The Mobility Reset: How to Move Better Without Adding Another Workout by Super Age

 I bet you're getting nothing like this from your doctor or therapists! Why the fuck are you paying them for incompetence? In my opinion incompetence is defined as knowing nothing about 100% recovery; and even worse; DOING NOTHING TO SOLVE IT!

So, a simple question to your doctor, therapists and board of directors. Are you competent or not based upon the above statement?

The Mobility Reset: How to Move Better Without Adding Another Workout

Prevalence of post-stroke poor sleep quality: a meta-analysis of Pittsburgh Sleep Quality Index results

Prevalence is totally useless! You need to create EXACT SLEEP PROTOLS! Are you that fucking incompetent you can't accomplish that?

You've known of poor sleep for how many years and STILL HAVEN'T SOLVED THE PROBLEM? Only 6+ years and why haven't you been fired yet?

30% poor sleep (16 posts to May 2019)

 Prevalence of post-stroke poor sleep quality: a meta-analysis of Pittsburgh Sleep Quality Index results

Yu Zhou¹Bi Guan²Rong Tang³Qiongyao Zhong⁴Liangnan Zeng^5*

• 1Department of Operating Room, Chengdu Fifth People’s Hospital, Chengdu, China
• 2Department of Nursing, Chengdu Fifth People’s Hospital, Chengdu, China
• 3Department of Orthopedics, Chengdu Fifth People’s Hospital, Chengdu, China
• 4Department of Neurology, Chengdu Fifth People’s Hospital, Chengdu, China
• 5Department of Nursing, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China

Objective: To assess the prevalence of post-stroke poor sleep quality using the Pittsburgh Sleep Quality Index (PSQI).

Methods: This study was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Following the PICO framework, a systematic search was conducted in PubMed, CINAHL, Cochrane Library, and Web of Science for relevant cohort, case-control, and cross-sectional studies published up to October 2024. The retrieved literature was then meta-analyzed using Stata 13.0 software.

Results: Eighteen studies were reviewed, showing a total poor sleep quality prevalence of 55% (95%CI = 0.47 to 0.62) and a PSQI score is 8.12 (95%CI = 6.71 to 9.53). Compared to normal people, stroke patients sleep onset latency (SL) was prolonged by 1.36 min (95%CI = 0.82 to 1.90), sleep efficiency (SE) decreased by 1.48% (95%CI = −0.20 to −0.92), and periodic leg movements per hour of sleep (PLMI) increased by 1.07 per hour (95%CI = 0.56 to 1.59). Subgroup analysis showed that, compared with hemorrhagic stroke patients, ischemic stroke patients had higher incidence of poor sleep quality at 52% (95%CI = 0.24 to 0.86); the incidence of poor sleep quality was 59% (95%CI = 0.49 to 0.70) higher in chronic stroke patients compared to acute and subacute stroke patients; the incidence of poor sleep quality was 61% (95%CI = 0.51 to 0.71) higher in community stroke patients than in hospitalized stroke patients; and the incidence of poor sleep quality was 59% (95%CI = 0.58 to 0.61) higher in stroke patients in developing countries than those in developed countries.

Conclusion: Current evidence suggests that quality of sleep worsens after a stroke, with symptoms being widespread. Factors such as stroke type, stroke phase, clinical setting, and research region can all impact sleep quality after stroke. These findings underscore the importance of monitoring sleep quality in these populations and implementing appropriate preventive and interventional strategies.

Systematic review registration: https://www.crd.york.ac.uk/PROSPERO, identifier CRD420251161167.

More at link.

Development of a prediction model for poor outcomes after thrombolysis in mild non-disabling ischemic stroke

Where is your scientific proof that ANY PREDICTION MODEL gets survivors recovered? NONE? I thought so! So, you're incompetently DOING NOTHING to help survivors? You'd be fired immediately in any business setting! Even proposing crapola like this should get you fired!

 Development of a prediction model for poor outcomes after thrombolysis in mild non-disabling ischemic stroke

Xiaopan Cao¹Zhijian Fu¹Li Li²Li Ren¹Yang Jiang^3*Xue Cong⁴Bing Xu^5*Xin Zhang⁶

• ¹Department of Neurology VIII, Shenyang First People’s Hospital, Shenyang, Liaoning, China
• ²Department of Neurology I, Shenyang First People’s Hospital, Shenyang, Liaoning, China
• ³Neurology Outpatient Department, Shenyang First People’s Hospital, Shenyang, Liaoning, China
• ⁴Department of Critical Care Medicine, Shenyang First People’s Hospital, Shenyang, Liaoning, China
• ⁵Department of Neurology, Shenyang Tenth People’s Hospital, Shenyang, Liaoning, China
• ⁶Department of Neurorehabilitation, Shenyang First People’s Hospital, Shenyang, Liaoning, China

Background: Mild non-disabling ischemic stroke (MNDIS) is increasingly treated with intravenous thrombolysis, yet a substantial proportion of patients still experience poor functional outcomes, and robust tools for individualized risk prediction are lacking.

Methods: In this retrospective cohort study, we analyzed 713 consecutive MNDIS patients who received intravenous thrombolysis within 4.5 h of symptom onset at an advanced stroke center between January 1, 2022 and December 31, 2024. Poor outcome was defined as a 90-day modified Rankin Scale (mRS) score ≥2. Candidate predictors, including demographic, clinical, laboratory, hemodynamic and imaging variables, were first screened by univariable analysis and then entered into a stepwise multivariable logistic regression model (entry p < 0.05, removal p > 0.10). A nomogram incorporating independent predictors was constructed in R, and its performance was evaluated using receiver operating characteristic (ROC) analysis, bootstrap calibration, and decision curve analysis.

Results: Of the 713 patients, 91 (12.8%) had poor 90-day outcomes (mRS 2–6) and 622 (87.2%) had good outcomes (mRS 0–1). Admission NIHSS score (OR 1.37; 95% CI 1.10–1.72), 24-h NIHSS score (OR 1.78; 95% CI 1.52–2.10), diastolic blood pressure (OR 1.02 per mmHg; 95% CI 1.00–1.05), and coronary heart disease (OR 1.88; 95% CI 1.05–3.35) were independently associated with poor outcome. The resulting nomogram showed good discrimination (AUC 0.835; 95% CI 0.805–0.861; sensitivity 71.4%; specificity 84.1%), excellent calibration (bootstrap mean absolute error 0.014), and provided positive net clinical benefit across a wide range of risk thresholds (0.03–0.89).

Conclusion: Admission and 24-h NIHSS scores, diastolic blood pressure, and coronary heart disease are key predictors of poor 90-day outcomes after thrombolysis in patients with MNDIS. The derived nomogram offers accurate, well-calibrated, and clinically useful individualized risk estimation, and may assist clinicians in early post-thrombolysis risk stratification and tailoring the intensity of monitoring and follow-up.

More at link.

Associations of eosinophil-to-monocyte ratio and C-reactive protein-to-high-density lipoprotein cholesterol ratio with early neurological deterioration after thrombolysis in acute ischemic stroke

'Associations' DO NOTHING FOR SURVIVOR RECOVERY! Are you that blitheringly stupid you don't know that survivors would like recovery rather than a completely fucking useless 'association'? 

Had you been thinking at all you would be solving the  5 causes of the neuronal cascade of death in the first week saving hundreds of million to billions of neurons! Thus, preventing early neurological deterioration. Or don't you have two functioning neurons to rub together for a spark of intelligence?

 Associations of eosinophil-to-monocyte ratio and C-reactive protein-to-high-density lipoprotein cholesterol ratio with early neurological deterioration after thrombolysis in acute ischemic stroke

Guohua HeGuilan XuYanqiao XiaoZhen WangYachun Yu^*

• Department of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China

Background: Inflammation mechanisms play critical roles in acute ischemic stroke (AIS). However, the correlations of the eosinophil-to-monocyte ratio (EMR) and blood C-reactive protein to high-density lipoprotein cholesterol (CRP/HDL-C) ratio with post-thrombolysis early neurological deterioration (END) in patients with AIS remain uncertain.

Methods: Patients with AIS who received intravenous thrombolysis therapy from January 2020 to February 2025 were retrospectively recruited for this study. CRP level, blood lipid concentrations, and complete blood count measurements were recorded within 24 h of admission. Post-thrombolysis END was defined as an increase in the U.S National Institutes of Health Stroke Scale (NIHSS) score of ≥ 4 points compared to the initial NIHSS score taken within 24 h of initiating intravenous thrombolysis. Multivariate logistic regression modeling was performed to evaluate the correlations of EMR and the CRP/HDL-C ratio to post-thrombolysis END. Receiver operating characteristic (ROC) curves were used to analyze the predictive value of both EMR and the CRP/HDL-C ratio in patients with post-thrombolysis END.

Results: Among 473 recruited patients, 103 (21.78%) were diagnosed with post-thrombolysis END. Patients with END had significantly higher systolic and diastolic blood pressures, white blood cell and monocyte counts, CRP levels, CRP/HDL-C ratios, and NIHSS scores on admission, while their eosinophil counts and EMRs were significantly lower. The multivariate logistic regression analysis indicated that EMR (odds ratio [OR], 0.03 [95% confidence interval (CI) 0.01–0.14]; p < 0.001) and CRP/HDL-C (odds ratio, 1.04[95%CI 1.01–1.08]; p = 0.025) were independently associated with END after adjusting for potential confounders. The areas under the receiver operating characteristic curve (AUC) for EMR and the CRP/HDL-C ratio were 0.757 (95% CI, 0.709–0.805) and 0.61 (95% CI, 0.545–0.675), respectively.

Conclusion: A lower EMR level and a higher CRP/HDL-C ratio in patients with AIS are independently associated with post-thrombolysis END. EMR and the CRP/HDL-C ratio may be potential biomarkers for post-thrombolysis END.

More at link.

Mitochondria magic: Exercise’s value soars with this news

 

Great Catch-22 here; you need exercise to recover, but you really need 100% recovery to do the required exercises. Have your competent? doctor EXACTLY EXPLAIN HOW TO GET AROUND THAT PROBLEM!

I can almost guarantee your doctor and hospital will KNOW NOTHING AND DO NOTHING! 

No human research will occur; nothing will be done! That is how fucking incompetent the whole stroke medical world is. Hopefully schadenfreude will hit them all with a stroke. And they can regret their incompetence in not solving stroke to 100% recovery!

Al this incompetence is a result of NO leadership firing the incompetent persons!

Mitochondria magic: Exercise’s value soars with this news

Japanese researchers found that exercise triggers muscle cells to send mitochondria through the bloodstream to protect and repair brain tissue after stroke

• By David Kesiena
• Jan 26, 2026
• 7:00 am

Photo credit: Shutterstock.com / LightField-Studios-2

Scientists at Juntendo University School of Medicine have uncovered a remarkable process that explains how exercise protects the brain from stroke damage. The research team discovered that physical activity triggers muscle cells to produce mitochondria that travel through the bloodstream and deliver healing benefits directly to injured brain tissue.

The study, published in the journal MedComm on Jan. 15, reveals that blood platelets act as tiny transport vehicles, carrying these cellular powerhouses from muscles to the brain. Once they arrive, the mitochondria help damaged neurons survive oxygen deprivation and support the repair of critical brain structures. The findings could eventually lead to new treatments for stroke patients who are too frail to exercise on their own.(Slight problem here, the penumbra resolves itself into dead brain in the first week, so you need this exercise immediately! HOW THE FUCK WILL YOUR DOCTOR ACCOMPLISH THAT?)

 

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Research Assistant Professor Toshiki Inaba led the investigation alongside colleagues Nobukazu Miyamoto and Nobutaka Hattori at Juntendo’s Department of Neurology. The team conducted experiments using mouse models designed to replicate both stroke and dementia conditions, providing insights into how cellular communication might be harnessed for therapeutic purposes.

Watching mitochondria travel between cells

Miyamoto’s interest in mitochondrial migration began during a research fellowship at Massachusetts General Hospital and Harvard Medical School, where he first observed these cellular structures moving from one cell to another. That observation sparked the realization that mitochondrial transfer might offer treatment possibilities for various neurological conditions.

For the current study, researchers divided mice into groups and had some perform low-intensity treadmill exercise while others remained sedentary. The team then carefully tracked brain damage, movement abilities, memory function and changes in brain and muscle cells among both groups. They also measured mitochondrial levels and activity throughout the experiment.

The results showed clear advantages for the mice that exercised. These animals experienced less damage to white matter and myelin, the protective coating around nerve fibers. They also demonstrated better memory retention and movement capabilities compared to sedentary mice, while experiencing fewer complications following stroke events.

Researchers have demonstrated how mitochondria, which are abundant in muscle, could aid in stroke recovery through exercise-induced migration.(Photo courtesy of Dr. Toshiki Inaba from Juntendo University School of Medicine, Japan)

Platelets serve as cellular delivery system

The research revealed that exercise significantly increased mitochondrial production in both muscle tissue and the bloodstream. Blood platelets, typically known for their role in clotting, took on an unexpected function by capturing mitochondria from muscle cells and transporting them to the brain.

Once in the brain, these traveling mitochondria didn’t just reach neurons. They also made their way to support cells including oligodendrocytes, which produce protective myelin, and astrocytes, star-shaped cells that help form the blood-brain barrier. The mitochondria provided crucial support to cells in the damaged area and the surrounding region called the penumbra, where brain tissue remains vulnerable but potentially salvageable.

Inside these brain cells, the delivered mitochondria helped them endure low-oxygen conditions that typically cause widespread cell death after stroke. They supported the repair of white matter, the brain’s communication infrastructure, and reduced the cascade of complications that often follow stroke events.

Limited options drive search for new approaches

Current stroke treatment relies heavily on clot removal or dissolution, but these interventions only work within a narrow window after symptoms begin. Once that critical time frame passes, patients face limited therapeutic options. Physical rehabilitation and symptom management become the primary focus, yet many stroke survivors continue struggling with walking difficulties, speech problems and memory decline.

Exercise has long been recognized as beneficial for both stroke prevention and recovery. However, many stroke patients are elderly and lack the physical stamina required to exercise intensively enough to gain those protective benefits. This reality makes the search for alternative approaches particularly urgent.

Inaba acknowledged that while the research team has identified several technical and biological challenges through additional experiments, the approach holds promise for reducing neurological problems after stroke. The applications might extend beyond stroke to include mitochondrial diseases and related neurodegenerative conditions where current treatment options remain limited.

From mice to potential human therapies

The pathway from laboratory findings to clinical treatments typically spans years and requires extensive testing for safety and effectiveness. If the mitochondrial transfer approach proves successful in human trials, it could potentially allow stroke patients to receive the benefits of exercise through transfusions of platelet preparations enriched with mitochondria.

Such a treatment would be particularly valuable for patients who cannot engage in physical rehabilitation due to age, frailty or the severity of their condition. The approach might also offer hope for preventing the progression of vascular dementia, a condition that currently has no established treatments.

The research team’s work builds on growing scientific understanding of how cells communicate and share resources. By revealing the specific mechanism through which exercise protects the brain, the scientists have opened a new avenue for developing therapies that could help millions of stroke survivors worldwide maintain better neurological function and quality of life.

SOURCE: juntendo

New Guidelines Expand Stroke Care, Add Pediatric Advice

 Survivors never want 'care'; THEY WANT FULL RECOVERY! Are you that blitheringly stupid? You have never talked to a survivor who demanded 'care'; HAVE YOU? Have you ever really talked to a survivor without talking down to them and using your tyranny of low expectations TO JUSTIFY YOUR FUCKING FAILURE TO NOT DELIVER 100% RECOVERY?

I'd fire everyone in this crapola guideline shit!

I will against my better nature hope all of you discover schadenfreude when you have your stroke and DON'T RECOVER!

New Guidelines Expand Stroke Care, Add Pediatric Advice

American Heart Association

Guideline Highlights:

• The 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke includes key advances in stroke treatment, such as expanded eligibility for clot-removal procedures, new evidence supporting the use of the clot-busting medication tenecteplase, and the implementation of mobile stroke units to deliver care(NOT RECOVERY!) faster and reduce the risk of long-term disability.
• Also included in the guideline are the first detailed recommendations for diagnosing and treating stroke in children.
• The new guideline is endorsed by the American Association of Neurological Surgeons/Congress of Neurological Surgeons, the Neurocritical Care Society, the Society for Academic Emergency Medicine, the Society of NeuroInterventional Surgery, and the Society of Vascular and Interventional Neurology. The American Academy of Neurology affirmed the guideline as an educational tool for neurologists.

DALLAS, Jan. 26, 2026 — Expanded eligibility for advanced stroke therapies and new recommendations for diagnosing and treating stroke in children and adults are among the major updates in the new 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke from the American Stroke Association, a division of the American Heart Association, published today in the Association's flagship journal Stroke.

According to the American Heart Association's 2026 Heart Disease and Stroke Statistics, stroke is now the #4 leading cause of death in the U.S. Every year, nearly 800,000 people in the U.S. have a stroke, and it is also a leading cause of serious, long-term disability. There are several types of strokes. Ischemic stroke is the most common type and occurs when blood flow to the brain is suddenly blocked in a vessel, usually by a blood clot.

The new guideline replaces the 2018 edition and its 2019 update to reflect a surge of new evidence in acute ischemic stroke care(NOT RECOVERY!). It provides an evidence-based roadmap for health care(NOT RECOVERY!) professionals to recognize, diagnose and treat ischemic stroke, from prehospital recognition to hospital management and early recovery.

"This update brings the most important advances in stroke care(NOT RECOVERY!) from the last decade directly into practice," said Shyam Prabhakaran, M.D., M.S., FAHA, chair of the writing group for the guideline and the James Nelson and Anna Louise Raymond Professor of Neurology and chair of the department of neurology at the University of Chicago Medicine. "New recommendations in the guideline expand access to cutting-edge treatments, such as clot-removal procedures and medications, simplify imaging requirements so more hospitals can act quickly, and introduce guidance for pediatric stroke for the first time."

Since the 2019 update, several landmark trials have transformed stroke care(NOT RECOVERY!), including interventions for large vessel occlusion in the brain, clot-busting or clot-removal therapies, and streamlined hospital workflows. The 2026 guideline brings that progress together to standardize stroke care(NOT RECOVERY!) across hospitals of all sizes and ensure rapid, evidence-based treatment for every patient, regardless of where they live.

The guideline reinforces that outcomes depend on what treatments are provided to stroke patients and how quickly and efficiently they are delivered. From the first 9-1-1 call to hospital discharge, coordinated systems of care(NOT RECOVERY!) can be a key factor in preventing lifelong disability. The updated recommendations focus on enhancing those systems, accelerating the use of imaging techniques and medication delivery, and expanding access to advanced procedures like endovascular thrombectomy (EVT, the mechanical removal of a blood clot).

First-time guidance for pediatric stroke

Though rare, stroke can occur in infants, children and teens, and prompt recognition is critical. Children can exhibit the same warning signs as adults described by the acronym F.A.S.T.: Face Drooping; Arm Weakness; Speech Difficulty; Time to Call 911. However, stroke warning signs in children more often may also include:

• Sudden severe headache, especially with vomiting and sleepiness
• New onset of seizures, usually on one side of the body
• Sudden confusion, difficulty speaking or understanding others
• Sudden trouble seeing in one or both eyes, and/or
• Sudden difficulty walking, dizziness, loss of balance or coordination

Currently available stroke screening tools have been developed for adults, so they do not accurately distinguish strokes in the pediatric population from mimics (conditions with similar symptoms). Some examples of mimics include migraine, seizure, traumatic brain injury, or brain tumor. The guideline advises rapidly performing magnetic resonance imaging (MRI) and angiography (MRA) to identify blockages to differentiate arterial ischemic stroke fromhemorrhagic stroke and rule out mimics in pediatric stroke. Computed tomography (CT) is reasonable if MRI is not available in a timely manner, according to the guideline.

For treating ischemic stroke in children, the guideline states that the intravenous (IV) clot-busting agent alteplase may be considered within 4.5 hours for children ages 28 days to 18 years with disabling deficits. Also, mechanical clot-removal performed by experienced neurointerventionalists may be effective for large-vessel blockages in children 6 years and older within 6 hours and may be reasonable up to 24 hours after symptoms begin if imaging shows salvageable brain tissue.

"These recommendations represent a major step toward standardized, evidence-based care for children," Prabhakaran said. "They also highlight how much more we still need to learn about pediatric stroke."

Faster care from the field to the hospital

The guideline emphasizes the need for regional stroke systems of care(NOT RECOVERY!) that link 9-1-1 call centers, emergency medical services (EMS) agencies, hospitals and telemedicine networks. Mobile stroke units, which are ambulances equipped with CT scanners and stroke-trained care(NOT RECOVERY!) teams, demonstrate how faster response times can accelerate recognition and treatment delivery.

In regions with reasonable access to thrombectomy-capable stroke centers (TSCs), EMS should transport patients with suspected large vessel occlusion to the nearest TSC for immediate evaluation. Direct transport to a TSC can be beneficial to reduce delays in diagnosis and treatment, helping more patients receive EVT when indicated. Further, in regions without geographic access to TSCs, the guideline focuses on reducing door-in-door-out times at hospitals transferring patients to TSCs.

Rapid diagnosis and imaging

Speed and accuracy are critical for diagnosing and treating stroke. Hospitals should complete an initial brain scan within 25 minutes of arrival to confirm that symptoms are caused by an ischemic stroke and not a brain bleed, so that the right treatment can begin immediately. Confirming the stroke type ensures that clot-dissolving or clot-removal treatments can begin safely and without delay.

Advanced brain imaging techniques such as MRI or CT perfusion can sometimes show how much the stroke has damaged the brain tissue. The new guideline also advises hospitals without advanced perfusion imaging to use a standard CT scoring system called ASPECTS to identify candidates for clot-removal procedures.

Clot-busting medications

The guideline endorses the use of either tenecteplase or alteplase within 4.5 hours of symptom onset. Both medications are effective at dissolving blood clots. However, tenecteplase, a single-dose IV infusion, has the advantage of simplifying treatment compared to the 60-minute period needed for alteplase infusion.

For some people who wake up with stroke symptoms or arrive at the hospital after the standard 4.5-hour window for treatment, clot-busting treatment may still be effective up to 24 hours after the onset of stroke symptoms, if advanced brain imaging shows brain tissue that has not been irreversibly damaged.

Clot-removal procedures (endovascular thrombectomy or EVT)

Removing clots directly from blocked brain arteries, a procedure called thrombectomy, remains a powerful treatment for major strokes caused by large-vessel blockages in eligible patients. Patients eligible for both clot-busting medications and thrombectomy should receive both, rapidly and sequentially, without delaying the procedure to "see if symptoms improve."

• EVT is now recommended in selected patients for up to 24 hours after symptom onset even if imaging shows certain large core infarcts by ASPECTS, meaning a significant area of brain tissue has been severely damaged due to lack of blood flow.
• Based on new evidence, eligibility for EVT also includes some patients with blockages in the back of the brain (posterior circulation stroke).
• Some people with mild or moderate preexisting disability may also benefit in the first 6 hours after symptom onset.
• EVT is not routinely recommended for smaller blockages in medium- or small arteries in the brain but may be considered in a clinical trial.

Improving survival and recovery

The guideline underscores that coordinated systems of care(NOT RECOVERY!) are essential for improving survival and recovery. Hospitals are encouraged to use reporting systems such as the American Stroke Association's Get With The Guidelines® - Stroke Registry to track treatment times and outcomes, expand telemedicine and imaging access, and establish transfer agreements that link primary and comprehensive stroke centers.

"Time is brain," Prabhakaran said. "This new guideline makes that concept real, showing how systems, from EMS to hospitals, can work together to cut 30 to 60 minutes off treatment time to improve patient outcomes and reduce the likelihood of disability."

2026 International Stroke Conference

The new guideline will be featured at the American Heart Association's 2026 International Stroke Conference, to be held February 4-6, 2026, in New Orleans.

• What's New in the 2026 Acute Ischemic Stroke Guideline: Process Overview and Key Updates from the Chairs; Thursday, February 5, 2:30-3:30 p.m. CT
• Acute Ischemic Stroke Guidelines: Q&A Part I (Fireside Chat); Thursday, February 5, 3:45-4:45 p.m. CT
• Acute Ischemic Stroke Guidelines: Q&A Part II (Fireside Chat); Thursday, February 5, 5:00-6:00 p.m. CT

This guideline was prepared by the volunteer writing group on behalf of the American Heart Association's Stroke Council and the American Stroke Association. Since 1990, the American Stroke Association has translated scientific evidence into clinical practice guidelines with recommendations to improve cerebrovascular health.

WOW! Look at all these M.D.s and Ph.D.s AND STILL HAVE NO COMMON SENSE ABOUT GETTING STROKE SOLVED TO 100% RECOVERY! NO leadership here at all!

Co-Vice Chairs of the volunteer writing group are Nestor R. Gonzalez, M.D., M.S.C.R., FAHA, and Kori S. Zachrison, M.D., M.Sc., FAHA. Co-authors and members of the writing group are Opeolu Adeoye, M.D., M.S.; Anne W. Alexandrov, Ph.D., A.G.A.C.N.P.-B.C., A.N.V.P.-B.C.; Sameer A. Ansari, M.D., Ph.D., FAHA; Sherita Chapman, M.D., FAHA; Alexandra L. Czap, M.D.; Oana M. Dumitrascu, M.D., M.Sc., FAHA; Koto Ishida, M.D.; Ashutosh P. Jadhav, M.D., Ph.D., FAHA; Brenda Johnson, D.N.P., M.S.N., F.N.P.-B.C., A.N.V.P.-B.C., FAHA; Karen C. Johnston, M.D., M.Sc.; Pooja Khatri, M.D., M.Sc., FAHA; W. Taylor Kimberly, M.D., Ph.D., FAHA; Vivien H. Lee, M.D., FAHA; Thabele M. Leslie-Mazwi, M.D.; Brian Mac Grory, M.B., B.Ch., B.A.O., M.H.Sc., M.R.C.P., FAHA; Tracy E. Madsen, M.D., M.C.T.R., Ph.D., FAHA; Bijoy Menon, M.D.; Eva A. Mistry, M.B.B.S., M.S.C.I., FAHA; Soojin Park, M.D.; Natalia Perez de la Ossa, M.D., Ph.D.; Mathew Reeves, B.V.Sc., Ph.D., FAHA; Tania Saiz; Phillip A. Scott, M.D., M.B.A., FAHA; Dana Schwartzberg; Sunil A. Sheth, M.D.; Peter Sporns, M.D., M.H.B.A.; Sabrina Times, D.H.Sc., M.P.H.; Stavropoula Tjoumakaris, M.D., M.B.A., FAHA; Stacey Q. Wolfe, M.D.; and Shadi Yaghi, M.D., FAHA. Authors' disclosures are listed in the manuscript.