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.My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Tuesday, November 24, 2020

Coassessment framework to identify person-centred unmet needs in stroke rehabilitation: a case report in Norway

One question assessment is all you need. Did you get 100% recovered? Yes/No? Based on that you provide EXACT STROKE PROTOCOLS to get 100% recovered.

Coassessment framework to identify person-centred unmet needs in stroke rehabilitation: a case report in Norway

  1. Kari Jorunn Kværner1,2,
  2. Linn Nathalie Støme1,
  3. Jonathan Romm3,
  4. Karianne Rygh3,
  5. Frida Almquist3,
  6. Sveinung Tornaas4,
  7. Marianne Storen Berg3

Abstract

Objective To describe unmet needs and values in stroke rehabilitation using the Health Value Framework and the associated coassessment tool Health Value Spider, a framework designed to identify and prioritise unmet needs based on health technology assessment (HTA).

Setting The study took place at Oslo University Hospital, Norway, from February to April 2019. Participants in three consecutive workshops were recruited from Sunnaas Rehabilitation Hospital, Oslo Municipality, Hospital Procurement Trust and Oslo University Hospital. Twenty-four hospital workers (medical and allied health staff and administrative staff) participated in workshop 1 and 29 patients, user representatives and hospital workers in workshop 2. Twenty-one patients and hospital workers participated in workshop 3.

Interventions Stakeholder analysis and scenario building was performed in a coassessment setting where unmet needs were identified applying the Health Value Framework. Two of the authors are also the developers of the Health Value Framework (KJK and LNS).

Results In the two first workshops where health workers, patients and next of kin perspectives were elicited, three needs were identified: patient insecurity in patient journey transitions, lack of stroke rehabilitation expertise in primary care and invisible patient problems, such as fatigue and cognitive impairment. In workshop 3, 12 opportunity areas were identified. Four opportunity areas were selected by the stakeholders based on a prioritisation process: early discovery of cognitive impairment, rehabilitation continuity, empowered patients and next of kin and remote monitoring and digital touchpoints.

Conclusion Health Value Spider successfully identified and prioritised unmet needs and described associated values.

http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Effectiveness of an Innovative Cognitive Treatment and Telerehabilitation on Subjects With Mild Cognitive Impairment: A Multicenter, Randomized, Active-Controlled Study

 Since you lost 5 cognitive years from the stroke maybe you want your doctor to have this available for you. Up to you if you want to enforce competence in your stroke hospital. It might help your children and grandchildren when they have strokes.

Effectiveness of an Innovative Cognitive Treatment and Telerehabilitation on Subjects With Mild Cognitive Impairment: A Multicenter, Randomized, Active-Controlled Study

Rosa Manenti1*, Elena Gobbi1, Francesca Baglio2, Ambra Macis3, Clarissa Ferrari3, Ilaria Pagnoni1, Federica Rossetto2, Sonia Di Tella2, Federica Alemanno4, Vincenzo Cimino5, Giuliano Binetti6, Sandro Iannaccone4, Placido Bramanti5, Stefano F. Cappa7,8 and Maria Cotelli1*
  • 1Neuropsychology Unit, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy
  • 2IRCCS, Fondazione Don Carlo Gnocchi – ONLUS, Milan, Italy
  • 3Service of Statistics, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy
  • 4Department of Rehabilitation and Functional Recovery, IRCCS San Raffaele Hospital and Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy
  • 5IRCCS Centro Neurolesi “Bonino Pulejo,” Messina, Italy
  • 6MAC Memory Clinic and Molecular Markers Laboratory, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy
  • 7NEtS, Scuola Universitaria Superiore IUSS-Pavia, Pavia, Italy
  • 8IRCCS Fondazione Mondino, Pavia, Italy

Background: In recent years, the potential usefulness of cognitive training procedures in normal aging and mild cognitive impairment (MCI) have received increased attention.

Objective: The main aim of this study was to evaluate the efficacy of the face-to-face cognitive virtual reality rehabilitation system (VRRS) and to compare it to that of face-to-face cognitive treatment as usual for individuals with MCI. Moreover, we assessed the possibility of prolonging the effects of treatment with a telerehabilitation system.

Methods: A total of 49 subjects with MCI were assigned to 1 of 3 study groups in a randomized controlled trial design: (a) those who received face-to-face cognitive VRRS (12 sessions of individualized cognitive rehabilitation over 4 weeks) followed by telerehabilitation (36 sessions of home-based cognitive VRRS training, three sessions for week); (b) those who received face-to-face cognitive VRRS followed by at-home unstructured cognitive stimulation (36 sessions of home-based unstructured cognitive stimulation, three sessions for week); and (c) those who received face-to-face cognitive treatment as usual (12 sessions of face-to-face cognitive treatment as usual).

Results: An improvement in memory, language and visuo-constructional abilities was observed after the end of face-to-face VRRS treatment compared to face-to-face treatment as usual. The application of home-based cognitive VRRS telerehabilitation seems to induce more maintenance of the obtained gains than home-based unstructured stimulation.

Discussion: The present study provides preliminary evidence in support of individualized VRRS treatment and telerehabilitation delivery for cognitive rehabilitation and should pave the way for future studies aiming at identifying optimal cognitive treatment protocols in subjects with MCI.

Clinical Trial Registration: www.ClinicalTrials.gov, identifier NCT03486704.

Introduction

In recent years, there has been growing interest in the use of telerehabilitation methods in patients with neurodegenerative diseases (Cherney and van Vuuren, 2012; Cotelli et al., 2019).

Given the limited effectiveness of pharmacological treatments, there is a critical need to develop novel interventions aimed at preventing or delaying the onset of Alzheimer’s disease (AD), and mild cognitive impairment (MCI) might represent a potential target for intervention trials (Kidd, 2008; Hong et al., 2015; Janoutova et al., 2015).

Traditional cognitive training involves intensive in-person sessions that may not prove to be feasible and cost-effective in the case of large-scale implementation. The average lifespan in the world almost doubled during the 20th century and has resulted in a large number of people living to old ages, causing an increased risk of developing age-related diseases, disability and dementia (Fratiglioni et al., 1999; Brown, 2015). In the coming years, the growing demand and the need to contain the costs of health care will dictate the need to reorganize the services dedicated to people at risk of developing cognitive impairment by taking advantage of technological developments (Bharucha et al., 2009; Astell, 2019; Moyle, 2019). Telerehabilitation via information and communication technologies (Brennan et al., 2011; Realdon et al., 2016; Pitt et al., 2019) represents an innovative approach to overcome the obstacles associated with face-to-face intervention. Telerehabilitation technologies allow to provide services remotely in patients’ homes or other environments, allowing access to health care to patients living in rural settings or with mobility difficulties (Brennan et al., 2002, 2009, 2011; Forducey et al., 2003; Mashima and Doarn, 2008; Zampolini et al., 2008; Hailey et al., 2011; Peretti et al., 2017). In addition, the telerehabilitation modality offers the advantage of providing rehabilitation within the natural environment of the patient’s home, making the treatment more realistic and possibly more generalizable to the person’s daily life (McCue et al., 2010).

Recent studies have shown that the application of telerehabilitation methodology in individuals with physical impairments, post-stroke participants and patients with neurodegenerative diseases leads to clinical improvements that are generally equal to those induced by conventional face-to-face rehabilitation programs (Brennan et al., 2002; Rosen, 2004; Poon et al., 2005; Mashima and Doarn, 2008; Kairy et al., 2009; Cherney and van Vuuren, 2012; Jelcic et al., 2014; Antonietti et al., 2016; Vermeij et al., 2016; Burton and O’Connell, 2018; Isernia et al., 2019).

A recent systematic review showed the efficacy of telerehabilitation on cognitive abilities in individuals with MCI and in patients with neurodegenerative diseases associated with cognitive impairment (Cotelli et al., 2019). MCI is a condition associated with risk of progression to dementia, and represents a well-suited target for prevention studies (Petersen et al., 1999, 2014; Petersen, 2004; Livingston et al., 2017). However, these treatments are delivered in several ways and there is not a clinical consensus about content-design of telerehabilitation. A fixed schedule approach has proved to be effective in the treatment of elderly people with high risk of conversion in dementia resulting in a significant improvement in global cognitive functioning, memory and processing speed (Lampit et al., 2014). In other studies, participants were given the opportunity to choose free among the activities available in each session of training (Medalia and Freilich, 2008; Gooding et al., 2016). A third alternative consisted in the user-centered approach, which customized the choice of rehabilitative contents based on the performance obtained by the individual to the set up tests implemented in the software at the beginning of the rehabilitation path (Solana et al., 2015; Vance et al., 2018). So far, the majority of studies are feasibility or pilot studies with small-medium sample size and are very heterogeneous in terms of intensity and duration of treatment (Burdea et al., 2015; Espay et al., 2016; Dodakian et al., 2017). For this reason, in the light of this ongoing deep transformation of health care, it is of great relevance the effort to harmonize intervention protocols and randomized controlled trials (RCTs) are strongly needed to demonstrate the effectiveness of these home-based technology-enhanced treatment protocols with respect to the gold-standard, named the usual face-to-face care (Linden et al., 2016; Fetta et al., 2017; Topol, 2019).

The main aim of the current study was to evaluate the efficacy of the cognitive face-to-face virtual reality rehabilitation system (VRRS) and to compare it to that of face-to-face cognitive treatment as usual for subjects with MCI. We hypothesized that the face-to-face VRRS system would ameliorate memory and attentional abilities more than treatment as usual in subjects with MCI.

Moreover, we tested the hypothesis that the implementation of home-based treatment through the cognitive VRRS system could induce long-term benefits, prolonging the beneficial effects of face-to-face.

 

Brain Entropy Mapping in Healthy Aging and Alzheimer’s Disease

I have zero understanding of this but you will want your doctor to know what to do about this because of your heightened risks of dementia. Assuming that your doctor even knows about those risks. 

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

But maybe this: which you doctor needs to come up with EXACT amounts of caffeine to consume. YOUR DOCTOR'S RESPONSIBILITY!

Caffeine causes widespread brain entropy (and that's a good thing)

April 2018

 

The latest here:

Brain Entropy Mapping in Healthy Aging and Alzheimer’s Disease

Ze Wang* and for the Alzheimer’s Disease Neuroimaging Initiative
  • Department of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore, United States

Alzheimer’s disease (AD) is a progressive neurodegenerative disease, for which aging remains the major risk factor. Aging is under a consistent pressure of increasing brain entropy (BEN) due to the progressive brain deteriorations. Noticeably, the brain constantly consumes a large amount of energy to maintain its functional integrity, likely creating or maintaining a big “reserve” to counteract the high entropy. Malfunctions of this latent reserve may indicate a critical point of disease progression. The purpose of this study was to characterize BEN in aging and AD and to test an inverse-U-shape BEN model: BEN increases with age and AD pathology in normal aging but decreases in the AD continuum. BEN was measured with resting state fMRI and compared across aging and the AD continuum. Associations of BEN with age, education, clinical symptoms, and pathology were examined by multiple regression. The analysis results highlighted resting BEN in the default mode network, medial temporal lobe, and prefrontal cortex and showed that: (1) BEN increased with age and pathological deposition in normal aging but decreased with age and pathological deposition in the AD continuum; (2) AD showed catastrophic BEN reduction, which was related to more severe cognitive impairment and daily function disability; and (3) BEN decreased with education years in normal aging, but not in the AD continuum. BEN evolution follows an inverse-U trajectory when AD progresses from normal aging to AD dementia. Education is beneficial for suppressing the entropy increase potency in normal aging.

Introduction

Alzheimer’s disease (AD) is a neurodegenerative disease that has impacted millions of elderly people but still remains incurable (Ferri et al., 2005; Reitz and Mayeux, 2014). Although AD has been well characterized by AD pathology and clinical symptoms, a major barrier to research progress is the unclear mechanism for how and when normal aging progresses into AD dementia (Kumar and Singh, 2015; Mehta and Yeo, 2017) and why AD symptoms often emerge many years later than AD pathology. This pathology vs. symptom discrepancy (Jack et al., 2010; Jack and Holtzman, 2013) suggests that there may exist a reserve of brain function according to the seminal “cognitive reserve” (CR; Stern, 2006; Stern et al., 2018) model. This reserve may compensate brain damage–induced functional abnormalities in normal aging but fails to do that after disease conversion. To characterize the brain function reserve, we need a more tangible proxy. One candidate is the resting-state brain activity which matches the latent function reserve in two perspectives: first, it is an ongoing process non-specific to any overt brain function; second, it has been postulated to play a role in brain function facilitation (Raichle et al., 2001; Raichle and Gusnard, 2002; Raichle, 2011). Resting-state fMRI (rsfMRI) represents the most widely used tool for studying resting brain activity and has been used to assess neural correlates of brain reserve through the inter-regional functional connectivity (FC) analysis (Arenaza-Urquijo et al., 2013; Bozzali et al., 2015; Marques et al., 2016; Franzmeier et al., 2017; Li et al., 2020). An overall picture revealed by these studies is that higher CR measures are related to stronger FC in distributed brain regions including the default mode network (DMN) area and weaker FC in other restricted focal regions. Because FC is defined by the inter-regional signal correlation in the seed-based FC (Biswal et al., 1995) or the associations to a common temporal fluctuation pattern in the spatial independent component decomposition (Calhoun et al., 2001; Hyvärinen et al., 2001; Beckmann and Smith, 2004), it does not tell anything specific to regional brain activity.

In this study, we proposed entropy of each local voxel as a regional proxy of brain reserve. Entropy is a physical measure for a dynamic system with high entropy indicating less order and more irregularity. It may be informative for delineating the aforementioned AD pathology vs. symptom discrepancy because aging is known to have progressive brain deteriorations (Hayflick, 2004; Drachman, 2006) which inevitably increase the brain entropy. High entropy corresponds to low temporal coherence, which is detrimental to brain functional organization and has to be counteracted to keep the normal brain functionality. Because brain reserve is defined by brain function facilitation and compensation, assessing entropy of functional brain activity may provide a direct outcome measure of the latent brain reserve. In a pilot study (Wang, 2020a,b; full article under separate review) based on data from 862 healthy adults from the human connectome project (Van Essen et al., 2013), we found that brain entropy (BEN) in the DMN (including precuneus, bilateral parietal cortex, and part of temporal cortex) and the executive control network (ECN; including the dorsolateral prefrontal cortex and lateral parietal cortex) increases with age but decreases with education years (an indicator of cognitive reserve for compensating brain dysfunctions) and that lower BEN in DMN and ECN is associated with better performance of cognitive functions. These data suggest the feasibility of BEN for characterizing the latent brain reserve compensation outcome. Although the compensation may be sufficient in normal aging, they may become insufficient when disease progresses, which can reciprocally trigger reserve overactions, leading to a catastrophic reduction of BEN as found in previous biophysiological recording–based AD entropy studies (Stam et al., 2003; Jeong, 2004; Abásolo et al., 2006; Gómez and Hornero, 2010; Mizuno et al., 2010; Yang et al., 2013). To explain this apparent opposed entropy change pattern in normal aging and AD, we proposed a heuristic BEN model as shown in Figure 1. This model considers low BEN in DMN and ECN as beneficial for normal aging because low brain entropy corresponds to high temporal coherence which is evidenced to be important for brain function (Buzsáki and Draguhn, 2004; Buzsaki, 2006; Schroeder and Lakatos, 2009; Saleh et al., 2010; Buzsáki and Watson, 2012; Henry and Obleser, 2012; Lega et al., 2012; Thut et al., 2012; Calderone et al., 2014; Reinhart and Nguyen, 2019). However, in AD, our model predicts a detrimental large BEN reduction in DMN/ECN, indicating a failure of the functional compensation role of brain reserve in AD (Stern, 2006, 2012; Stern et al., 2018). The accumulating brain errors or deteriorations will increase BEN and the risk of brain dysfunction if no compensations occur. This potency, however, can be substantially counteracted by brain reserve or other compensatory mechanisms, resulting in a slowly increasing and then flat topping BEN evolution curve in normal aging (the dashed blue line in Figure 1). When the BEN increase latency reaches a critical point where brain dysfunction cannot be fully compensated anymore, reserve overaction may be triggered, leading to an apparent BEN reduction (the red solid curve in Figure 1). When disease progresses, BEN reduction may be accelerated further by other detrimental factors such as the accumulation of Aβ deposition and perfusion deficits. Both Aβ decomposition and hypoperfusion may cause or be associated with BEN reductions through the CBF vs. brain coherence associations: lower CBF correlates with higher brain activity coherence (Sharbrough et al., 1973; Foreman and Claassen, 2012; higher coherence corresponds to lower BEN).

FIGURE 1
www.frontiersin.org

Figure 1. A hypothetical brain entropy (BEN) model for normal aging and Alzheimer’s disease (AD). The dotted line shows the latent BEN evolution trend as a result of the aging-related accumulated brain deteriorations. The dashed line represents the actual BEN evolution curve after brain reserve compensation which imposes negative entropy brings down the total BEN. Catastrophic BEN reduction may start at the disease conversion time due to a potential overaction of the brain reserve.

The main purpose of this study was to assess the feasibility of BEN as an outcome measure of the latent brain function reserve and to evaluate the hypothetical BEN model by leveraging the relatively large data from the AD Neuroimaging Initiative (ADNI)1 and our recently developed rsfMRI-based BEN mapping tool (Wang et al., 2014). The model was assessed using the cross-sectional ADNI rsfMRI data. We hypothesized that AD patients have lower BEN than cognitively healthy elderlies; BEN increases with age in normal aging but not in AD. The association of BEN to function reserve was examined through the correlation between BEN and education, cognitive function measures, and AD pathology measures. Education is a main contributing factor of cognitive reserve (Stern et al., 2018). Longer education years have been demonstrated to be beneficial for combating cognitive impairments. In accordance with the BEN model, we hypothesized that longer education years are associated with reduced BEN in normal aging but not in AD. The entire study reported in this paper is a full expansion of a small sample-based preliminary study (Li and Wang, 2016).

 

Videogames to help rehabilitate stroke patients

 We don't need you to tell us the obvious, it's been known for over a decade.  

WE NEED YOU TO CREATE EXACT STROKE REHAB PROTOCOLS.

  • video games (81 posts to March 2012 and I had video games 14 years ago)

But nothing like that will occur until we get survivors in charge.

Videogames to help rehabilitate stroke patients

 
 

Monday, November 23, 2020

Protective Effects of Leisure Activity on Dementia Risk Called Into Question

Well shit, there goes one of my prevention plans, although I will continue my social contacts and physical activity as much as possible anyway.

There is always coffee:

Coffee May Lower Your Risk of Dementia

Feb. 2013 

And this: Coffee's Phenylindanes Fight Alzheimer's Plaque 

How coffee protects against Parkinson’s Aug. 2014  

How Coffee May Protect Brain Health: A New Study Suggests The Benefits Aren't Just From Caffeine December 2018

The latest here:

Protective Effects of Leisure Activity on Dementia Risk Called Into Question

Previous short-term studies may reflect consequences of preclinical dementia

Study Authors: Andrew Sommerlad, Séverine Sabia, et al.; Victor W. Henderson, Merrill F. Elias

Target Audience and Goal Statement: Geriatricians, neurologists, primary care physicians, psychiatrists

The goal of this study was to examine the association between participation in leisure activities and incident dementia.

Questions Addressed:

  • Was leisure activity participation associated with lower risk of incident dementia in a large longitudinal study with an average 18-year follow-up?
  • How does length of follow-up affect the associations between activity participation and dementia; specific activities and dementia; and leisure activity change over 10 years and subsequent incident dementia?

Study Synopsis and Perspective:

The aging population and the lack of any disease-modifying treatments for dementia have increased interest in modifiable lifestyle factors that might help prevent or delay cognitive decline and onset of dementia, and maintain quality of life in old age.

Action Points

  • There was no evidence of a protective association between leisure activity participation and dementia, and no specific type of leisure activity was consistently associated with dementia risk, according to a large longitudinal study of London-based civil servants.
  • The findings suggest that decreases in leisure activity participation may be a prodromal feature of dementia, and simply increasing activities may not be a strategy for preventing dementia.

Leisure activities, i.e., pursuits engaged in for relaxation or pleasure outside of work and household responsibilities, have been studied extensively in this regard, since such activity involves three key aspects of cognitive reserve: mental activity, physical activity, and social engagement.

According to recent results from the longitudinal Whitehall II study, participating in leisure activities such as reading or going to the movies at age 56 was not linked to less dementia risk 18 years later.

However, higher participation at age 66 was tied to a lower likelihood of dementia over 8.3 years, suggesting leisure activity declines during the preclinical stage of dementia, reported Andrew Sommerlad PhD, of University College London, and colleagues in Neurology.

For each standard deviation higher on total leisure activity, dementia risk was 18% lower (HR 0.82, 95% CI 0.69-0.98) when the mean follow-up was 8.3 years, 12% lower (HR 0.88, 95% CI 0.76-1.03) at 13 years of follow-up, and 8% lower (HR 0.92, 95% CI 0.79-1.06) at 18 years.

While the outcomes may appear to contradict earlier research suggesting that leisure activity may protect against dementia, most of those studies had shorter follow-up periods, assessing the effects of leisure activity that occurred less than a decade before diagnosis of dementia, the researchers noted.

Sommerlad and team evaluated the activities of 8,280 London-based civil servants in the Whitehall II prospective cohort study; 69% were men, 91% were white, and mean age at the start of follow-up was about 56.

At three points -- 1997-1999, 2002-2004, and 2007-2009 -- Sommerlad and team assessed how frequently participants engaged in 13 types of leisure activities in the past year. Leisure activities ranged from reading, music, and taking classes to cultural, religious, and social events. Dementia diagnoses were derived from three linked electronic health records.

Overall, 360 incident dementia cases were recorded over the follow-up period (incidence 2.4 per 10,000 person-years). Mean age at diagnosis was about 76. No specific activities were consistently associated with dementia risk.

Participants whose activity level dropped over the course of the study were more likely to develop dementia than those whose activity, even if low, stayed the same. Five percent of 1,159 people whose activity decreased developed dementia compared with 2% of 820 people whose activity level stayed low over the years.

The finding doesn't question the importance of keeping active, "but it does suggest that simply increasing leisure activity may not be a strategy for preventing dementia," Sommerlad said in a statement.

"More research is needed to confirm these results, but we know that early changes in the brain can start decades before any symptoms emerge," he added. "It's plausible that people may slow down their activity level up to 10 years before dementia is actually diagnosed, due to subtle changes and symptoms that are not yet recognized."

One limitation of the study was that dementia diagnoses were gathered from electronic health records and some cases may not have been diagnosed, the researchers noted. The study also did not consider dementia subtypes or physical intensity of leisure activity.

Source References: Neurology 2020; DOI: 10.1212/WNL.0000000000010966

Editorial: Neurology 2020; DOI: 10.1212/WNL.0000000000010962

Study Highlights and Explanation of Findings:

In contrast to previous, mostly shorter-term, studies (lasting less than 10 years), this longitudinal study found no robust evidence for a protective association between leisure activity participation and dementia, and no specific type of leisure activity was consistently associated with dementia risk.

"Leisure activity is linked to reduced risk of cognitive decline, mild cognitive impairment, and dementia, but these associations are often based on activity occurring less than a decade before dementia is diagnosed," noted Victor Henderson, MD, of Stanford University in Palo Alto, California, and Merrill Elias, PhD, MPH, of the University of Maine in Orono, in an accompanying editorial.

Among previous studies of specific activities, a large Australian assessment of computer use among 5,506 community-dwelling men ages 69 to 87 followed for up to 8.5 years found that, compared with no computer use, the adjusted risk for dementia appeared to decrease with increasing frequency of computer use, by almost 40% with at least weekly or daily use.

One recent study of people in England age 50 or older participating in cognitively stimulating activities over an 8-year follow-up found that volunteering and internet use were associated with reduced risk of cognitive impairment.

One interpretation proposed by Henderson and Elias is that leisure activity may help stave off dementia symptoms even when subclinical neuropathology is present, perhaps by enhancing cognitive reserve. "A second possibility is that early neural dysfunction in pathways that underlie motivation and goal-directed behavior makes it more difficult to initiate and sustain leisure activity," they added.

Indeed, apathy may be significant: in cognitively normal older people, a recent prospective study showed that those with severe apathy were nearly twice as likely to develop probable dementia compared with those who had low levels of apathy (HR 1.9, 95% CI 1.5-2.5, P<0.001) over 9 years of follow-up, providing novel evidence for apathy as a prodrome of dementia. While it is often concurrent with depression, apathy is neuroanatomically distinct in being correlated to the dorsolateral prefrontal cortex and associated sub-regions in the basal ganglia.

Apathy was also associated with an approximately two-fold increased risk of dementia in a meta-analysis involving over 7,000 memory clinic patients. Adjustment for apathy definition and duration of follow-up explained 95% of heterogeneity in patients with mild cognitive impairment; these results seem generalizable to memory clinic populations, suggesting that apathy deserves more attention as a relevant, cheap, noninvasive, and easily measureable marker of increased risk for incident dementia, particularly because these vulnerable patients may forgo healthcare.

Thus, clinicians should be alert for signs of apathy -- marked by decreases in motivation and initiative, energy and enthusiasm, and gradual social withdrawal, which generally occur about 1 to 2 years before other symptoms of dementia. One expert geriatrician characterized apathy as a spectrum that follows that of dementia, and links worsening apathy with cognitive decline -- a process that can be slowed if apathy is assessed using a validated scale, such as the Apathy Evaluation Scale, and if diagnosed, treated.

"Large, long duration, randomized controlled trials could provide even stronger evidence of any causal relationship" between leisure activity and dementia, Henderson and Elias wrote. Studies that focus on lifestyle interventions, like POINTER in the U.S., may shed better light.

"Midlife and late-life leisure activity certainly does no harm, but its role in dementia prevention is not yet clear," they observed. "There is more work to be done."

Sommerlad and colleagues suggested that future research should investigate the socio-behavioral, cognitive, and neurobiological drivers of decline in leisure activity participation to determine potential approaches to improving social participation in those developing dementia.

"Our novel finding of association of dementia with activity decline and the timing of this decline suggests that changes in leisure activity participation may be a prodromal feature of dementia, which is consistent with retrospective accounts of decline in participation in activities preceding dementia onset. There should therefore be awareness among clinicians that those who decrease leisure activities in the absence of other causes might be developing dementia," the group concluded.

Reviewed by Henry A. Solomon, MD, FACP, FACC Clinical Associate Professor, Weill Cornell Medical College
 

2 Plant Extracts That Reverse Alzheimer’s Disease

This readable article explains this much better.

 But if you want the research behind it. Remember you can't do this on your own, it is not clinically proven yet. And since I'm not medically trained, don't listen to me.

You can't do this on your own, no human clinical research to back it up and no amounts or protocol to follow. 

Be very careful with green tea extract:

Herbal supplements linked to at least six Australian organ transplants since 2011, data shows  March 2016 

The research behind this:

Combined treatment with the phenolics (−)-epigallocatechin-3-gallate and ferulic acid improves cognition and reduces Alzheimer-like pathology in mice

The readable article here:

2 Plant Extracts That Reverse Alzheimer’s Disease

The extracts work by preventing the build up of sticky amyloid beta in the brain.

Compounds found in carrots and green tea have been shown to reverse Alzheimer’s, research finds.

The plant-based treatment was able to completely restore the memories of mice in the study.


Epigallocatechin-3-gallate (EGCG) is a compound found in green tea.

Meanwhile, ferulic acid is found in rice, tomatoes, carrots, oats and wheat.

For the study, mice genetically programmed to develop the disease were given plant-based supplements for three months.

Although mouse studies often do not translate into humans, the findings are still promising, said Professor Terrence Town, study co-author:

“You don’t have to wait 10 to 12 years for a designer drug to make it to market; you can make these dietary changes today.

I find that very encouraging.”

For the research, 32 mice with Alzheimer’s symptoms were randomly assigned to different diets.


Four groups were fed with different combinations of EGCG and ferulic acid.

The dosages were 30 mg per kilogram of body weight.

This amount could easily be consumed by a human as part of a healthy diet or in the form of supplements.

The mice were given a range of tests of their memory and learning.

These are the mouse-equivalent of tests given to assess dementia in humans.

Professor Town explained the results:

“After three months, combination treatment completely restored working memory and the Alzheimer’s mice performed just as well as the healthy comparison mice.”

The group of mice that did best were those that were given both compounds together.

The two compounds appear to work by preventing the build up of sticky amyloid beta in the brain.

These are the clumps of protein seen in the brains of people with Alzheimer’s.


The compounds also reduced neuroinflammation and oxidative stress.

About the author

Psychologist, Jeremy Dean, PhD is the founder and author of PsyBlog. He holds a doctorate in psychology from University College London and two other advanced degrees in psychology.

He has been writing about scientific research on PsyBlog since 2004. He is also the author of the book “Making Habits, Breaking Habits” (Da Capo, 2003) and several ebooks:

Dr Dean’s bio, Twitter, Facebook and how to contact him.

The study was published in the Journal of Biological Chemistry (Mori et al., 2019).

 


Is a Full Recovery from Stroke Possible? How to Push Your Potential: Flint Rehab

Notice very precisely that your stroke doctor has nothing to do for your recovery because they totally blew it by not figuring out how to stop the 5 causes of the neuronal cascade of death in the first week. My doctor allowed 5.4 billion neurons to die that first week. By preventing that I could have easily fully recovered with only 171 million neurons dying(tPA in 90 minutes).

Is a Full Recovery from Stroke Possible? How to Push Your Potential: Flint Rehab

 

PH DuBois, PH Elk(DuBois, Pa) Receive American Heart Association Quality Achievement Awards for Stroke

 

Big fucking whoopee.

 

 But you tell us NOTHING ABOUT RESULTS. They remind us they 'care' about us multiple times but never tell us how many 100% recovered.  You have to ask yourself why they are hiding their incompetency by not disclosing recovery results. ARE THEY THAT FUCKING BAD?

Three measurements will tell me if the stroke hospital is possibly not completely incompetent; DO YOU MEASURE ANYTHING?  I would start cleaning the hospital by firing the board of directors, you can't let incompetency continue for years at a time.

There is no quality here if you don't measure the right things.

  1. tPA full recovery? Better than 12%?
  2. 30 day deaths? Better than competitors?
  3. rehab full recovery? Better than 10%?

 

You'll want to know results so contact Jolene below.  RESULTS are; tPA efficacy, 30 day deaths, 100% recovery. Because there is no point in going to that hospital if they are not willing to publish results.

 The latest invalid chest thumping here:

PH DuBois, PH Elk(DuBois, Pa) Receive American Heart Association Quality Achievement Awards for Stroke

DUBOIS ? Penn Highlands DuBois and Penn Highlands Elk have received the American Heart Association/American Stroke Association’s Get With The Guidelines®-Stroke Quality Achievement Award. The award recognizes a hospital’s commitment to ensuring stroke patients receive the most appropriate treatment according to nationally recognized, research-based guidelines based on the latest scientific evidence. This year Penn Highlands DuBois has won the Gold Plus award for the fifth year in a row, while Penn Highlands Elk has won the Silver award for the first time.

The two hospitals have earned these awards by meeting specific quality achievement measures for the diagnosis and treatment of stroke patients at a set level for a designated period. These measures include evaluation of the proper use of medications and other stroke treatments aligned with the most up-to-date, evidence-based guidelines with the goal of speeding recovery and reducing death and disability for stroke patients. Before discharge, patients also receive education on managing their health, get a follow-up visit scheduled, as well as other care transition interventions.


“Penn Highlands Healthcare is dedicated to improving the quality of care for our stroke patients by implementing the American Heart Association’s Get with the Guidelines Stroke initiative,” said Rose Campbell, Chief Nursing Officer at Penn Highlands Healthcare. “The tools and resources offered with this program help us track and measure our success in meeting evidenced-based clinical guidelines developed to improve patient outcomes.”

To qualify for this recognition, hospitals must meet quality measures developed to reduce the time between the patient’s arrival at the hospital and treatment with the clot-buster tissue plasminogen activator, or tPA, the only drug approved by the U.S. Food and Drug Administration to treat ischemic stroke

“We are pleased to recognize Penn Highlands DuBois and Penn Highlands Elk for their commitment to stroke care,” said Lee H. Schwamm, M.D., national chairperson of the Quality Oversight Committee and Executive Vice Chair of Neurology, Director of Acute Stroke Services, Massachusetts General Hospital, Boston, Massachusetts. “Research has shown that hospitals adhering to clinical measures through the Get With The Guidelines quality improvement initiative can often see fewer readmissions and lower mortality rates.”

According to the American Heart Association/American Stroke Association, stroke is the number-five cause of death and a leading cause of adult disability in the United States. On average, someone in the U.S. suffers a stroke every 40 seconds and nearly 795,000 people suffer a new or recurrent stroke each year.


To learn more about stroke care and prevention at Penn Highlands Healthcare, contact stroke coordinator Jolene Barbazzeni, BSN, RN, SCRN, PHRN at jabarbazzeni@phhealthcare.org.

 

Guidelines for Adult Stroke Rehabilitation and Recovery; American Heart Association/American Stroke Association

You can immediately tell from the title that this is worthless. GUIDELINES, NOT PROTOCOLS.  Nothing here has any chance of guaranteeing 100% recovery.

Guidelines for Adult Stroke Rehabilitation and Recovery; American Heart Association/American Stroke Association 

Endorsed by the American Academy of Physical Medicine and Rehabilitation and the American Society of Neurorehabilitation The American Academy of Neurology affirms the value of this guideline  as  an educational  tool  for  neurologists  and  the  American  Congress  of  Rehabilitation  Medicine  also  affirms  the educational  value  of  these  guidelines  for  its  members
Carolee J. Winstein, PhD, PT, Chair; Joel Stein, MD, Vice Chair; Ross Arena, PhD, PT, FAHA; Barbara Bates, MD, MBA; Leora R. Cherney, PhD; Steven C. Cramer, MD; Frank Deruyter, PhD; Janice J. Eng, PhD, BSc; Beth Fisher, PhD, PT; Richard L. Harvey, MD; Catherine E. Lang, PhD, PT; Marilyn MacKay-Lyons, BSc, MScPT, PhD; Kenneth J. Ottenbacher, PhD, OTR; Sue Pugh, MSN, RN, CNS-BC, CRRN, CNRN, FAHA; Mathew J. Reeves, PhD, DVM, FAHA; Lorie G. Richards, PhD, OTR/L; William Stiers, PhD, ABPP (RP); Richard D. Zorowitz, MD; on behalf of the American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Quality of Care and Outcomes Research
Purpose
—The  aim  of  this  guideline is to provide a synopsis of best clinical practices in the rehabilitative care of adults recovering from stroke.
Methods
—Writing group members(Notice that not a single survivor was even thought of being put on the committee. Which is why we get shitty guidelines rather than protocols. Hope you are OK with such crapola when you are the 1 in 4 per WHO that has a stroke )  were nominated by the committee chair on the basis of their previous work in relevant topic areas and were approved by the American Heart Association (AHA) Stroke Council’s Scientific Statement Oversight Committee and the AHA’s Manuscript Oversight Committee. The panel reviewed relevant articles  on  adults  using  computerized  searches  of  the  medical  literature  through  2014.  The evidence  is  organized  within  the  context  of  the  AHA  framework  and  is  classified  according  to  the  joint AHA/American  College  of  Cardiology  and  supplementary  AHA  methods  of  classifying  the  level  of  certainty  and  the  class  and  level  of  evidence.  The  document  underwent  extensive AHA internal  and  external peer  review,  Stroke  Council  Leadership  review,  and  Scientific  Statements  Oversight  Committee  review before  consideration  and  approval  by  the  AHA  Science  Advisory  and  Coordinating  Committee.
 Results
—Stroke  rehabilitation  requires  a  sustained  and  coordinated  effort  from  a  large  team,  including  the  patient and  his  or  her  goals(But nothing here is going to get survivors to 100% recovery; the only goal in stroke.),  family  and  friends, other caregivers (eg, personal care attendants), physicians, nurses, physical and occupational therapists, speech-language pathologists, recreation therapists, psychologists, nutritionists, social workers, and others. Communication and coordination among these team members are paramount in maximizing the effectiveness and efficiency of rehabilitation and underlie this entire guideline. Without communication and coordination, isolated efforts to rehabilitate the stroke survivor are unlikely to achieve their full potential.
 

Exercise for This Many Minutes for a Longer Life, Says Science; 12 minutes of vigorous exercise

The responsibility is your doctors to get you recovered well enough to do 12 minutes of vigorous exercise. YOUR DOCTOR'S RESPONSIBILITY!

 

Exercise for This Many Minutes for a Longer Life, Says Science

For many of us, it's been a tough year for maintaining healthy habits. As our living situations change and our options for exercising outside the house decrease with the recent country-wide spike in cases, it can be tough to figure out what our usual workout routine looks like. Good news: it turns out, working the benefits of regular exercise into your life may be easier than you thought. A study published in the American Heart Association journal Circulation has found that bursts of exercise as short as twelve minutes can increase your life expectancy and decrease your risk of heart disease and diabetes.

The study, conducted by researchers at the Harvard-affiliated Massachusetts General Hospital, looked at the levels of hundreds of different metabolites in 411 middle-aged men and women before and after about twelve minutes of strenuous exercise. They found that the amount of DMGV, a biomarker linked to increased risk of diabetes and fatty liver disease, dropped 18 percent. Similarly, Glutamate, which is associated with heart disease, diabetes, and shorter life expectancy, decreased 29 percent. This is great news for anyone with a packed schedule—just 12 minutes of vigorous exercise can fight off deadly diseases and make you live longer. (Related:21 Best Healthy Cooking Hacks of All Time.)

"We're starting to better understand the molecular underpinnings of how exercise affects the body and use that knowledge to understand the metabolic architecture around exercise response patterns," co-lead author Ravi Shah, MD, explains to the Harvard Gazette. "This approach has the potential to target people who have high blood pressure or many other metabolic risk factors in response to exercise, and set them on a healthier trajectory early in their lives."

Still not motivated to set aside just twelve minutes of your day to commit to living a healthier life? Consider how harmful the alternative can be—here's What Happens to Your Body When You Don't Move All Day.