CT vs MRI: Assessing Stroke and Dementia Risk in White Matter Disease

 

My incompetent? 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. I have zero cognitive impairment and I'm 20 years out.

CT vs MRI: Assessing Stroke and Dementia Risk in White Matter Disease

 Patients with incidentally discovered white matter disease on computed tomography have a higher risk for future stroke or dementia than those with disease detected only on magnetic resonance imaging. White matter disease (WMD) detected on computed tomography (CT) identified patients at greater risk for future stroke or dementia than WMD detected only on magnetic resonance imaging (MRI), according to study results published in Neurology. Covert cerebrovascular disease (CCD), which includes covert brain infarction (CBI) and WMD, is frequently identified incidentally during neuroimaging in patients without a history of stroke or dementia. Although MRI is generally considered more sensitive for detecting these abnormalities, CT remains the most commonly used neuroimaging modality in routine clinical practice. Researchers therefore compared incidentally discovered CCD detected on CT and MRI to determine whether findings from each modality differed in their association with subsequent neurologic outcomes. Researchers conducted a retrospective cohort study of adults aged 50 years and older who underwent both head CT and brain MRI within a 30-day period between 2009 and 2022. They excluded patients with a prior history of stroke or dementia, as well as those with major neurologic symptoms suggestive of acute stroke. They used natural language processing to identify CBI and WMD from radiology reports and classify WMD severity. These findings highlight the importance of modality-specific interpretation of CCD in clinical practice and research. The analysis included 18,628 participants with a mean age of 64.9 years; 59.1% were women. The cohort was racially and ethnically diverse, with 41.4% identifying as non-Hispanic White, 32.7% as Hispanic, 12.0% as Asian or Pacific Islander, and 11.3% as African American. Cardiovascular risk factors were common, including hypertension (63.3%), hypercholesterolemia (71.3%), diabetes (30.3%), and a history of tobacco use (44.9%). The prevalence of CBI was similar across imaging modalities, occurring in 6.3% of CT scans and 6.1% of MRI scans. Overall agreement for CBI presence or absence was 91.6%. Among patients with CBI on MRI, 33.3% also had CBI on CT. Among patients with CBI on CT, 31.9% also had CBI on MRI. Researchers identified WMD in 60.5% of MRI reports compared with 24.4% of CT reports. Agreement for WMD presence was 57.6%. Among patients with WMD severity classified on both modalities, 47.9% received different severity classifications, and MRI assigned a higher severity grade than CT in 92.3% of those discordant cases. During a mean follow-up period of 4.4 years, 985 patients experienced stroke alone, 716 developed dementia alone, and 330 experienced both outcomes. Patients without WMD on either imaging modality had an incidence rate of stroke or dementia of 12.7 events per 1000 person-years. Rates increased to 22.6 among patients with WMD detected only on MRI, 37.0 among those with WMD detected only on CT, and 52.2 among those with WMD detected on both CT and MRI (all per 1000 person-years). After adjustment for demographic characteristics and vascular risk factors, patients with WMD detected only on MRI had a 23% higher risk for stroke or dementia than those without WMD on either modality (hazard ratio [HR], 1.23; 95% CI, 1.07-1.41). Patients with WMD detected only on CT had an even greater risk (HR, 1.46; 95% CI, 1.11-1.92), and those with WMD identified on both modalities had the greatest risk (HR, 1.82; 95% CI, 1.58-2.11). The researchers observed a similar pattern for CBI. Compared with patients without CBI on either modality, those with MRI-only CBI had a higher adjusted risk for stroke or dementia (HR, 1.47; 95% CI, 1.23-1.76), as did patients with CT-only CBI (HR, 1.26; 95% CI, 1.04-1.53) and those with CBI detected on both modalities (HR, 1.68; 95% CI, 1.33-2.11). The researchers suggested that MRI appears to detect a broader spectrum of white matter abnormalities, including milder disease that may not be visible on CT. In contrast, WMD identified on CT may represent more advanced or clinically significant cerebrovascular injury, potentially explaining its stronger association with future stroke or dementia. Study limitations include reliance on natural language processing of radiology reports rather than direct image review and the inclusion of only patients who underwent both CT and MRI. “These findings highlight the importance of modality-specific interpretation of CCD in clinical practice and research,” the study authors concluded.  Disclosures: This research was supported by the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health. One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures.

Higher Education Linked to Lower White Matter Hyperintensity Burden

 

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. So, I can't compare mine to anything here.  I got within 2 classes of getting my master's before realizing it would do nothing for my career. 

Higher Education Linked to Lower White Matter Hyperintensity Burden

Higher education was associated with reduced white matter hyperintensity volume across multiple brain regions, particularly in posterior lobes, suggesting that educational attainment may confer resilience to brain changes linked to aging and dementia risk.

Higher educational attainment is associated with a lower burden of white matter hyperintensities (WMHs), partially explained by differences in vascular risk profiles, according to study findings published in Alzheimer’s & Dementia.

White matter hyperintensities are magnetic resonance imaging (MRI)-detectable markers of cerebral small vessel disease that are associated with cognitive decline, progression to mild cognitive impairment, and increased dementia risk. Although higher educational attainment is thought to protect against cognitive aging, it remains unclear whether this benefit is mediated by differences in cerebrovascular health, prompting researchers to examine the role of vascular risk factors in the relationship between education and WMH burden.

Researchers conducted a cross-sectional analysis using data from the National Alzheimer’s Coordinating Center, including 1443 participants aged 55 years and older with available MRI and vascular risk data. Participants had normal cognition or had diagnoses of mild cognitive impairment or Alzheimer disease. Education was measured as years of formal schooling completed. The researchers quantified WMH burden using automated segmentation of T1-weighted and fluid-attenuated inversion recovery MRI scans and normalized for intracranial volume. Analyses evaluated both total WMH volume and regional WMH burden across frontal, temporal, parietal, and occipital lobes.

At baseline, the mean age of the cohort was 74.3 years, and 59% of participants were women. The mean educational attainment was 15.1 years, though substantial differences were observed across racial and ethnic groups. Vascular risk factors were common: 47% of participants had hypertension, 50% had hypercholesterolemia, 16% had diabetes, and 60% had a body mass index (BMI) of 25 kg/m² or greater. Smoking history was reported by 40% of participants. The mean composite vascular risk score, which incorporated diabetes, hypertension, hypercholesterolemia, smoking, alcohol abuse, BMI, and blood pressure, was 2.7 out of a possible 8 points.

Higher educational attainment was consistently associated with a more favorable vascular risk profile. In adjusted regression models, education was inversely associated with diabetes, hypertension, hypercholesterolemia, BMI, smoking exposure, alcohol abuse, and systolic blood pressure (all P <0.001). Education was also significantly associated with lower cumulative vascular burden, as reflected by both the composite vascular risk score and a BMI-based atherosclerotic cardiovascular disease risk score.

Education was independently associated with lower WMH burden after adjusting for age, sex, race, and cognitive diagnosis. Each additional year of education was associated with a modest but significant reduction in total WMH volume (β=-0.05; P =.004). Region-specific analyses showed inverse associations across all lobes, with the strongest effects observed in the parietal and occipital regions.

Mediation analyses demonstrated that vascular risk factors partially mediated the relationship between education and WMH burden. The indirect effect of education on total WMH volume through the composite vascular risk score was significant (a*b=-0.02; P <.001), accounting for approximately 27% of the total association. Similar results were observed when vascular risk was indexed using the BMI-based cardiovascular risk score, which mediated 22% of the education-WMH relationship. No single vascular risk factor independently explained the mediation effect, suggesting that the pathway reflects cumulative vascular burden rather than an isolated risk factor.

Study limitations include a cross-sectional design, reduced statistical power in non-White subgroups, and reliance on binary vascular risk indicators.

“[O]ur findings offer a better understanding of how education protects the cerebrovascular system in aging populations and emphasize integrating educational equity and vascular risk prevention in public health strategies to mitigate cerebrovascular disease and slow cognitive aging,” the study authors concluded.

Disclosures: This research was supported by the National Institute on Aging of the National Institutes of Health, the Canadian Institutes of Health Research, the Fonds de Recherche du Québec—Santé, the Natural Sciences and Engineering Research Council of Canada, and Brain Canada. Please see the original reference for a full list of disclosures.

Biomarkers of Impaired Distal Perfusion in ICAS

Hopefully your competent? doctor knows EXACTLY WHAT TO DO WITH THIS TO PREVENT YOUR NEXT STROKE!

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?

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.

Biomarkers of Impaired Distal Perfusion in ICAS

Johanna Seiden

, MD, MPH, @JohannaSeidenMDYaghi S, Khan F, Lewis S, Stipanovich A, Choi R, Baker R, Al Kasab S, Abu Qdais A, Yaddanapudi SS, Sultana S, et al. Impaired Perfusion and Early Ischemic Stroke Recurrence in Symptomatic Intracranial Atherosclerosis: BIORISK ICAS Study. Stroke. 2025. 

The risk of recurrent ischemic stroke due to intracranial atherosclerosis (ICAS) among medically treated patients is higher than other etiologies.¹ There are a number of different submechanisms within ICAS — distal embolization, perforator disease, and hypoperfusion — and risk of subsequent ischemic stroke may not be the same for all causes. Prior studies suggest that impaired distal perfusion may be associated with increased risk of stroke recurrence,^2,3 but these studies did not acutely enroll patients after their index events. They beg the question: Are specific biomarkers of impaired distal perfusion — Anterior Circulation borderzone infarcts (ACBI) and hypoperfusion mismatch volume — associated with higher risk of recurrence within 90 days? The Biomarkers and Recurrence Risk in Symptomatic Intracranial Atherosclerosis (BIORISK ICAS) is a multicenter retrospective international study of 2050 patients with symptomatic ICAS (50-99% luminal stenosis of the intracranial vertebral, basilar, distal ICA or proximal MCA) who did not receive endovascular therapy as first line therapy. The study was conducted between 2019 and 2024. The primary outcome was recurrent ischemic stroke in the territory of the symptomatic artery within 90 days. The primary analysis examined acute ACBI, and secondary analysis performed on patients presenting within 72 hours of last known normal with perfusion imaging studied hypoperfusion mismatch volume at Tmax of 6 seconds. The primary analysis included 1891 patients. Mean age was 67 years, and 54.7% were men. ACBI was seen in 31.7% of patients, and 71.7% had 70-99% stenosis. 174 (9.2%) patients had recurrent ischemic stroke in the symptomatic arterial territory within 90 days. In univariate analysis, ACBI was associated with recurrent stroke at 90 days (38.5% [67/174] vs. 31% [532/1717], p=0.042). Hyperlipidemia, degree of stenosis 70-99% vs 50-69%, and nonsmokers had increased risk of recurrent stroke. Among patients who underwent perfusion imaging (509 patients), hypoperfusion mismatch was also associated with increased risk of recurrent stroke within 90 days (67.7% [42/62] vs. 53.5% [221/413], p=0.036). Hyperlipidemia and atrial fibrillation were also associated with increased risk of recurrent stroke. Patients with ACBI had increased risk of recurrent stroke within 90 days; this finding persisted even after adjustment for variables associated with recurrent ischemic stroke risk (aHR 1.40, 95% CI 1.02-1.93, p=0.038). In the interaction analyses, the association between ACBI and recurrent stroke was more pronounced in patients with 50-69% stenosis (aHR 3.10 95% CI 1.47-6.52) versus 70-99% stenosis (aHR 1.18 95% CI 0.83-1.68), P Interaction=0.026. In the perfusion imaging analysis, hypoperfusion mismatch >10 mL at Tmax 6 seconds was associated with recurrent stroke at 90 days even after adjustment (aHR 1.83, 95% CI 1.03-3.28, p=0.041). This multicenter international study of patients with symptomatic ICAS demonstrated that patients with impaired distal perfusion, measured either directly (through perfusion imaging) or indirectly (via evidence of ACBI), were at a higher risk of recurrent stroke at 90 days. Interestingly, this study found that the association between ACBI and recurrent ischemic stroke was more pronounced in patients with moderate stenosis versus severe stenosis. This finding could very well be due to chance, but the authors also hypothesize that the presence of borderzone infarcts in patients with severe stenosis may not be as helpful in risk stratification because they are inherently more common; however, in those with moderate stenosis, borderzone infarcts may portend a higher recurrence risk. Future studies will be important to further evaluate this finding. Limitations of this study include the retrospective and observational nature, while strengths include the large sample size and multicenter international population. Methods to risk stratify ICAS patients could help determine which patients might benefit from angioplasty, stenting, or other targeted interventions. Randomized trials testing maximal medical therapy against early reperfusion in these high-risk patients will be important moving forward.

References:Derdeyn CP, Chimowitz MI, Lynn MJ, Fiorella D, Turan TN, Janis LS,Montgomery J, Nizam A, Lane BF, Lutsep HL, et al. Aggressive medical treatment with or without stenting in high-risk patients with intracranial artery stenosis (SAMMPRIS): The final results of a randomised trial. Lancet (London, England). 2014;383:333-341

Wabnitz AM, Derdeyn CP, Fiorella DJ, Lynn MJ, Cotsonis GA, Liebeskind DS, Waters MF, Lutsep H, López-Cancio E, Turan TN, et al. Hemodynamic markers in the anterior circulation as predictors of recurrent stroke in patients with intracranial stenosis. Stroke. 2018:Strokeaha11802084

Wang T, Yang Y, Wang H, Liu D, Wang J, Luo J, Yang R, Li T, Gong H, Sun X, et al. Ct perfusion for predicting ischemic stroke in patients with symptomatic carotid or middle cerebral artery occlusion: A post hoc analysis of the CMOSS study. Stroke. 2025;56:2579-2587

Periodic Limb Movements Linked to White Matter Changes After Minor Stroke

 Ask your competent? doctor what this means, I have no clue.

Periodic Limb Movements Linked to White Matter Changes After Minor Stroke

Individuals with an elevated PLM index had significantly higher Fazekas and ARWMC total scores than those with a lower PLM index.

Periodic limb movements (PLMs) during sleep are associated with white matter hyperintensities (WMHs) among patients with incident minor stroke and transient ischemic attack (TIA), according to study results published in Sleep.

Previous studies have reported that PLMs during sleep are associated with nocturnal fluctuations in heart rate and blood pressure and vascular events. As such, some researchers posit that PLMs may contribute to cerebrovascular and cardiovascular disease – although this relationship remains debated.

To evaluate the relationship between PLMs and cerebral small vessel disease, investigators conducted a study using data from the Sleep Disorders Managed and Assessed Rapidly in TIA and In Early Stroke (SMARTIES; NCT01528462) and SLEep APnea Screening Using Mobile Ambulatory Recorders After TIA/Stroke (SLEAP SMART; NCT02454023) studies. The investigators assessed periodic limb movement index (PLMI), PLM arousal index (PLMAI), and signs of cerebral small vessel disease (CSVD) among patients (N=86) with recent, first-ever stroke or TIA. Limb movement outcomes were measured using polysomnography and CSVD outcomes were measured using magnetic resonance imaging.

Of the 86 patients included in the study, 66.3% were male, 52.3% had hypertension, 10.5% had diabetes mellitus, 29.1% smoked, 29.1% had microbleeds, and 24.4% had lacunar infarcts. The patients had a mean age of 62.2 (SD=14.3) years and a body mass index (BMI) of 28.1 (SD=5.7) kg/m².

In conclusion, this study adds to the literature examining the relationship between PLMs and CSVD in patients with cerebrovascular disease,

The patients had a median Fazekas total score of 2 (IQR, 1-3) and an age-related white matter changes (ARWMC) total score of 5 (IQR, 2-10). The subset of patients with a PLMI of 5 or greater (n=36) had significantly higher Fazekas (P =.003) and ARWMC (P =.007) total scores than those with lower PLMI.

In the adjusted models, Fazekas total score was significantly associated with a PLMAI of 5 or greater (adjusted odds ratio [aOR], 5.9; 95% CI, 1.5-23.8; P =.01), PLMI of 5 or greater (aOR, 2.8; 95% CI, 1.2-6.8; P =.02), and a PLMI of the upper limit of normal or higher (aOR, 2.6; 95% CI, 1.0-6.5; P =.04). Additionally, ARWMC total scores were associated with a PLMAI of 5 or greater (adjusted b [ab], 3.8; 95% CI, 0.5-7.1; P =.027) and a PLMI of 5 or greater (ab, 2.3; 95% CI, 0.07-4.4; P =.043).

In a subgroup analysis among only patients with an elevated PLMI, no significant trends in CSVD outcomes were observed on the basis of obstructive sleep apnea status.

“In conclusion, this study adds to the literature examining the relationship between PLMs and CSVD in patients with cerebrovascular disease,” the study authors noted. “These findings suggested that an elevated PLM index was independently associated with WMHs; further work is needed to determine the directionality of this association.”

Study limitations include potential unaccounted confounding and the inability to determine the directionality of the findings.

This article originally appeared on Sleep Wake Advisor

White matter aging and its impact on brain function

 You competent? doctor has known of myelin problems from your stroke a long time ago, was anything done to solve it? NO? So, pure incompetence in action!

(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.)

demyelinating (23 posts to May 2012)

demyelination (7 posts to November 2021)

White matter aging and its impact on brain function

Janos Groh^1,2,3 janos.groh@tum.de ∙ Mikael Simons^1,2,3,4 mikael.simons@dzne.de

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Summary

Aging has a detrimental impact on white matter, resulting in reduced volume, compromised structural integrity of myelinated axons, and an increase in white matter hyperintensities. These changes are closely linked to cognitive decline and neurological disabilities. The deterioration of myelin and its diminished ability to regenerate as we age further contribute to the progression of neurodegenerative disorders. Understanding these changes is crucial for devising effective disease prevention strategies. Here, we will discuss the structural alterations in white matter that occur with aging and examine the cellular and molecular mechanisms driving these aging-related transformations. We highlight how the progressive disruption of white matter may initiate a self-perpetuating cycle of inflammation and neural damage.

Keywords

1. aging
2. white matter
3. myelin
4. neuroinflammation

Introduction

In his pioneering work, De Humani Corporis Fabrica (1543), Renaissance anatomist Andreas Vesalius provided one of the earliest descriptions of white matter structure, noting the corpus callosum as a whitish substance distinct from the softer, yellowish cerebrum.¹ Although Vesalius recognized that the corpus callosum connected the two hemispheres, he did not understand that its fibers originated from nerve cell bodies. At the time, white matter was believed to be composed of excretory ducts filled with a “spongy substance” and was thought to be the center of spirit and imagination.¹ Now, we know that white matter primarily consists of myelinated axons, glial cells, blood vessels, and extracellular matrix. Oligodendrocytes, the main cells in white matter, produce myelin sheaths that are crucial for fast signal transmission and for maintaining the functional and structural integrity of axons.^2,3 Because white matter largely lacks neuronal cell bodies and mainly serves to connect different gray matter areas, it has not received as much as attention as the cortical areas of the brain. Yet, its significance becomes evident when looking at its evolution in primates. Unlike neocortical gray matter, which grows in direct proportion to brain size, white matter mass has increased at a much higher rate, highlighting the crucial role of enhanced connectivity for higher brain function.⁴ Consequently, the proportion of white matter in the human brain has risen to about 40%, with myelinated axons being a major component.⁴ However, this expansion of white matter also introduces risks, providing a surface for diseases and the effects of aging. As we age, our white matter undergoes several changes. It experiences a reduction in overall volume and exhibits a decline in its microstructural integrity, and there is an accumulation of focal lesions, contributing to a decline in cognitive functions and to the risk for age-related neurological diseases, including dementia and stroke.^5,6,7,8 Many of these changes follow non-linear kinetics, starting slowly and then accelerating at a certain age.⁹ In this context, we explore the structural changes in white matter associated with aging and investigate the cellular and molecular mechanisms underlying these age-related transformations. We hypothesize that chronic inflammation and vascular changes are closely linked to the degeneration of myelin and axons with age.

Why brain aging can vary dramatically between people

 I think I'm doing good in this category.

Why brain aging can vary dramatically between people

             Researchers are uncovering deeper insights into how the human brain ages and what factors may be tied to healthier cognitive aging, including exercising, avoiding tobacco, speaking a second language or even playing a musical instrument.

Some aspects of cognitive abilities in older age may be connected to test scores around age 11, according to a review paper published Thursday in the journal Genomic Psychiatry from Genomic Press New York.

video

Related video Nearly 40% of dementia cases can be prevented with one small health change

The paper, based on data from the Lothian Birth Cohorts studies in Scotland, suggests that about half of the variabilities in people’s cognition at older ages – why some people may have greater cognitive decline than others – may already have been present in their childhoods.

Yet some adult lifestyle factors still appeared to be linked with improved cognitive performance and slower aging of the brain.

“We have found that things like keeping physically and mentally active and engaged, having few ‘vascular’ risk factors (such as high blood pressure, cholesterol, smoking, BMI), speaking a second language, playing musical instruments, and having a younger-looking brain and many more show detectable-but-small associations,” Simon Cox, an author of the new paper and director of the Lothian Birth Cohort Studies at the University of Edinburgh, said in an email.

“We came up with the idea that ‘Marginal Gains, Not Magic Bullet’ is a good way to think about a recipe for better cognitive ageing: rather than finding that one single thing has a huge risk, we see lots and lots of (often partly-overlapping) factors that each probably contributes a little bit to your risk for cognitive ageing,” Cox said.

He added that such lifestyle factors – when they are considered all together – can add up to explaining “about 20%” of the differences seen in cognitive declines across the ages of 70 to 82.

The Lothian Birth Cohorts involve data from two studies of older adults: a group of Scottish adults born in 1921 and another group born in 1936. They all took a validated cognitive test at age 11 and were then tested in their 70s, 80s and 90s for cognitive functions and fitness, among other factors.

Related article Humans age dramatically at two key points in their life, study finds

“We first took MRI scans of the participants when they were 73 years old. One of the most striking things about the study for me is how wide the differences are between their scans,” Cox wrote.

“Even though they were all the same age, some brains looked perfectly healthy (and wouldn’t be out of place amongst scans of 30 or 40 year olds),” he said. “Whereas others showed lots of shrinkage and damage to the white matter connections(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.)

, along with other features that are related to cognitive ageing and dementia.”

White matter is the tissue that forms connections between brain cells and the rest of the nervous system, helping these regions communicate with each other through nerve signals. Having decreased or damaged white matter can slow the brain’s ability to process information.

Overall, “it shows us that brain ageing at age 73 is not an inevitability, while also strongly motivating us to research what we can do to emulate those lucky few who arrive at that age with such pristine brains,” Cox said.

Older adults whose memory seems as sharp as that of people 20 to 30 years younger have been referred to as cognitive super agers.

“Not all of the aspects of brain ageing happen together in the same people,” Cox said. “We are now looking into whether different constellations of brain ageing features are driven by particular subsets of risk factors.”

As a researcher of the aging brain, Dr. Richard Isaacson said, the new paper spoke to him.

Related article What’s your Brain Care Score? The answer may indicate your dementia risk

“It was a really practical, narrative overview of the ‘nuts and bolts’ about why this type of research is so hard, and several best practices to retain as much value as you can when you start a long-term study like this,” said Isaacson, director of research at the Institute for Neurodegenerative Diseases in Florida, who was not involved in the paper.

There is a robust body of research on key differences in lifestyle that may contribute to differences in an aging brain. For instance, poor sleep is a key risk factor for cognitive decline, and mental health issues such as depression are known risk factors for developing dementia.

Getting regular exercise by walking or cycling just three times a week may improve thinking skills, according to a 2018 study. Adding a heart-healthy diet to your routine also can help slow brain aging and reduce dementia risk. And a 2020 study suggests that daily meditation could slow brain aging.

Experts developed a tool named the Brain Care Score and a study published last year showed that it may help assess a person’s risk of developing dementia or having a stroke as they age.

The 21-point score refers to how a person fares on 12 health-related factors concerning physical, lifestyle and social-emotional components of health, according to the study, published in the journal Frontiers in Neurology. The researchers found that participants with a higher score had a lower risk of dementia or stroke later in life.

Those 12 factors are 

blood pressure, (Mine is controlled by two blood pressure meds; Nifedipine and lisinopril.)

blood sugar, (No problem here)

 cholesterol, (Controlled by atorvastatin)

body mass index, (At 28.4 but this suggests not a problem; 

What's overweight enough for lower disability after stroke?)

nutrition, (Could be better, but not going to worry about it.)

alcohol consumption, (Necessary for excellent social connections at bars for playing trivia and listening to jazz.)

smoking, (Occasional cigars)

 aerobic activities, (Not possible since my doctor and therapists completely failed at getting me recovered!)

sleep, (Much better since retiring)

stress, (None, hey I'm retired and having the time of my life.)

social relationships (Lots, three different groups of friends I travel internationally with, lots of women friends which is quite entertaining)

finding meaning or purpose in life. (Yeah, to get stroke solved to 100% recovery!)

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For anyone hoping to improve the health of their aging brain, “seeing your doctor at least every year or twice a year” to talk about your overall physical health, vascular health and chronic diseases is important, Isaacson said.

“Those things may not exactly cause Alzheimer’s, but it can fast forward cognitive aging and fast forward cognitive decline. So seeing your primary care doctor and getting your blood pressure taken – everyone needs to know their numbers. What is your blood pressure? What is your fasting blood sugar? What are your cholesterol numbers?” he said. “Another important thing is to track bone health. I think a lot of people are unaware that bone health, muscle strength and grip strength are things that are absolutely imperative and predict brain health outcomes over time.”     

Association between fibrinogen and white matter lesions and cerebral atrophy in patients with acute ischemic stroke

 ABSOLUTELY FUCKING USELESS RESEARCH! Associations DO NOTHING to get survivors recovered!

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.

This told me nothing useful. Like how to reverse white matter hyperintensities.

Association between fibrinogen and white matter lesions and cerebral atrophy in patients with acute ischemic stroke

, , , , , , , , ,

https://doi.org/10.1016/j.jstrokecerebrovasdis.2024.108008

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Highlights

• •

  In patients with acute ischemic stroke (AIS), increased fibrinogen levels were independently associated with white matter hyperintensity.

• •

  Moreover, higher levels of fibrinogen were also independently associated with increased risk of cerebral atrophy in AIS.

• •

  Fibrinogen has the potential to serve as a biomarker for identifying cerebral small vessel disease (CSVD).

Abstract

Background

Inflammation is a potential mechanism underlying the development of white matter lesions (WMLs) and cerebral atrophy. We aimed to investigate the relationship of fibrinogen levels with WMLs and cerebral atrophy in patients with acute ischemic stroke (AIS).

Methods

A total of 701 AIS patients were enrolled. Participants were divided into four groups according to the quartiles of fibrinogen levels: Q1 < 2.58 g/L, Q2: 2.58-3.12 g/L, Q3: 3.12-3.67 g/L, Q4: ≥ 3.67 g/L. White matter hyperintensity (WMH), periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH) were defined according to the Fazekas scale. Cerebral atrophy was defined according to global cortical atrophy scores. Univariate and multivariate logistic regression were used to explore the relationship of fibrinogen levels and WMHs, PVH, DWMH and cerebral atrophy.

Results

Among 701 AIS patients, 498 (71.0 %), 425 (60.6 %), 442 (63.1 %), and 560 (79.9 %) had WMHs, PVH, DWMH and cerebral atrophy, respectively. After adjustment for potential covariates, the highest fibrinogen quartiles were significantly associated with increased risk of WMHs (odds ratio [OR] 1.97, 95 % confidence intervals [CI] 1.10-3.50), PVH (OR 1.85, 95 % CI 1.08-3.16) and cerebral atrophy (OR 2.53, 95 % CI 1.19-5.40) but not DWMH (OR 1.37 95 % CI 0.81-2.31) compared with the lowest fibrinogen quartile. Moreover, the association between elevated fibrinogen levels and the risk of WMLs and cerebral atrophy remained significant as continuous variables.

Conclusions

Increased baseline fibrinogen levels were independently associated with WMHs, PVH and cerebral atrophy in patients with ischemic stroke. Fibrinogen could be the potential blood biomarker of WMLs and cerebral atrophy.

Effects of White Matter Hyperintensities on Cognitive Decline and Neurodegeneration

 

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.

This told me nothing useful. Like how to reverse white matter hyperintensities.

Effects of White Matter Hyperintensities on Cognitive Decline and Neurodegeneration

Tao-Ran Li ^1* Bai-Le Li ¹ Zhong Jin ¹ Xu Xinran ¹ Tai-Shan Wang ² Feng-Qi Liu ¹

• ¹ Nanjing Medical University, Nanjing, China
• ² yangzhou friendship hospital, Yang zhou, China

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Background: 

The relationship between white matter hyperintensities (WMH) and the core features of Alzheimer’s disease (AD) remains controversial. Further, due to the prevalence of co-pathologies, the precise role of WMH in cognition and neurodegeneration also remains uncertain. 

 

Methods: 

Herein, we analyzed 1803 participants with available WMH volume data, extracted from the ADNI database, including 756 cognitively normal controls, 783 patients with mild cognitive impairment (MCI), and 264 patients with dementia. Participants were grouped according to cerebrospinal fluid (CSF) pathology (A/T profile) severity. Linear regression analysis was applied to evaluate the factors associated with WMH volume. Modeled by linear mixed-effects, the increase rates (Δ) of the WMH volume, cognition, and typical neurodegenerative markers were assessed. The predictive effectiveness of WMH volume was subsequently tested using Cox regression analysis, and the relationship between WMH/ΔWMH and other indicators such as cognition was explored through linear regression analyses. Furthermore, we explored the interrelationship among amyloid-β deposition, cognition, and WMH using mediation analysis. 

Results: 

Higher WMH volume was associated with older age, lower CSF amyloid-β levels, hypertension, and smoking history (all p ≤ 0.001), as well as cognitive status (MCI, p < 0.001; dementia, p = 0.008), but not with CSF tau levels. These results were further verified in any clinical stage, except hypertension and smoking history in the dementia stage. Although WMH could not predict dementia conversion, its increased levels at baseline were associated with a worse cognitive performance and a more rapid memory decline. Longitudinal analyses showed that baseline dementia and positive amyloid-β status were associated with a greater accrual of WMH volume, and a higher ΔWMH was also correlated with a faster cognitive decline. In contrast, except entorhinal cortex thickness, the WMH volume was not found to be associated with any other neurodegenerative markers. To a lesser extent, WMH mediates the relationship between amyloid-β and cognition. 

Conclusion: 

WMH are non-specific lesions that are associated with amyloid-β deposition, cognitive status, and a variety of vascular risk factors. Despite evidence indicating only a weak relationship with neurodegeneration, early intervention to reduce WMH lesions remains a high priority for preserving cognitive function in the elderly.

New study reveals age-related brain changes influence recovery after stroke

 

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.

This told me nothing useful. Like how to reverse white matter hyperintensities.

New study reveals age-related brain changes influence recovery after stroke

Date:

May 6, 2024

Source:

Keck School of Medicine of USC

Summary:

A new study has revealed that areas of age-related damage in the brain relate to motor outcomes after a stroke -- a phenomenon that may be under-recognized in stroke research. The new observational study looked at the relationship between stroke recovery and white matter hyper-intensities (WMHs) -- areas of age-related damage in the brain's white matter, which represent vascular dysfunction and are known to impact cognitive functions.

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FULL STORY

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A new study by a global team of researchers, led by Sook-Lei Liew, PhD, of USC's Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI), has revealed that areas of age-related damage in the brain relate to motor outcomes after a stroke -- a phenomenon that may be under-recognized in stroke research. The study was published online on May 3, 2024, in Neurology®, the medical journal of the American Academy of Neurology.

A stroke often leads to motor impairment, which is traditionally linked to the extent of damage to the corticospinal tract (CST), a crucial brain pathway for motor control. Signaling along the CST is involved in a variety of movements, including walking, reaching, and fine finger movements like writing and typing. However, stroke recovery outcomes aren't fully predicted by damage to the CST, suggesting other factors are at play.