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.

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.

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