1 and Ming Liu1*
    • 1Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, China
    • 2Department of Radiology, West China Hospital, Sichuan University, Chengdu, China
    • 3Cardiac Ultrasound Office, Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China

    Background and objectives: Atrial fibrillation (AF) has been linked to dementia risk, partly explained by cerebral small vessel disease (CSVD). Since AF and cardiovascular comorbidities were associated with cardiac dysfunction, we aimed to determine the association between echocardiographic parameters and neuroimaging markers of CSVD in patients with AF-related ischemic stroke.

    Methods: This cross-sectional study enrolled patients with AF-related ischemic stroke from March 2013 to December 2019 who underwent transthoracic echocardiography and brain 3T MRI, including T1, T2, Flair, and SWI imaging sequences. We assessed the presence of lacunes and cerebellar microbleeds (CMBs), the severity of white matter hyperintensity (WMH) scored by the Fazekas scale (0-6), and the severity of enlarged perivascular spaces (EPVS) in basal ganglia (BG) and centrum semiovale (CSO) classified into three categories (0–10, 10–25, and >25). CSVD burden was rated on a 0-to-4 ordinal scale. Generalized linear regression analysis and post hoc comparisons with Bonferroni correction were performed to assess the association between various echocardiographic parameters and these lesions, adjusted for demographics and potential confounders.

    Results: 119 patients (68.38 ± 12.692 years; male 45.4 %) were included for analysis, of whom 55 (46.2%) had lacunes, 40 (33.6%) had CMBs, and median severity for WMH, BG-EPVS, CSO-EPVS, and CSVD burden were 2 (IQR: 1–3), 1 (IQR: 1–2), 1 (IQR: 0–1), and 1 (IQR: 1–2) respectively. In multivariable, fully adjusted models, left ventricular posterior wall thickness (LVPW) was associated with a higher risk of lacunes (RR 1.899, 95% CI: 1.342–2.686) and CSVD burden (RR = 2.081, 95%CI: 1.562–2.070). Right atrial diameter (RAD) was associated with greater CSO-EPVS (RR = 2.243, 95%CI: 1.234–4.075). No echocardiographic parameters were revealed to be associated with CMBs and WMH.

    Conclusion: In patients with AF-related ischemic stroke, LVPW is associated with a higher risk of lacunes and CSVD burden, while RAD was associated with greater CSO-EPVS. Larger studies are required to determine these associations and to elucidate if these associations can help facilitate cognitive evaluation and brain MRI screening.

    Introduction

    Increasing evidence suggests that atrial fibrillation (AF) appears to be correlated with cognitive decline independent of clinical stroke (1, 2). Cerebral small vessel disease (CSVD) is one of the pathological mechanisms through which AF might lead to cognitive impairment. A more recent large sample of study (3) has demonstrated that nearly 25% of patients with AF-related ischemic stroke or transient ischemic attack have preexisting cognitive impairment. They found imaging markers of CSVD were independently associated with cognitive impairment prior to ischemic events.

    There is no complete explanation of the mechanism that links AF and CSVD, but chronic cerebral hypoperfusion, inflammation, and shared vascular risk factors, such as hypertension and diabetes mellitus, may all be involved. Patients with AF are more likely to develop cardiac dysfunction, for example, many patients with AF develop an enlarged left atrium (LA) and enlarged left ventricular (LV), and are also associated with an increased incidence of heart failure. Conversely, patients with cardiac dysfunction are known to contribute to AF development and maintenance (46). According to previous studies, some cardiac subclinical indicators, such as left ventricular structure and LV systolic dysfunction, may contribute to greater white matter hyperintensity (WMH) (6), and LA volume, may contribute to silent brain infarcts (7) even in the absence of AF. However, none of them investigated whether cardiac structural or functional abnormalities correlated with neuroimaging markers of CSVD in patients with AF-related ischemic stroke. Thus, we evaluated the cross-sectional association of the echocardiographic parameters of cardiac structure or function with the neuroimaging markers of CSVD on MRI in patients with AF-related ischemic stroke.

    More at link.

    Saturday, August 27, 2022

    Effect of Antihypertensives by Class on Cerebral Small Vessel Disease: A Post Hoc Analysis of SPRINT-MIND

    So you described something but didn't give us a protocol on what EXACTLY NEEDS TO BE DONE. Useless.  No objective damage diagnosis which should lead directly to an EXACT protocol.  Does no one know how to do research that actually helps survivors? Obviously the mentors and senior researchers here don't.

    Effect of Antihypertensives by Class on Cerebral Small Vessel Disease: A Post Hoc Analysis of SPRINT-MIND

    Originally publishedhttps://doi.org/10.1161/STROKEAHA.121.037997Stroke. 2022;53:2435–2440

    Background:

    Treatment of uncontrolled arterial hypertension reduces the risk of cerebral small vessel disease (CSVD) progression, although it is unclear whether this reduction occurs due to blood pressure control or class-specific pleiotropic effects, such as improved beat-to-beat arterial pressure variability with calcium channel blockers. The goal of this study was to investigate the influence of antihypertensive medication class, particularly with calcium channel blocker, on accumulation of white matter hyperintensities (WMH), a radiographic marker of CSVD, within a cohort with well-controlled hypertension.

    Methods:

    We completed an observational cohort analysis of the SPRINT-MIND trial (Systolic Blood Pressure Trial Memory and Cognition in Decreased Hypertension), a large randomized controlled trial of participants who completed a baseline and 4-year follow-up brain magnetic resonance image with volumetric WMH data. Antihypertensive medication data were recorded at follow-up visits between the magnetic resonance images. A percentage of follow-up time participants were prescribed each of the 11 classes of antihypertensive was then derived. Progression of CSVD was calculated as the difference in WMH volume between 2 scans and, to address skew, dichotomized into a top tertile of the distribution compared with the remaining.

    Results:

    Among 448 individuals, vascular risk profiles were similar across WMH progression subgroups except age (70.1±7.9 versus 65.7±7.3 years; P<0.001) and systolic blood pressure (128.3±11.0 versus 126.2±9.4 mm Hg; P=0.039). Seventy-two (48.3%) of the top tertile cohort and 177 (59.2%) of the remaining cohort were in the intensive blood pressure arm. Those within the top tertile of progression had a mean WMH progression of 4.7±4.3 mL compared with 0.13±1.0 mL (P<0.001). Use of angiotensin-converting enzyme inhibitors (odds ratio, 0.36 [95% CI, 0.16–0.79]; P=0.011) and dihydropyridine calcium channel blockers (odds ratio, 0.39 [95% CI, 0.19–0.80]; P=0.011) was associated with less WMH progression, although dihydropyridine calcium channel blockers lost significance when WMH was treated as a continuous variable.

    Conclusions:

    Among participants of SPRINT-MIND trial, angiotensin-converting enzyme inhibitor was most consistently associated with less WMH progression independent of blood pressure control and age.

    Sunday, July 24, 2022

    Gait in Cerebral Small Vessel Disease, Pre-Dementia and Dementia: A Systematic Review

    With no next steps on what EXACTLY THE FOLLOWUP RESEARCH should be. Useless.  Whenever I came upon a problem in programming, if I didn't have an exact plan to fix it I would have been fired immediately. The same should apply here.

    Gait in Cerebral Small Vessel Disease, Pre-Dementia and Dementia: A Systematic Review

    First Published July 7, 2022 Research Article 

    Background: 

    The interrelationships between gait, cerebral small vessel disease (CSVD), and cognitive impairments in aging are not well-understood – despite their common co-occurrence.

    Objective: 

    To systematically review studies of gait impairment in CSVD, pre-dementia, and dementia and to identify key gaps for future research and novel pathways toward intervention.

    Methods:  

    A PRISMA-guided search strategy was implemented in PubMed to identify relevant studies. Potential articles (n=263) published prior to December 1st, 2021 were screened by two reviewers. Studies with sample sizes >20 and including some adult over >65 years (n=202) were included.

    Results: 

    The key findings were that 1) adverse gait and cognitive outcomes were associated with several (rather than select) CSVD pathologies distributed across the brain, and 2) poor gait and CSVD pathologies were more strongly associated with dementia with a vascular, rather than an Alzheimer’s disease-related, cause.

    Discussion:  

    A better understanding of the interrelationships between gait performance in CSVD, pre-dementia and dementia requires studies examining a) comprehensive patterns in the clinical manifestations of CSVD, b) racially/ethnically diverse samples, c) samples followed for extended periods of time or across the adult lifespan, d) non-traditional CSVD neuroimaging markers (e.g., resting-state fMRI), and e) continuous (e.g., wearable sensors) and complex (e.g., dual-task) walking performance.

    Sunday, July 10, 2022

    Gait in Cerebral Small Vessel Disease, Pre-Dementia and Dementia: A Systematic Review

     My gait is still impaired 16 years post stroke and will stay that way until I die. I have zero cognitive impairment.

    Gait in Cerebral Small Vessel Disease, Pre-Dementia and Dementia: A Systematic Review

    First Published July 7, 2022 Research Article 

    Background:  

    The interrelationships between gait, cerebral small vessel disease (CSVD), and cognitive impairments in aging are not well-understood – despite their common co-occurrence.

    Objective:  

    To systematically review studies of gait impairment in CSVD, pre-dementia, and dementia and to identify key gaps for future research and novel pathways toward intervention.

    Methods:  

    A PRISMA-guided search strategy was implemented in PubMed to identify relevant studies. Potential articles (n=263) published prior to December 1st, 2021 were screened by two reviewers. Studies with sample sizes >20 and including some adult over >65 years (n=202) were included.

    Results: 

    The key findings were that 1) adverse gait and cognitive outcomes were associated with several (rather than select) CSVD pathologies distributed across the brain, and 2) poor gait and CSVD pathologies were more strongly associated with dementia with a vascular, rather than an Alzheimer’s disease-related, cause.

    Discussion: 

    A better understanding of the interrelationships between gait performance in CSVD, pre-dementia and dementia requires studies examining a) comprehensive patterns in the clinical manifestations of CSVD, b) racially/ethnically diverse samples, c) samples followed for extended periods of time or across the adult lifespan, d) non-traditional CSVD neuroimaging markers (e.g., resting-state fMRI), and e) continuous (e.g., wearable sensors) and complex (e.g., dual-task) walking performance.

    Friday, May 6, 2022

    Effect of Antihypertensives by Class on Cerebral Small Vessel Disease: A Post Hoc Analysis of SPRINT-MIND

    No clue.

    Effect of Antihypertensives by Class on Cerebral Small Vessel Disease: A Post Hoc Analysis of SPRINT-MIND

    Originally publishedhttps://doi.org/10.1161/STROKEAHA.121.037997Stroke. 2022;0:10.1161/STROKEAHA.121.037997

    Background:

    Treatment of uncontrolled arterial hypertension reduces the risk of cerebral small vessel disease (CSVD) progression, although it is unclear whether this reduction occurs due to blood pressure control or class-specific pleiotropic effects, such as improved beat-to-beat arterial pressure variability with calcium channel blockers. The goal of this study was to investigate the influence of antihypertensive medication class, particularly with calcium channel blocker, on accumulation of white matter hyperintensities (WMH), a radiographic marker of CSVD, within a cohort with well-controlled hypertension.

    Methods:

    We completed an observational cohort analysis of the SPRINT-MIND trial (Systolic Blood Pressure Trial Memory and Cognition in Decreased Hypertension), a large randomized controlled trial of participants who completed a baseline and 4-year follow-up brain magnetic resonance image with volumetric WMH data. Antihypertensive medication data were recorded at follow-up visits between the magnetic resonance images. A percentage of follow-up time participants were prescribed each of the 11 classes of antihypertensive was then derived. Progression of CSVD was calculated as the difference in WMH volume between 2 scans and, to address skew, dichotomized into a top tertile of the distribution compared with the remaining.

    Results:

    Among 448 individuals, vascular risk profiles were similar across WMH progression subgroups except age (70.1±7.9 versus 65.7±7.3 years; P<0.001) and systolic blood pressure (128.3±11.0 versus 126.2±9.4 mm Hg; P=0.039). Seventy-two (48.3%) of the top tertile cohort and 177 (59.2%) of the remaining cohort were in the intensive blood pressure arm. Those within the top tertile of progression had a mean WMH progression of 4.7±4.3 mL compared with 0.13±1.0 mL (P<0.001). Use of angiotensin-converting enzyme inhibitors (odds ratio, 0.36 [95% CI, 0.16–0.79]; P=0.011) and dihydropyridine calcium channel blockers (odds ratio, 0.39 [95% CI, 0.19–0.80]; P=0.011) was associated with less WMH progression, although dihydropyridine calcium channel blockers lost significance when WMH was treated as a continuous variable.

    Conclusions:

    Among participants of SPRINT-MIND trial, angiotensin-converting enzyme inhibitor was most consistently associated with less WMH progression independent of blood pressure control and age.

     

    Thursday, March 31, 2022

    Advanced MRI in cerebral small vessel disease

     Is your doctor testing for this? To implement the protocols to prevent the next stroke and to cure the cerebral small vessel disease? Why not? Isn't your doctor supposed to be competent in all things stroke?

    Advanced MRI in cerebral small vessel disease

     

    First Published March 21, 2022 Research Article Find in PubMed 

    Cerebral small vessel disease (cSVD) is a major cause of stroke and dementia. This review summarizes recent developments in advanced neuroimaging of cSVD with a focus on clinical and research applications.

    In the first section we highlight how advanced structural imaging techniques, including diffusion MRI, enable improved detection of tissue damage, including characterization of tissue appearing normal on conventional MRI. These techniques enable progression to be monitored and may be useful as surrogate endpoint in clinical trials. Quantitative MRI, including iron and myelin imaging, provides insights into tissue composition on the molecular level.

    In the second section, we cover how advanced MRI techniques can demonstrate functional or dynamic abnormalities of the blood vessels, which could be targeted in mechanistic research and early-stage intervention trials. Such techniques include the use of dynamic contrast enhanced MRI to measure blood-brain barrier permeability, and MRI methods to assess cerebrovascular reactivity.

    In the third section we discuss how the increased spatial resolution provided by ultra-high field MRI at 7T allows imaging of perforating arteries, and flow velocity and pulsatility within them.

    The advanced MRI techniques we describe are providing novel pathophysiological insights in cSVD and allow improved quantification of disease burden and progression. They have application in clinical trials, both in assessing novel therapeutic mechanisms, and as a sensitive endpoint to assess efficacy of interventions on parenchymal tissue damage. We also discuss challenges of these advanced techniques and suggest future directions for research.