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.

Thursday, June 3, 2021

Carotid Atherosclerotic Calcification Characteristics Relate to Post-stroke Cognitive Impairment

My doctors never found the 80% blockage in my right carotid artery, which thankfully completely closed up in three years.  I think my post stroke cognitive impairment is zilch.

Carotid Atherosclerotic Calcification Characteristics Relate to Post-stroke Cognitive Impairment

 
Yingzhe Wang1†, Chanchan Li2†, Mengyuan Ding1, Luyi Lin2, Peixi Li1, Yizhe Wang3, Qiang Dong1,4, Yanmei Yang2*‡ and Mei Cui1,4*‡
  • 1Department of Neurology, Huashan Hospital, Fudan University, Shanghai, China
  • 2Department of Radiology, Huashan Hospital, Fudan University, Shanghai, China
  • 3Department of Medicine, Nanchang University, Nanchang, China
  • 4The State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, China

Background: Together with cerebral small vessel disease (CSVD), large vessel atherosclerosis is considered to be an equally important risk factor in the progression of vascular cognitive impairment. This article aims to investigate whether carotid atherosclerotic calcification is associated with the increased risk of post-stroke cognitive impairment (PSCI).

Methods: A total of 128 patients (mean age: 62.1 ± 12.2 years, 37 women) suffering from ischemic stroke underwent brain/neck computer tomography angiography examination. The presence and characteristic of carotid calcification (size, number and location) were analyzed on computer tomography angiography. White matter hyperintensity (WMH) was assessed using Fazekas scales. PSCI was diagnosed based on a battery of neuropsychological assessments implemented 6−12 months after stroke.

Results: Among 128 patients, 26 developed post-stroke dementia and 96 had carotid calcification. Logistic regression found carotid calcification (odds ratio [OR] = 7.15, 95% confidence interval [CI]: 1.07–47.69) and carotid artery stenosis (OR = 6.42, 95% CI: 1.03–40.15) both significantly increased the risk for post-stroke dementia. Moreover, multiple, thick/mixed, and surface calcifications exhibited an increasing trend in PSCI (Ptrend = 0.004, 0.016, 0.045, respectively). The prediction model for post-stroke dementia including carotid calcification (area under curve = 0.67), WMH (area under curve = 0.67) and other covariates yielded an area under curve (AUC) of 0.90 (95% CI: 0.82–0.99).

Conclusion: Our findings demonstrated that the quantity and location of carotid calcifications were independent indicators for PSCI. The significant role of large vessel atherosclerosis in PSCI should be concerned in future study.

Introduction

Stroke is considered to be one of the most widespread and serious cerebrovascular diseases affecting millions of people worldwide. With a high prevalence of 20–80%, post-stroke cognitive impairment (PSCI) is one of the major complications suffered during the chronic stage of ischemic stroke (Sun et al., 2014). As cognitive function can fluctuate due to neurological deficits and subsequent improvement of perfusion in early phases, the diagnosis of PSCI is often postponed by at least 3 months after the onset of stroke (Gottesman and Hillis, 2010). Thus, early identification of patients at high-risk of PSCI, based on patients’ baseline characteristics, is essential in the orchestration of appropriate preventataive management.

Several factors, including age, education level, vascular risk factors, extent of stroke, and neuroimaging features, are considered to be important determinants of PSCI (Rasquin et al., 2004; Leys et al., 2005; Lu et al., 2016). Apart from acute stroke, pre-existing cerebral small vessel disease (CSVD) is believed to be closely connected with both the prognosis of stroke and the occurrence of cognitive dysfunction. It has been reported that PSCI was significantly associated with several subtypes of baseline CSVD, including white matter hyperintensity (WMH), cerebral microbleed, enlarged perivascular space and brain atrophy (Wen et al., 2004; Gregoire et al., 2012; Kebets et al., 2015; Molad et al., 2017; Arba et al., 2018). Interestingly, although CSVD is often accompanied by pathological changes in large arteries, the relationship between large vessel diseases (such as stenosis, slow blood flow, malformation, or poor collateral circulation) and PSCI remains ambiguous. While some research has demonstrated that large vessel stenosis was highly predictive of PSCI (Kandiah et al., 2016; Li et al., 2017), not all studies have shown consistent results (Chaudhari et al., 2014). Understanding the relationship between atherosclerotic calcification and PSCI will provide a deeper insight into the pathology of PSCI, which would be beneficial for early diagnosis and prevention.

Therefore, in this study, we aimed to investigate whether the presence of carotid atherosclerotic calcification is an associated risk factor for the development and progression of PSCI, and whether this association depends on the characteristic of calcification.

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