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.

Tuesday, January 16, 2024

Predictors and outcomes of fluctuations in the clinical dementia rating scale

 How will your doctor use this information to put you in the reversion category after you start down the dementia pathway? If your doctor doesn't have a plan you don't have a functioning stroke doctor! Run away! I expect my doctor to know more than I do about stroke, you should also

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

The latest here:

Predictors and outcomes of fluctuations in the clinical dementia rating scale

First published: 15 January 2024

Abstract

INTRODUCTION

Reversion, or change in cognitive status from impaired to normal, is common in aging and dementia studies, but it remains unclear what factors predict reversion.

METHODS

We investigated whether reverters, defined as those who revert from a Clinical Dementia Rating® (CDR®) scale score of 0.5 to CDR 0) differed on cognition and biomarkers from unimpaired participants (always CDR 0) and impaired participants (converted to CDR > 0 and had no reversion events). Models evaluated relationships between biomarker status, apolipoprotein E (APOE) ε4 status, and cognition. Additional models described predictors of reversion and predictors of eventual progression to CDR > 0.

RESULTS

CDR reversion was associated with younger age, better cognition, and negative amyloid biomarker status. Reverters that eventually progressed to CDR > 0 had more visits, were older, and were more likely to have an APOE ε4 allele.

DISCUSSION

CDR reversion occupies a transitional phase in disease progression between cognitive normality and overt dementia. Reverters may be ideal candidates for secondary prevention Alzheimer's disease (AD) trials.

Highlights

  • Reverters had more longitudinal cognitive decline than those who remained cognitively normal.
  • Predictors of reversion: younger age, better cognition, and negative amyloid biomarker status.
  • Reverting from CDR 0.5 to 0 is a risk factor for future conversion to CDR > 0.
  • CDR reversion may be a transitional phase in Alzheimer's Disease progression.
  • CDR reverters may be ideal for Alzheimer's disease secondary prevention trials.

1 BACKGROUND

Gauging the presence and severity of dementia is critical for aging and dementia studies. One of the most common research instruments used for determining cognitive status is the Clinical Dementia Rating® (CDR®1). The CDR captures intraindividual changes in cognition and function using a semistructured interview conducted by an experienced clinician with the patient and a collateral source, who is typically a spouse, family member, or close friend. Important features of the CDR are that it is completed without referencing other cognitive tests or mental status exams, and for follow-up evaluations, the CDR is not informed by prior assessments. The CDR is used to define cognitive status in most large observational cohorts studying Alzheimer's disease (AD) and related dementias, such as the National Alzheimer's Coordinating Center (NACC), Alzheimer's Disease Neuroimaging Initiative (ADNI), Australian Imaging, Biomarker & Lifestyle Flagship Study of Ageing (AIBL), and all studies at the Joanne F. and Charles Knight Alzheimer Disease Research Center. The CDR and the CDR-Sum of Boxes (CDR-SB) score are also used in nearly every AD therapeutic trial, and the CDR-SB was a prominently featured outcome measure in the recently completed and successful trials of lecanemab2 and donanemab.3

Clinical trials investigating therapies to stop or slow the progression of AD target enrollment toward older adults who are most likely to show clinical change (e.g., asymptomatic cognitively normal individuals, and/or individuals with very mild to more moderate symptoms of dementia). Recruiting individuals at risk for AD requires tremendous time and resources. For example, the Anti-Amyloid Treatment in Asymptomatic Alzheimer's Disease (A4) trial screened over 4,486 individuals to recruit just 1,100 that were amyloid positive and had some indication of cognitive decline.4 Clinical reversion, or a pattern of fluctuation between a clinical classification of cognitively normal and cognitively impaired, maybe a meaningful predictor of impending clinical change. Studies of clinical reversion have found that reversion is common when tracking change from the classification of mild cognitive impairment (MCI5) back to normal cognition, with rates ranging from 14% in clinic-based studies6 to as much as 58% in population studies.7 At least two studies have found that reversion from MCI to cognitive normality is a risk factor for future progression to dementia.8, 9 Further, a meta-analysis of 17 studies found that individuals who revert from MCI to normal cognition tend to be younger, have higher education, not carry an apolipoprotein E (APOE) ε4 allele, and have better cognitive scores.10 Another recent study found that the presence of persistent neuropsychiatric symptoms was associated with less reversion to cognitive normality11 However, these studies tracked cognitive status with MCI criteria, which rely on cutoffs based on normative data which is subject to practice effects12 and misclassification due to inclusion of low performers.13

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