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, June 19, 2023

Arterial stiffness and its influence on cerebral morphology and cognitive function

 

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?

Do you prefer your  doctor incompetence NOT KNOWING? OR NOT DOING?

Arterial stiffness and its influence on cerebral morphology and cognitive function

Melanie Haidegger https://orcid.org/0000-0003-0180-7917, Simon Lindenbeck, and Reinhold Schmidt reinhold.schmidt@medunigraz.atView all authors and affiliations
All Articles
https://doi.org/10.1177/17562864231180715

Abstract

Background:

Recently, arterial stiffness has been associated with cerebral small vessel disease (SVD), brain atrophy and vascular dementia. Arterial stiffness is assessed via pulse wave velocity (PWV) measurement and is strongly dependent on arterial blood pressure. While circadian blood pressure fluctuations are important determinants of end-organ damage, the role of 24-h PWV variability is yet unclear.

Objectives:

We here investigated the association between PWV and its circadian changes on brain morphology and cognitive function in community-dwelling individuals.

Design:

Single-centre, prospective, community-based follow-up study.

Methods:

The study cohort comprised elderly community-based participants of the Austrian Stroke Prevention Family Study which was started in 2006. Patients with any history of cerebrovascular disease or dementia were excluded. The study consists of 84 participants who underwent ambulatory 24-h PWV measurement. White matter hyperintensity volume and brain volume were evaluated by 3-Tesla magnetic resonance imaging (MRI). A subgroup of patients was evaluated for cognitive function using an extensive neuropsychological test battery.

Results:

PWV was significantly related to reduced total brain volume (p = 0.013), which was independent of blood pressure and blood pressure variability. We found no association between PWV with markers of cerebral SVD or impaired cognitive functioning. Only night-time PWV values were associated with global brain atrophy (p = 0.005).

Conclusions:

This study shows a relationship of arterial stiffness and reduced total brain volume. Elevations in PWV during night-time are of greater importance than day-time measures.

Introduction

In recent studies, arterial stiffness has been related to cerebral small vessel disease (SVD), brain volume and cognitive function. With increasing age, the elasticity of the aortic wall is reduced, resulting in an increased aortic pulse wave transmitted to the cerebral microvasculature and consecutive brain tissue damage.1 This process is accelerated by exposure to vascular risk factors such as arterial hypertension, diabetes mellitus and cardiac disease.2,3
Arterial stiffness has been related to higher burden of white matter hyperintensities (WMHs).4,5 In addition, recent studies investigated a possible association between arterial stiffness and microstructural changes of the white matter captured by diffusion tensor imaging (DTI) techniques. Arterial stiffness related to lower fractional anisotropy and to higher mean diffusivity, suggesting that increased arterial stiffness exerts widespread detrimental effects on microstructural integrity of the white matter.6–8
Current literature also indicates an association of arterial stiffness and reduced brain volume as well as impaired cognitive abilities, including executive function and processing speed.2,9,10
The gold standard of measurement of arterial stiffness is assessment of carotid-femoral pulse wave velocity (PWV).11 New technological approaches of PWV measurements, however, have been developed. These include pulse wave analysis which can easily be combined with a blood pressure measurement device allowing repetitive evaluation in an ambulatory 24-h setting.12,13 As arterial stiffness is highly depending on arterial blood pressure, a circadian rhythm of PWV is assumed.14,15 Data on circadian changes of PWV and its associations to cerebral structural damage and impairment of cognitive function, however, are lacking.
Therefore, this study aims to investigate the associations between PWV and its circadian fluctuations and focal SVD-related brain lesions, the peak width of skeletonized mean diffusivity (PSMD), brain volume and cognitive functioning.
 
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