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.

Friday, April 17, 2026

Progressive Whole-Body Vertical Vibration with Conventional Rehabilitation for Upper Limb Function and Corticospinal Excitability in Subacute Stroke Patients

 

Didn't your competent? doctor propose this for you years ago? NO? So you don't have a functioning stroke doctor, do you?

Progressive Whole-Body Vertical Vibration with Conventional Rehabilitation for Upper Limb Function and Corticospinal Excitability in Subacute Stroke Patients




Summary

This randomized controlled trial aimed to examine the effects of progressive Whole-Body Vertical Vibration (WBVV) combined with conventional rehabilitation on upper limb motor function and corticospinal tract excitability in subacute stroke patients and to explore potential neurophysiological mechanisms.

Abstract

Stroke often results in upper limb impairment. Although many patients regain independent ambulation, upper limb function recovery remains incomplete, which limits activities of daily living (ADL) and reduces quality of life. Optimizing upper limb rehabilitation strategies continues to represent a major challenge in stroke care. This article presents a randomized controlled trial protocol investigating the effects of progressive WBVV training on upper limb function and corticospinal excitability in subacute stroke patients. Forty-eight subacute stroke patients are allocated to an experimental group (n = 24) and a control group (n = 24). The control group receives conventional rehabilitation training, while the experimental group receives additional progressive WBVV training. This intervention offers the advantages of easy implementation, low energy consumption, and favorable tolerability for subacute stroke patients. The WBVV protocol is gradually intensified over four weeks by adjusting frequency and amplitude. After four weeks of intervention, both groups showed significant improvements in upper limb function, ADL ability and neurophysiological indicators (< 0.05). The experimental group achieved significantly better outcomes in Fugl–Meyer Assessment of Upper Extremity (FMA-UE), Wolf Motor Function Test (WMFT) and Modified Barthel Index (MBI) scores compared with the control group (p < 0.05). Both groups presented shortened motor evoked potential latency and increased peak-to-peak amplitude, but no significant between-group differences were found in neurophysiological measures (p > 0.05). These findings indicate that WBVV combined with conventional rehabilitation can effectively promote upper limb functional recovery and ADL performance in subacute stroke patients. Further research is required to verify its effects on corticospinal excitability.

Asundexian for Secondary Stroke Prevention

 Your competent? doctor should have known of this trial as it started; IF COMPETENT AT ALL! We've already established your doctor is incompetent, so find a competent one to tell you what this research means for you!

Is it better than all these others that your doctor discussed with you?

Asundexian for Secondary Stroke Prevention


AuthorsMukul SharmaM.D. https://orcid.org/0000-0002-6119-342X
Qiang DongM.D.
Teruyuki HiranoM.D.
Scott E. KasnerM.D.
Jeffrey L. SaverM.D. https://orcid.org/0000-0001-9141-2251
Jaime MasjuanM.D., Ph.D.
Andrew M. DemchukM.D.+47 , for the OCEANIC-STROKE Investigators*
 Published April 15, 2026
N Engl J Med 2026;394:1467-1479
DOI: 10.1056/NEJMoa2513880

Abstract

Background

Patients with noncardioembolic ischemic stroke or transient ischemic attack (TIA) are at risk for recurrent stroke. Low factor XI levels are associated with a reduced risk of ischemic stroke. Asundexian inhibits activated factor XI. Whether the addition of asundexian to antiplatelet therapy would be superior to antiplatelet therapy alone for the secondary prevention of ischemic stroke is unclear.

Methods

In this phase 3, double-blind trial, we randomly assigned patients within 72 hours after the onset of a noncardioembolic ischemic stroke or high-risk TIA to receive asundexian (50 mg once daily) or placebo, in addition to planned dual or single antiplatelet therapy. Patients had at least one of the following: a nonlacunar infarct on imaging, a history of atherosclerosis, or evidence of atherosclerotic plaque at any location on cerebrovascular imaging. The primary efficacy outcome was ischemic stroke. The composite of death from cardiovascular causes, myocardial infarction, or stroke was a key secondary outcome. The primary safety outcome was major bleeding.

Results

Among 12,327 patients who underwent randomization (6162 to the asundexian group and 6165 to the placebo group), the incidence of ischemic stroke was lower in the asundexian group than in the placebo group (6.2% vs. 8.4%; cause-specific hazard ratio, 0.74; 95% confidence interval [CI], 0.65 to 0.84; P<0.001). The incidence of the composite of death from cardiovascular causes, myocardial infarction, or stroke was lower in the asundexian group than in the placebo group. The incidence of major bleeding was similar in the asundexian group and the placebo group (1.9% and 1.7%, respectively; cause-specific hazard ratio, 1.10; 95% CI, 0.85 to 1.44). The incidence of adverse events was 69.3% in the asundexian group and 70.1% in the placebo group; the incidence of serious adverse events was 19.2% and 19.5%, respectively.

Conclusions

Among patients with noncardioembolic ischemic stroke or high-risk TIA treated with antiplatelet therapy, asundexian at a daily dose of 50 mg resulted in lower risks of ischemic stroke and major cardiovascular events than placebo, without a higher risk of major bleeding. (Funded by Bayer; OCEANIC-STROKE ClinicalTrials.gov number, NCT05686070.)

Researchers are near a breakthrough drug for brain recovery after stroke

 

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 comeuppance will hit them all.

Let's see how long incompetence has existed!

  • DDL-920 (5 posts to March 2025)
  • Parvalbumin neurons (8 posts to June 2013)
  • Researchers are near a breakthrough drug for brain recovery after stroke

    Doctor holding a patient's MRI result with the senior patient sitting upright on the hospital bed in the background, next to a relative and the nurseSource: Shutterstock For millions of stroke survivors, recovery doesn’t end when they leave the hospital. While emergency treatments can save lives, the long road afterward often involves months or years of physical therapy, with no guarantee of regaining lost movement or coordination. Stroke remains the leading cause of long-term disability in adults, and many patients never fully recover.In the United States alone, nearly 800,000 people suffer a stroke each year, and an estimated 7.8 million adults are living as stroke survivors, many coping with lasting mobility or speech impairments. Despite the scale of the problem, treatment options focused specifically on repairing brain function after stroke remain limited.

    That may be starting to change. New research suggests scientists are closer than ever to developing a medication that could help the brain rewire itself after stroke, potentially reducing reliance on grueling rehabilitation alone.

    What the New Research Has Found

    study published in Nature Communications, researchers at UCLA identified a drug candidate that restored movement in mice after stroke by mimicking the effects of physical rehabilitation. The compound, known as DDL-920, was able to repair disrupted neural connections that typically limit recovery.The research builds on years of work examining how the brain heals after stroke. Scientists found that damage isn’t limited to the area where the stroke occurs. Instead, stroke disrupts communication among brain cells located far from the injury site, particularly a type called parvalbumin neurons.

    These neurons play a critical role in generating gamma oscillations, which are rhythmic brain signals that help coordinate movement. Physical therapy was shown to restore these rhythms in both humans and mice. The breakthrough came when researchers discovered that DDL-920 could activate the same recovery pathway without physical rehabilitation in mouse models.

    Why This Approach is Different

    Most past stroke treatments have focused on preventing additional damage rather than repairing what’s already been lost. The UCLA findings mark a shift toward treating recovery itself as a biological process that can be targeted with medicine, a single pill.

    According to the researchers, DDL-920 works by re-exciting parvalbumin neurons and restoring synchronized brain activity necessary for movement control. In mice, the drug produced improvements nearly equivalent to those seen with intensive physical therapy.This matters because many stroke patients are unable to participate fully in rehabilitation due to mobility limitations or lack of access. A medication that enhances or replicates the effects of rehab could dramatically expand recovery options, especially for older adults and those in underserved communities.

    Still, researchers emphasize that the work is in early stages. The drug has only been tested in animals, and extensive safety and efficacy studies are required before human trials can begin. No clinical trials in people are currently underway.

    What Comes Next for Stroke Recovery

    If future research confirms the drug’s safety and effectiveness in humans, it could fundamentally reshape how stroke recovery is treated. Instead of relying solely on physical therapy, doctors may one day prescribe medications that help the brain rebuild its own neural networks

    Researchers caution that the drug is not intended to replace rehabilitation entirely, but to complement it — potentially making therapy more effective or accessible. The ultimate goal is to move stroke recovery into what scientists call an era of molecular medicine, where biology and rehabilitation work together.

    For now, the findings represent a significant step forward rather than a finished solution. But for a field that has gone decades without a single recovery-focused drug, the possibility of a pill that helps the brain heal offers something long missing from stroke care: cautious optimism.

    Predicting post-stroke functional outcome using explainable machine learning and integrated data

     Predictions like this ARE ABSOLUTELY FUCKING USELESS! Because only 10% get fully recovered from rehab!  So, the OBVIOUS THING TO DO IS: Get to work creating 100% recovery protocols! Leaders would work on this but instead we have fucking failures of stroke associations that do nothing for survivors! I'd have you all fired for incompetence!

    Predicting post-stroke functional outcome using explainable machine learning and integrated data


    Abstract

    Functional outcome after acute ischemic stroke (AIS) varies widely, and existing prognostic scores may not capture complex relationships. We evaluated a diverse set of clinical characteristics and blood biomarkers with multiple machine learning models to predict 3-month functional outcome after AIS, and used explainable artificial intelligence to identify key drivers of performance. Models were trained on 506 patients aged 18–69 years with AIS enrolled at four stroke units in western Sweden. We compared extreme gradient boosting, multilayer perceptron (MLP), and L1- and L2-regularized logistic regression. Feature importance was assessed with Shapley additive global explanations. Of the 506 patients, 105 had an unfavorable outcome (modified Rankin Scale score > 2). All models showed high area under the curve (AUROC, 0.900–0.906). The MLP achieved the highest precision–recall performance (AUPRC, 0.773 ± 0.080) and sensitivity (0.655 ± 0.096), though with lower specificity (0.920 ± 0.035). Stroke severity (NIH Stroke Scale score) was the dominant predictor across models. Among biomarkers, brain-derived tau (BD-tau) was most informative, followed by inflammation-related plasma proteins. In conclusion, machine learning accurately predicted functional outcome after AIS. BD-tau and inflammation-related proteins contributed predictive information above stroke severity, suggesting a potential for blood biomarkers to enhance individualized prognostication after AIS.

    Thursday, April 16, 2026

    DoctorSpeak: Why early detection can save stroke patients

     The lie about full recovery at the end of the article means I can't trust anything this person says!

    many stroke survivors can achieve total recovery and return to their routine lives.(A COMPLETE BALDFACED LIE! (Only 10% fully recover!)

    DoctorSpeak: Why early detection can save stroke patients

    Morinda-based Devinder (35) had a typically 'Punjabi' lifestyle - a diet high in oily and spicy foods; he smoked and also liked his Patiala peg.

    Consequently, he had high BP, diabetes and hypercholesterolemia (high levels of cholesterol, specifically LDL or 'bad' cholesterol). He was also not regular in taking his medications.

    One day he experienced sudden weakness on the left side of his body, slurred speech, and fell down. He was rushed to a nearby hospital where a CT scan suggested a stroke, following which he was referred for advanced treatment and care.

    Devinder had been experiencing fatigue or dizziness for days preceding this incident but he dismissed these, as do many such patients, which often results in a serious episode sooner or later.

    Often called a 'silent killer', a stroke usually begins quietly - a slight slurring of speech, sudden weakness in the arm, or a brief moment of confusion. Because these early warning signs can appear mild, many people dismiss them as fatigue or dizziness. Unfortunately, even a short delay in treatment can have life-altering consequences for stroke patients.

    A stroke occurs when the blood supply to a part of the brain is suddenly interrupted, either due to a blockage in an artery or bleeding within the brain. Without oxygen and nutrients, brain cells begin to die rapidly, which is why a stroke is considered one of the most time-sensitive medical emergencies.

    India records nearly 1.8 million new stroke cases every year, and doctors are increasingly seeing patients getting a stroke at much younger age than before. In Punjab, the concern is particularly significant because several major stroke risk factors are widely prevalent.

    Not just in Punjab, but in rest of India too, the incidence of hypertension, diabetes, obesity and high cholesterol is rising rapidly. People affected with these medical problems have a high risk of their blood vessels being damaged over time, increasing their likelihood of having a stroke.

    Diets high in salt and saturated fats, along with tobacco use and alcohol consumption, further increase the risk. A sedentary lifestyle and rising stress levels have also contributed to the rise in many lifestyle diseases. Consequently, doctors are now seeing strokes among younger people in their 30s and 40s.

    It highlights an urgent need for lifestyle modification, regular health check-ups, and adherence to prescribed treatment, especially among the young, who may otherwise underestimate their stroke risk. However, the encouraging news is that the treatment for stroke has advanced significantly. Clot-dissolving medications can restore blood flow if administered early. Many modern procedures like mechanical thrombectomy, recommended by the American Stroke Association, allow doctors to remove the clot from the blocked brain artery, without opening the brain. But this is a time-sensitive procedure, meant only for eligible patients, and can be performed up to 24 hours after the stroke.

    This makes awareness crucial - recognising symptoms early and getting the right treatment can dramatically change a patient's chances of recovery.

    Advancements in neurosurgical technology have further strengthened stroke management. Various sophisticated, image-guided technologies allow neurosurgeons to precisely locate and target affected areas of the brain in real time. In complex stroke cases, especially those involving bleeding or requiring surgical intervention, these can enhance accuracy, minimise damage to surrounding healthy brain tissue, and improve overall surgical outcomes.

    Post-stroke rehabilitation is equally important, as it plays a crucial role in helping patients regain independence and quality of life. Recovery often requires a structured, multi-disciplinary approach involving physiotherapy, speech therapy, occupational therapy, and psychological support. Early rehabilitation, sometimes initiated within 24-48 hours after stabilisation, can significantly improve mobility, speech, and cognitive functions.

    Family support and consistent follow-up are vital, as recovery timelines vary for each patient. With the right rehabilitation plan and medical guidance, many stroke survivors can achieve total recovery and return to their routine lives.(A COMPLETE BALDFACED LIE! (Only 10% fully recover!)

    The writer is Director, Neuro & Spine Surgery, Livasa Hospital, Mohali

    SIGNS YOU SHOULD NEVER IGNORE

    F Face drooping: One side of the face appears uneven or numb

    A Arm weakness: Sudden weakness or numbness in one arm

    S Speech difficulty: Slurred speech or difficulty in speaking

    Time to seek help: Seek emergency medical care immediately

    Other warning signs may include sudden severe headache, dizziness, vision problems, confusion, or difficulty in walking.

    MAJOR RISK FACTORS

    High blood pressure

    Diabetes

    High cholesterol

    Smoking or tobacco use

    Excessive alcohol consumption

    Obesity and sedentary lifestyle

    Heart disease or family history of stroke

    QUICK FACTS ABOUT STROKE

    - Stroke can occur at any age, although risk increases with age.

    - Women are slightly more likely to suffer a stroke than men.

    - Most patients, who suffer a stroke, have at least one major risk factor such as hypertension, high cholesterol, or smoking.

    FACTCHECK

    Stroke is a leading cause of death and disability in India, with an estimated incidence of 105-152/100,000 people per year. The crude incidence rate is estimated at 138.1 per 100,000 population, with significant regional variations. The total number of stroke cases in India has risen by 130.4% from 1990 to 2019. Studies indicate a rising burden, with over 1.25 million new cases in 2021, a 51% increase over three decades, and a high prevalence of ischemic stroke (70-80%). Key factors include hypertension, diabetes, and smoking, often exacerbated by delayed care and low awareness.

    Dailyhunt
    Disclaimer: This content has not been generated, created or edited by Dailyhunt. Publisher: The Tribune

    Naringin Reverses Chronic Stress-Induced Cognitive Deficits and Enhances Hippocampal Neuroplasticity in Mice

     

    All stroke patients are under massive stress because your incompetent? doctor doesn't have 100% RECOVERY PROTOCOLS. Will you doctor and hospital get human testing going?

    Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

    OH NO! your doctor KNOWS NOTHING AND DOES NOTHING! 

    Here's all the previous information on naringin which your incompetent doctor doesn't know about, have them prove me wrong!

    You do expect your doctor to be up-to-date on stroke research? Otherwise, you would be selecting a better doctor, right?

    Nitric oxide mechanism in the protective effect of naringin against post-stroke depression (PSD) in mice 2010 


    Preventive effects of hesperidin, glucosyl hesperidin and naringin on hypertension and cerebral thrombosis in stroke‐prone spontaneously hypertensive rats 2012


    Therapeutic potential of naringin in neurological disorders 2019


    Naringin reverses neurobehavioral and biochemical alterations in intracerebroventricular collagenase-induced intracerebral hemorrhage in rats 2017


    The beneficial role of Naringin-a citrus bioflavonoid, against oxidative stress-induced neurobehavioral disorders and cognitive dysfunction in rodents: A systematic … 2017


    Protective effect of naringin against ischemic reperfusion cerebral injury: possible neurobehavioral, biochemical and cellular alterations in rat brain 2009


    Naringin attenuates cerebral ischemia-reperfusion injury through inhibiting peroxynitrite-mediated mitophagy activation 2018


    The effect of ozone and naringin on intestinal ischemia/reperfusion injury in an experimental model 2015


    Preclinical evidence for the pharmacological actions of naringin: a review 2014

    And that's just the first page of 'naringin and stroke' in Google Scholar. 

    The latest here:

    Naringin Reverses Chronic Stress-Induced Cognitive Deficits and Enhances Hippocampal Neuroplasticity in Mice


    Abstract

    Chronic stress, such as chronic unpredictable mild stress (CUMS), induces hippocampal oxidative stress, inflammation, and neurochemical imbalances, resulting in cognitive and synaptic deficits. However, the role of naringin, a citrus bioflavonoid with antioxidant and neurotrophic properties in reversing hippocampal oxidative–inflammatory effects in CUMS remains largely unexplored. This study uniquely elucidates the neurocognitive and synaptic mechanisms through which naringin restores hippocampal integrity, emphasizing its dual antioxidant and neurogenic actions against CUMS-induced cognitive dysfunction. Adult male mice were divided into six groups (n = 9/group): control, CUMS, naringin (2.5, 5, 10 mg/kg), and fluoxetine (10 mg/kg). All mice except the control group were exposed to CUMS daily for 21 days. After 21 days of treatment post-CUMS exposure, behavioral assessments, biochemical assays, immunohistochemical assay for neuroplasticity-related proteins, and histological analyses were conducted. Naringin significantly improved memory performance in the Y-Maze and NORT, as evidenced by increased % alternation and discrimination index. Naringin significantly reduced nitrite and acetylcholinesterase enzyme activity while attenuating the depletion of reduced glutathione, superoxide dismutase and catalase activities in the brains of CUMS mice. CUMS exposure increased proinflammatory cytokines (TNF-α and IL1-β), which were attenuated by naringin. Likewise, hippocampal neurotransmitters, including serotonin, dopamine and noradrenaline, were restored by naringin relative to CUMS group. Naringin upregulated neurotrophic (BDNF), neuronal (NeuN), and proliferative (Ki-67) markers while suppressing astroglia activation (GFAP), indicating enhanced neuronal survival, synaptic remodeling, and hippocampal neurogenesis that collectively supported behavioral recovery. In conclusion, naringin ameliorates CUMS-induced cognitive impairment through inhibition of oxidative stress, inflammation, neurotransmitter imbalance, and enhancing hippocampal neurogenesis.