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, April 13, 2021

An Exercise Mimetic Approach to Reduce Poststroke Deconditioning and Enhance Stroke Recovery

 I'm sure your eyes immediately glassed over upon seeing the word 'mimetic'.

An Exercise Mimetic Approach to Reduce Poststroke Deconditioning and Enhance Stroke Recovery

First Published April 7, 2021 Research Article 

Evidence supports early rehabilitation after stroke to limit disability. However, stroke survivors are typically sedentary and experience significant cardiovascular and muscular deconditioning. Despite growing consensus that preclinical and clinical stroke recovery research should be aligned, there have been few attempts to incorporate cardiovascular and skeletal muscle deconditioning into animal models of stroke. Here, we demonstrate in rats that a hindlimb sensorimotor cortex stroke results in both cardiovascular and skeletal muscle deconditioning and impairments in gait akin to those observed in humans. To reduce poststroke behavioral, cardiovascular, and skeletal muscle perturbations, we then used a combinatorial intervention consisting of aerobic and resistance exercise in conjunction with administration of resveratrol (RESV), a drug with exercise mimetic properties. A combination of aerobic and resistance exercise mitigated decreases in cardiovascular fitness and attenuated skeletal muscle abnormalities. RESV, beginning 24 hours poststroke, reduced acute hindlimb impairments, improved recovery in hindlimb function, increased vascular density in the perilesional cortex, and attenuated skeletal muscle fiber changes. Early RESV treatment and aerobic and resistance exercise independently provided poststroke benefits, at a time when individuals are rapidly becoming deconditioned as a result of inactivity. Although no additive effects were observed in these experiments, this approach represents a promising strategy to reduce poststroke behavioral impairments and minimize deconditioning. As such, this treatment regime has potential for enabling patients to engage in more intensive rehabilitation at an earlier time following stroke when mechanisms of neuroplasticity are most prevalent.

With advances in acute care, stroke has transitioned from a disease of survivability to one of chronic disability.1 To optimize behavioral recovery, preclinical evidence suggests that high-intensity rehabilitation should be initiated during the early subacute stroke recovery phase to harness the brain’s endogenous repair mechanisms.2-5 Instead, at this time stroke patients are extremely inactive, spending more than 50% of their time lying in bed and ~87% of time in a sedentary state.6,7 As such, stroke survivors experience significant deconditioning and fatigue, which reduces their capacity to engage in high-intensity rehabilitation and accomplish most activities of daily living.8-11

International consensus groups recognize that preclinical and clinical research must become better aligned to advance the field of stroke recovery.12,13 In humans, the stroke-affected limb undergoes significant muscular atrophy, hypertrophy of slow-twitch fibers, and atrophy of fast-twitch fibers.8,9,14 Similarly, stroke survivors experience significant cardiovascular deconditioning.8-11 Currently, these aspects of cardiovascular and skeletal muscle dysfunction have not been incorporated into animal models of stroke, nor has consideration been given to the idea that the benefits of poststroke interventions might be a result of central as well as peripheral actions.8,9,11,14,15

Exercise is viewed as a powerful poststroke therapeutic, enhancing brain repair through multiple mechanisms such angiogenesis, upregulation of growth factors, reducing inflammation, and attenuating deteriorations in cardiovascular and skeletal muscle health.11,16,17 However, implementing aerobic exercise following stroke is challenging, largely because of fatigue and deconditioning.8,18 Thus, poststroke deconditioning is a significant barrier that limits patients’ ability to engage in early, intensive rehabilitation programs. A possible solution is to administer drugs that induce central and peripheral effects similar to physical exercise (ie, exercise mimetics). In this context, resveratrol (RESV), a naturally occurring polyphenol (found in grapes, blueberries, peanuts, etc), has the potential to enhance neurological recovery and attenuate poststroke cardiovascular and skeletal muscle deconditioning by activation of sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC1α), and angiogenesis in a variety of body tissues (eg, brain, heart, muscle) similar to exercise.19-23

Because lack of mobility is such an important issue for patients following stroke, we used a rat model of hindlimb motor cortex stroke to assess poststroke changes in skeletal muscle and cardiovascular deconditioning. We hypothesized that both RESV and delayed aerobic and resistance exercise (DEx) following stroke would enhance behavioral recovery and attenuate poststroke deconditioning but that the combination would be most effective. In summary, this study aimed to address a number of interrelated research questions: (1) In conjunction with persistent hindlimb deficits, do rats experience cardiovascular deconditioning and skeletal muscle fiber changes as observed clinically? (2) Does early RESV administration reduce acute hindlimb deficits? (3) Does RESV alone or in combination with exercise rehabilitation improve long-term hindlimb recovery? (4) Does RESV alone or in combination with exercise mitigate perturbations in cardiovascular fitness and skeletal muscle after stroke?

 

Baduanjin Qigong Improves Balance, Leg Strength, and Mobility in Individuals With Chronic Stroke: A Randomized Controlled Study

I guess you'll have to find and figure out what Baduanjin Qigong is since they tell you nothing. Where to get it? What is is? How long to do it? This is pretty much useless as is. Since this is for chronic it means you are likely not seeing any stroke medical professionals anymore. You're on your own to figure this out.

Baduanjin Qigong Improves Balance, Leg Strength, and Mobility in Individuals With Chronic Stroke: A Randomized Controlled Study

First Published April 7, 2021 Research Article 

Effective and sustainable exercise training methods for improving balance poststroke are needed.

To evaluate the effect of Baduanjin Qigong for improving balance after stroke.

This was a single-blinded randomized controlled study in which only the assessor was blinded. Fifty-eight people with chronic stroke (mean age: 62.5 ± 11.8 years) were randomly assigned to the experimental (n = 29) or control group (n = 29). The experimental group underwent 8 weeks of supervised Baduanjin training (3 sessions per week). This was followed by home-based practice of the same exercises 3 days a week for another 8 weeks. The control group underwent 2 sessions of supervised conventional fitness training in the first week, followed by home-based exercise practice 3 days a week until the end of week 16. All outcomes were measured at baseline, week 8, and week 16.

Significantly greater improvements in the Mini-Balance Evaluation Systems Test (Mini-BESTest), composite equilibrium score (Sensory Organization Test), 5 Times Sit to Stand, and Timed Up and Go test were detected at week 8 in the experimental group than in the control group (P < .017). Further improvement in the Mini-BESTest was observed from week 8 to 16 in the experimental group (P < .001). Other outcomes (Limit of Stability, Fall-Efficacy Scale, Modified Barthel Index, Stroke-Specific Quality of Life) showed no significant results.

Baduanjin is effective in improving balance, leg strength, and mobility and is a safe and sustainable form of home-based exercise for people with chronic stroke.

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Number of Retrieval Attempts Rather Than Procedure Time Is Associated With Risk of Symptomatic Intracranial Hemorrhage

 

IT IS YOUR RESPONSIBILITY  to have the proper stroke that only needs one pass.  All because your doctors and stroke hospital have not taken the proper steps to create 100% recovery protocols for ANY situation. 

IT IS YOUR RESPONSIBILITY to ensure your hospital does create those protocols. Without your push your stroke hospital will do nothing.  If your want your children and grandchildren to 100% recover from a stroke YOU  have to start right now.

The latest here:

Number of Retrieval Attempts Rather Than Procedure Time Is Associated With Risk of Symptomatic Intracranial Hemorrhage

Originally publishedhttps://doi.org/10.1161/STROKEAHA.120.031242Stroke. ;0:STROKEAHA.120.031242

Background and Purpose:

Endovascular therapy is the standard of care in the treatment of acute ischemic stroke due to large-vessel occlusion. A direct association between the number of device passes and the occurrence of symptomatic intracranial hemorrhage (SICH) has been suggested. This study represents an in-depth investigation of the hypothesis that >3 retrieval attempts is associated with an increased rate of SICH in a large multicenter patient cohort.

Methods:

Two thousand six hundred eleven patients from the prospective German Stroke Registry were analyzed. Patients who received Endovascular therapy for acute large-vessel occlusion of the anterior circulation with known admission National Institutes of Health Stroke Scale and Alberta Stroke Program Early CT Score, final Thrombolysis in Cerebral Infarction, and number of retrieval passes were included. The primary outcome was defined as SICH. The secondary outcome was any type of radiologically confirmed intracranial hemorrhage within the first 24 hours. Multivariate mixed-effects models were used to adjust for cluster effects of the participating centers, as well as for confounders.

Results:

Five hundred ninety-three patients fulfilled the inclusion criteria. The median number of retrieval passes was 2 [interquartile range, 1–3]. SICH occurred in 26 cases (4.4%), whereas intracranial hemorrhage was identified by neuroimaging in 85 (14.3%) cases. More than 3 retrieval passes was the strongest predictor for SICH (odds ratio, 3.61 [95% CI, 1.38–9.42], P=0.0089) following adjustment for age, admission National Institutes of Health Stroke Scale, admission Alberta Stroke Program Early CT Score, and Thrombolysis in Cerebral Infarction, as well as time from symptom onset to flow restoration. Baseline Alberta Stroke Program Early CT Score of 8 to 9 (odds ratio, 0.26 [95% CI, 0.07–0.89], P=0.032) or 10 (odds ratio, 0.21 [95% CI, 0.06–0.78], P=0.020) were significant protective factors against the occurrence of SICH.

Conclusions:

More than 3 retrieval attempts is associated with a significant increase in SICH risk, regardless of patient age, baseline National Institutes of Health Stroke Scale, or procedure time. This should be considered when deciding whether to continue a procedure, especially in patients with large baseline infarctions.(So you are going to let 1.9 million neurons die per minute. Good to know the incompetence involved.)

REGISTRATION:

URL: https://www.clinicaltrials.gov; Unique identifier: NCT03356392.

 

Endovascular reperfusion outcomes in patients with a stroke and low ASPECTS is highly dependent on baseline infarct volumes

IT IS YOUR RESPONSIBILITY  to have the proper stroke  All because your doctors and stroke hospital have not taken the proper steps to create 100% recovery protocols for ANY situation. 

IT IS YOUR RESPONSIBILITY to ensure your hospital does create those protocols. Without your push your stroke hospital will do nothing.  If your want your children and grandchildren to 100% recover from a stroke YOU  have to start right now.

The latest here:

Endovascular reperfusion outcomes in patients with a stroke and low ASPECTS is highly dependent on baseline infarct volumes

  1. Mehdi Bouslama1,
  2. Clara M Barreira2,
  3. Diogo C Haussen2,
  4. Gabriel Martins Rodrigues1,
  5. Leonardo Pisani3,
  6. Michael R Frankel1,
  7. Raul G Nogueira4
  1. Correspondence to Dr Raul G Nogueira, Department of Neurology and Interventional Neuroradiology, Emory University, Atlanta, GA 30303, USA; rnoguei@emory.edu

Abstract

Background Patients with large vessel occlusion stroke (LVOS) and a low Alberta Stroke Program Early CT Score (ASPECTS) are often not offered endovascular therapy (ET) as they are thought to have a poor prognosis.

Objective To compare the outcomes of patients with low and high ASPECTS undergoing ET based on baseline infarct volumes.

Methods Review of a prospectively collected endovascular database at a tertiary care center between September 2010 and March 2020. All patients with anterior circulation LVOS and interpretable baseline CT perfusion (CTP) were included. Subjects were divided into groups with low ASPECTS (0–5) and high ASPECTS (6-10) and subsequently into limited and large CTP-core volumes (cerebral blood flow 30% >70 cc). The primary outcome measure was the difference in rates of 90-day good outcome as defined by a modified Rankin Scale (mRS) score of 0 to 2 across groups.

Results 1248 patients fit the inclusion criteria. 125 patients had low ASPECTS, of whom 16 (12.8%) had a large core (LC), whereas 1123 patients presented with high ASPECTS, including 29 (2.6%) patients with a LC. In the category with a low ASPECTS, there was a trend towards lower rates of functional independence (90-day modified Rankin Scale (mRS) score 0-2) in the LC group (18.8% vs 38.9%, p=0.12), which became significant after adjusting for potential confounders in multivariable analysis (aOR=0.12, 95% CI 0.016 to 0.912, p=0.04). Likewise, LC was associated with significantly lower rates of functional independence (31% vs 51.9%, p=0.03; aOR=0.293, 95% CI 0.095 to 0.909, p=0.04) among patients with high ASPECTS.

Conclusions Outcomes may vary significantly in the same ASPECTS category depending on infarct volume. Patients with ASPECTS ≤5 but baseline infarct volumes ≤70 cc may achieve independence in nearly 40% of the cases and thus should not be excluded from treatment.


 

Very Early Exercise Rehabilitation After Intracerebral Hemorrhage Promotes Inflammation in the Brain

You came to the wrong conclusion. The hemorrhage cascade of death is probably responsible for the inflammation rather than the exercise. Do you people have any understanding of stroke at all?  And your mentors and senior researchers didn't correct that misunderstanding?

Very Early Exercise Rehabilitation After Intracerebral Hemorrhage Promotes Inflammation in the Brain

First Published April 7, 2021 Research Article 

Very early exercise has been reported to exacerbate motor dysfunction; however, its mechanism is largely unknown.

This study examined the effect of very early exercise on motor recovery and associated brain damage following intracerebral hemorrhage (ICH) in rats.

Collagenase solution was injected into the left striatum to induce ICH. Rats were randomly assigned to receive placebo surgery without exercise (SHAM) or ICH without (ICH) or with very early exercise within 24 hours of surgery (ICH+VET). We observed sensorimotor behaviors before surgery, and after surgery preexercise and postexercise. Postexercise brain tissue was collected 27 hours after surgery to investigate the hematoma area, brain edema, and Il1b, Tgfb1, and Igf1 mRNA levels in the striatum and sensorimotor cortex using real-time reverse transcription polymerase chain reaction. NeuN, PSD95, and GFAP protein expression was analyzed by Western blotting.

We observed significantly increased skillful sensorimotor impairment in the horizontal ladder test and significantly higher Il1b mRNA levels in the striatum of the ICH+VET group compared with the ICH group. NeuN protein expression was significantly reduced in both brain regions of the ICH+VET group compared with the SHAM group.

Our results suggest that very early exercise may be associated with an exacerbation of motor dysfunction because of increased neuronal death and region-specific changes in inflammatory factors. These results indicate that implementing exercise within 24 hours after ICH should be performed with caution.

 

Resting State Connectivity Is Modulated by Motor Learning in Individuals After Stroke

 

I have no understanding of how this helps recovery.  In my case since most of my premotor cortex is dead there can be no transfer from prefrontal to premotor.  And since I'm not healthy it wouldn't transfer anyways. When I follow the higher cognitive load reference24 I find nothing explaining that at all. I was hoping for some explanation of the mental fatigue post stroke.

Resting State Connectivity Is Modulated by Motor Learning in Individuals After Stroke

First Published April 7, 2021 Research Article 

Activity patterns across brain regions that can be characterized at rest (ie, resting-state functional connectivity [rsFC]) are disrupted after stroke and linked to impairments in motor function. While changes in rsFC are associated with motor recovery, it is not clear how rsFC is modulated by skilled motor practice used to promote recovery. The current study examined how rsFC is modulated by skilled motor practice after stroke and how changes in rsFC are linked to motor learning.

Two groups of participants (individuals with stroke and age-matched controls) engaged in 4 weeks of skilled motor practice of a complex, gamified reaching task. Clinical assessments of motor function and impairment, and brain activity (via functional magnetic resonance imaging) were obtained before and after training.

While no differences in rsFC were observed in the control group, increased connectivity was observed in the sensorimotor network, linked to learning in the stroke group. Relative to healthy controls, a decrease in network efficiency was observed in the stroke group following training.

Findings indicate that rsFC patterns related to learning observed after stroke reflect a shift toward a compensatory network configuration characterized by decreased network efficiency.

Damage resulting from stroke disrupts cortical networks and patterns of synchronized brain activity between disparate brain regions (termed functional connectivity).1-3 Synchronized patterns of brain activity can be characterized across the brain at rest (ie, resting-state functional connectivity [rsFC]) and their relationships represented as coherence. These patterns characterize functional reorganization of the brain after stroke and are reliable measure that characterize neural changes across the stages of recovery.4 While altered rsFC is associated with motor recovery (ie, improvements in function characterized by clinical assessments),5 it is not clear how rsFC is modulated by skilled motor practice after stroke (ie, behavioral improvements associated with a specific motor task). Even though rsFC does not rely on task performance, there is evidence showing that active networks mapped with rsFC overlap with regions involved in task performance.6-8 As rsFC does not rely on participant effort or compliance, it may be used to characterize neural changes that accompany motor impairment poststroke. Typically, in individuals with stroke, rsFC is disrupted in the sensorimotor network relative to healthy individuals.9,10 Increases in rsFC in both the sensorimotor network and between regions implicated in cognitive processes (ie, working memory) have been observed as motor recovery is achieved.9,11,12 For instance, poorly recovered individuals showed decreased connectivity within the sensorimotor network, while no differences in connectivity were observed between individuals who were well-recovered and healthy controls.9 Yet a typical pattern of connectivity is not necessarily restored during recovery after stroke. Even in well-recovered individuals, relative to healthy controls, reduced connectivity persists between brain regions associated with cognitive processes.9,13 To date, changes in rsFC have largely characterized functional reorganization that occurs in association with recovery from stroke.11,12,14,15 It remains unclear whether or not skilled motor practice drives changes in rsFC patterns.

Importantly, rsFC is thought to reflect the processing of information gained during skilled motor practice associated with motor consolidation and learning.16,17 Short-term changes in rsFC in areas previously shown to be critical to planning and executing visually guided movement18,19 including a network of frontal, posterior parietal, and cerebellar regions are associated with learning a visuomotor task.16,17,20,21 However, as behavioral change associated with task-specific learning plateaus, limited long-term changes in rsFC in healthy individuals are noted.21 While learning (and relearning) motor skills are critical to promoting functional recovery, we know little about the alterations in processes underlying motor learning after stroke. Thus, rsFC can be employed to characterize change in consolidation of motor memories and learning that result from functional reorganization after stroke.

Specifically, functional magnetic resonance imaging (fMRI) shows that healthy individuals shift brain activity from the prefrontal regions early in skilled motor practice to premotor cortical activation after learning occurs.16,22 This shift is not observed after stroke.23 The persistent and greater recruitment of frontal-parietal regions during motor tasks may reflect higher cognitive load during skilled motor practice after stroke.24 It also may be related to an overall decrease in network efficiency after stroke,25,26 that represents a lower overall capacity to transmit information and indicates that a compensatory network (ie, not restored to a neurotypical pattern of functioning) underlies motor processes.23 Taken together, alterations in consolidation and learning processes may arise after stroke, reflected by decreased network efficiency and greater reliance on cognitive processes during skilled motor practice. To test this idea, we probed (long-term) changes in rsFC induced by skilled motor practice to examine how brain reorganization supports learning after stroke.

The primary aim of the current study was to examine how rsFC is modulated by skilled motor practice after stroke. Furthermore, we sought explore how changes in rsFC are linked to motor learning. To address our objectives, we employed a between-group design whereby 2 groups of participants (individuals with stroke and age-matched controls) engaged in 4 weeks of skilled motor practice of a complex, gamified reaching task, that was designed to prevent early plateaus in performance. Clinical assessments of motor function and impairment, and brain activity were obtained before and after training.

We expected that rsFC would be differentially modulated from pre- to posttraining between groups. Because past work showed that individuals with stroke rely on prefrontal regions during skilled motor practice,23,27,28 and that greater recovery is linked to increased functional connectivity of frontal regions implicated in working memory,9,24 we expected to observe increased connectivity within the sensorimotor network, and between the sensorimotor network and prefrontal areas. In exploring the association between changes in rsFC and motor learning, we hypothesized that (1) improvements in motor behavior associated with task-specific learning would be related to decreased connectivity between regions implicated in working memory in individuals with stroke and (2) healthy controls would show minimal connectivity changes. Finally, we predicted that changes in network efficiency induced by skilled motor practice would occur differentially after stroke relative to healthy controls. Specifically, we predicted that healthy controls would show enhanced network efficiency that would reflect their increased capacity to transmit information. In contrast, we expected that individuals with stroke would show decreases in network efficiency reflecting a shift toward a compensatory network configuration to support learning.

 

OUR 12 COMMANDMENTS FOR AGEING WELL, PRINCE PHILIP AND MORE

I think I'll be aging well, I need to get to 100.

 OUR 12 COMMANDMENTS FOR AGEING WELL, PRINCE PHILIP AND MORE

Diffusion weighted imaging in acute ischemic stroke: A review of its interpretation pitfalls and advanced diffusion imaging application

But are these others faster and better?

But you're not comparing it to these much faster diagnosis options. 

TIME IS BRAIN you know. 

Maybe you want these much faster objective diagnosis options.

Hats off to Helmet of Hope - stroke diagnosis in 30 seconds; February 2017

 

Microwave Imaging for Brain Stroke Detection and Monitoring using High Performance Computing in 94 seconds March 2017

 

New Device Quickly Assesses Brain Bleeding in Head Injuries - 5-10 minutes April 2017

Ski-Mask Design AIR Coil Offers Whole-Brain Imaging Without Claustrophobia

The latest here:

Diffusion weighted imaging in acute ischemic stroke: A review of its interpretation pitfalls and advanced diffusion imaging application

Published:April 03, 2021DOI:https://doi.org/10.1016/j.jns.2021.117435

Highlights

  • DWI is useful to evaluate stroke mechanism, predict complications and outcome.
  • DWI reversal, DWI negative stroke and DWI stroke mimics are interpretation pitfalls.
  • Reversal of DWI lesion occurs in 26.5% of stroke and associated with reperfusion.
  • DWI negative stroke is noted in 6.8% to 21% of clinically diagnosed stroke.

Abstract

Diffusion weighted imaging (DWI) is a widely used imaging technique to evaluate patients with stroke. It can detect brain ischemia within minutes of stroke onset. However, DWI has few potential pitfalls that should be recognized during interpretation. DWI lesion could be reversible in the early hours of stroke and the entire lesion may not represent ischemic core. False negative DWI could lead to diagnosis of DWI negative stroke or to a missed stroke diagnosis. Ischemic stroke mimics can occur on DWI with non-cerebrovascular neurological conditions. In this article, the history of DWI, its clinical applications, and potential pitfalls for use in acute ischemic stroke are reviewed. Advanced diffusion imaging techniques with reference to Diffusion Kurtosis Imaging and Diffusion Tensor Imaging that has been studied to evaluate ischemic core are discussed.

Keywords

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