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.

Showing posts with label hate mail. Show all posts
Showing posts with label hate mail. Show all posts

Wednesday, August 12, 2026

Improving stroke care and innovation

The key word signifying incompetence is 'CARE'; NOT RECOVERY!  You don't have to go any farther than the word 'care' to declare incompetence.

 

Survivors want 100% recovery OR DON'T YOU CARE ABOUT THAT? 

Anyone who touts standards/'care' and NOT RECOVERY! IS A COMPLETE FUCKING FAILURE!

Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and title(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHERE I'M WRONG. I want to hear your excuses for failure(not getting to 100% recovery IS FAILURE!) so I can demolish them! You aren't solving to 100% recovery protocols with NO EXCUSES! I've never received any communications from any stroke association. You'd think they would want to talk to their fiercest critic, but no, they are hiding under a rock someplace, probably don't even know I exist! Swearing at me is allowed, I'll return the favor. Don't even attempt to use the excuse that brain research is hard.

Improving stroke care and innovation

Every 40 seconds, someone in the U.S. has a stroke, according to the Centers for Disease Control and Prevention. Because stroke is a leading cause of long-term disability and death, there is a growing need to develop innovative therapies to protect the brain and approach stroke rehabilitation in new ways. Investigators at Feinberg are working from multiple angles along the stroke care pathway, leading research that may improve recovery after a stroke occurs. When a person suffers a stroke, physicians must restore blood flow to the brain as quickly as possible to save their life. But, ironically, that lifesaving rush of blood can also trigger a second wave of damage—killing brain cells, fueling inflammation and increasing the odds of long-term disability.published in the journal Neurotherapeutics, Northwestern scientists developed an injectable regenerative nanomaterial that helps protect the brain during this vulnerable window. The findings suggest the new therapy could eventually complement existing stroke treatments by limiting secondary brain injury and supporting recovery. In the preclinical study, the team delivered a single intravenous dose immediately after restoring blood flow in a mouse model of ischemic stroke, the most common type of stroke. The therapy successfully crossed the blood-brain barrier—a major challenge for most drugs—to reach and repair brain tissue. The material significantly reduced brain damage and showed no signs of side effects or organ toxicity."Current clinical approaches are entirely focused on blood flow restoration," said co-senior author Ayush Batra, M.D., associate professor in the Ken and Ruth Davee Department of Neurology in the Division of Neurocritical Care. "Any treatment that facilitates neuronal recovery and minimizes injury would be very powerful, but that holy grail doesn't yet exist. This study is promising because it's leading us down a pathway to develop these technologies and therapeutics for this unmet need." Batra is also a professor of pathology and co-director of the NeuroVascular Inflammation Laboratory. This research is a collaboration with Samuel Stupp, Ph.D., the Board of Trustees Professor of Materials Science and Engineering, Chemistry, Medicine and Biomedical Engineering, who developed the injectable therapy based on supramolecular therapeutic peptides (STPs). The work builds on his study published in Science in 2021, which demonstrated how the STP technology—nicknamed "dancing molecules"—and the highly dynamic nature of its therapeutic agents could reverse paralysis and repair tissue in mice after a single injection at the site of severe spinal cord injury.

The new study found that similar dynamic molecular assemblies can be administered intravenously without requiring surgery or an invasive injection directly into the brain.

"One of the most promising aspects of this study is that we were able to show this therapeutic technology, which has shown incredible promise in spinal cord injury, can now begin to be applied in a stroke model and that it can be delivered systemically," said Stupp, who was co-senior author of the study. "This systemic delivery mechanism and the ability to cross the blood-brain barrier is a significant advance that could also be useful in treating traumatic brain injuries and neurodegenerative diseases such as ALS."

Acute ischemic stroke, which accounts for 80% of all strokes in the U.S., is a devastating condition and one of the leading causes of morbidity and mortality worldwide, Batra said. Ischemic strokes occur when a clot blocks blood flow to the brain. Physicians reopen the vessel by administering "clot-busting" drugs or using devices to surgically remove the clot.

Severe strokes can lead to permanent, significant disability that affects a patient's quality of life and their ability to return to work and engage with their family and society.

"It has not only a significant personal and emotional burden on patients, but also a financial burden on families and communities," Batra said. "Reducing this level of disability with a therapy that could potentially help restore function and minimize injury would really have a powerful long-term impact."

The findings are highly relevant for future clinical applications because the scientists tested the approach in a mouse model that closely mimics real-world ischemic stroke treatment, Batra said.

Further studies will need to assess whether this treatment can support longer-term functional recovery. For instance, many stroke patients suffer significant cognitive decline throughout the year after a stroke. According to Batra, the new therapy is primed to address that secondary injury, but the studies will require a longer follow-up period and more sophisticated behavioral testing.

Building video games that offer therapeutic benefit

A customized throwback video game may offer a surprisingly futuristic path to stroke recovery. In a recent study, published in Neurorehabilitation and Neural Repair, Marc Slutzky, '02 M.D., '00 Ph.D., '06 GME, professor of neurology and neuroscience, and his team developed a '90s-style video game to help chronic stroke survivors regain lost arm function.

While wearing a small device on their impaired arm and using a laptop computer, players use their arm muscles to complete tasks such as flying a helicopter around the screen to hit a moving target. The muscle retraining helps separate the brain's uncoordinated movement signals, enabling muscles to work independently again.

Patients in the study had moderate to severe arm impairment from a stroke that occurred at least six months before beginning the study. They could move their arm only slightly and extend their elbow. The average patient was 6.4 years out from their stroke, while some were 12 years out.

After six weeks of game-based therapy, chronic stroke survivors improved arm function by 7.8 times as much as those in the control group. They also kept improving even after stopping the therapy.

Being able to play the game at home allowed better access to therapy and increased repetitions. Participants performed more than 300 repetitions per day, compared with physical therapy in a clinic, where they might get only 30 repetitions three days per week, said Slutzky, who was senior author of the paper.

Most stroke rehabilitation today focuses on helping survivors perform daily tasks, which often leads them to compensate for impaired arm function. For example, they may lean forward with their whole body to reach for an object rather than reaching for it with just the arm. While this technique is useful, it doesn't directly aim to improve movement of the arm. This study, however, found that the therapy improved the range of motion in participants' arms during reaching tasks, as well as their ability to perform daily activities.

"Here we're doing something different," Slutzky said. "We're treating the impairment directly and measuring how much the actual arm improved in addition to performing certain functions. We found our conditioning really caused their improvement."

The team, along with Northwestern bioelectronics pioneer John A. Rogers, Ph.D., the Louis Simpson and Kimberly Querrey Professor of Materials Science and Engineering, Biomedical Engineering and Neurological Surgery, is working to make the game's wearable device completely wireless. They're also upgrading the games to be more engaging, and in the future, they plan to test them on stroke survivors' legs.

Addressing stroke treatment and recovery is vital to improving quality of life and health outcomes for many patients. These two studies offer novel ways Northwestern investigators continue to move the science forward.

Publication details

Zijun Gao et al, Toward development of a dynamic supramolecular peptide therapy for acute ischemic stroke, Neurotherapeutics (2026). DOI: 10.1016/j.neurot.2025.e00820

Journal information: Neurorehabilitation and Neural Repair  , Science  , Neurotherapeutics 

Monday, July 13, 2026

Quantitative multi-slice spiral CT perfusion parameters as predictors of collateral status and 90-day functional outcome in acute ischemic stroke

 

Predicting failure to recover IS STUPIDER THAN HELL! Deliver recovery you blithering idiots!

Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and title(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHERE I'M WRONG.

Exactly what in this research gets survivors recovered? 100% recovery is the only goal in stroke; NOT PREDICTIONS, BIOMARKERS, PROGNOSTICATION, OR ASSESSMENTS! I'd fire anyone doing these!

Quantitative multi-slice spiral CT perfusion parameters as predictors of collateral status and 90-day functional outcome in acute ischemic stroke


  • D

    Dan Zhu

  • X

    Xiaozhou Ma

  • Y

    Yingzhi Jiao

  • S

    Shuai Liu

  • J

    Jinzhu Yan

  • Lixin Zhang

    Lixin Zhang *

  • Imaging Center, Qianwei Hospital of Jilin Province, Changchun, Jilin, China

Abstract

Objective: 

To evaluate the utility of quantitative computed tomography perfusion parameters for assessing collateral circulation and predicting 90-day functional outcomes in acute ischemic stroke.

Methods: 

This retrospective study included 82 patients who underwent perfusion imaging within 24 h of symptom onset. Parameters including relative cerebral blood flow, relative cerebral blood volume, mean transit time, time to maximum, and hypoperfusion intensity ratio were analyzed. Collateral status was classified using multiphase angiography, and 90-day outcomes were assessed using the modified Rankin Scale.

Results: 

Patients with robust collateral circulation showed higher relative cerebral blood flow and volume and shorter perfusion times compared with those with poor collaterals. Hypoperfusion intensity ratio demonstrated strong diagnostic performance (area under the curve 0.925). For predicting unfavorable 90-day outcome, HIR achieved an AUC of 0.912 and showed greater discrimination than mismatch ratio in the present cohort, while the combined HIR–rCBF–Tmax model achieved an AUC of 0.938. Hypoperfusion intensity ratio correlated positively with functional disability, while relative cerebral blood flow correlated negatively with infarct volume. Favorable outcomes were more frequent in patients with robust collaterals.

Conclusion: 

Quantitative CTP parameters bridge a natomical collateral assessment and downstream tissue-level perfusion. HIR may provide a particularly informative functional marker of collateral efficiency and 90-day prognosis beyond conventional mismatch assessment.

Platelet to high-density lipoprotein cholesterol ratio predicts clinical outcomes after acute ischemic stroke: a prospective cohort study

 

Predicting failure to recover IS STUPIDER THAN HELL! Deliver recovery you blithering idiots!

Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and title(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHERE I'M WRONG.

Exactly what in this research gets survivors recovered? 100% recovery is the only goal in stroke; NOT PREDICTIONS, BIOMARKERS, PROGNOSTICATION, OR ASSESSMENTS! I'd fire anyone doing these!

Platelet to high-density lipoprotein cholesterol ratio predicts clinical outcomes after acute ischemic stroke: a prospective cohort study

  • 1. Department of Clinical Laboratory, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, China

  • 2. Department of Neurology, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, China

Abstract

Background: 

The platelet/high-density lipoprotein cholesterol ratio (PHR), a marker of hypercoagulable states and disordered lipid metabolism, has been confirmed as a predictor of cardiovascular disease. However, the effects of PHR on the prognosis of acute ischemic stroke (AIS) remain unknown. We aimed to assess the associations of PHR with the risk of clinical outcomes in patients with AIS.

Methods: 

This prospective observational study included 820 patients (median age, 68 years; female, 34.6%; median NIHSS at admission, 3) with AIS. The median time from symptom onset to admission was 2 days (interquartile range [IQR], 0–4), and from admission to blood sampling was 15 h (IQR, 12–19). PHR was calculated as platelet count (PC; 109 cells/L)/HDL-C (mmol/L) at admission. PHR was analyzed both as a continuous variable and in tertile form (tertile 1-tertile 3). To analyze the associations between PHR and clinical outcomes including all-cause death, stroke recurrence and poor functional outcome at 3 months, 6 months and 1 year, we used multivariable Cox and logistic regression, Kaplan–Meier survival curves, restricted cubic splines, subgroup analysis, concordance statistic (C-statistic), net reclassification index (NRI), and integrated discrimination improvement index (IDI).

Results: 

The median PHR was 202.155 (IQR, 153.120–262.365). Kaplan–Meier survival curves identified tertile 3 as the group with the highest risk for all-cause death and stroke recurrence. After adjustment, multivariable Cox regression (tertile 1 as reference) showed that the highest PHR tertile 3 was associated with increased risk for both all-cause death and stroke recurrence across all three follow-up intervals (3 months, 6 months and 1 year). In parallel, multivariable logistic regression (tertile 1 as reference) showed that tertile 3 was associated with a greater likelihood of poor functional outcome across the same three time points. Continuous PHR showed a positive dose–response relationship with clinical outcomes. Subgroup analysis revealed significant interactions of age (p < 0.05) with PHR for all-cause death, and of BMI (p < 0.05) with PHR for mRS 3–6. A basic model’s predictive ability was strengthened by the addition of PHR (C-statistic, NRI, IDI).

Conclusion: 

A higher PHR level in patients with AIS is strongly associated with an increased risk of all-cause death, stroke recurrence and poor functional outcome. As a valuable predictive biomarker, PHR may provide a simple and effective tool for predicting clinical outcomes in patients with AIS.

Graphical Abstract

Friday, July 10, 2026

Transthyretin at the crossroads of neurodegeneration: a silent guardian in Parkinson’s disease

 Will your competent? doctor be doing something with this because of your risk of Parkinsons post stroke? Oh NO, NOTHING DOING! So, INCOMPETENCE REIGNS AGAIN! Your doctor is becoming an expert at incompetence and your board of directors is so incompetent they can't recognize it in their hospital! 

Transthyretin at the crossroads of neurodegeneration: a silent guardian in Parkinson’s disease

Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disease characterised by disruption of brain homeostasis and degeneration of dopaminergic neurons in the substantia nigra. PD is characterised by motor symptoms, like tremor, rigidity, bradykinesia, and postural instability, as well as non-motor symptoms like cognitive impairment, mood disorders, sleep disturbances, and autonomic abnormalities that significantly affect quality of life. The molecular pathogenesis of PD involves Oxidative stress, neuroinflammation, mitochondrial dysfunction, α-synuclein (α-syn) misfolding and aggregation, insufficient autophagy-lysosomal clearance, and synaptic degeneration, leading to progressive neuronal loss. Transthyretin (TTR), a tetrameric transport protein that is primarily produced in the liver and choroid plexus, is well-known for carrying thyroxine and retinol-binding protein. Experimental studies have shown that TTR can protect neurons by binding misfolded proteins, such as α-syn, decreasing toxic aggregation, regulating oxidative stress responses, and affecting selective autophagic degradation. PD-related changes in TTR expression in brain tissue and cerebrospinal fluid provide strong evidence of TTR’s significance as a molecular biomarker and a physiological regulator in the pathogenesis of the disease. This review highlights TTR involvement in neuroinflammation, oxidative stress, and α-syn aggregation, and discusses emerging evidence supporting TTR stabilizers as potential biomarkers and therapeutic targets for modulating disease progression in PD.

 This is a preview of subscription content, log in via an institution  to check access.

Sunday, July 5, 2026

Early Temperature Rise Within First 24 Hours of Stroke Onset Predicts Poor Outcomes

 Predicting failure to recover IS STUPIDER THAN HELL! Deliver recovery you blithering idiots!

Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and title(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHERE I'M WRONG.

Exactly what in this research gets survivors recovered? 100% recovery is the only goal in stroke; NOT PREDICTIONS, BIOMARKERS, PROGNOSTICATION, OR ASSESSMENTS! I'd fire anyone doing these!

Early Temperature Rise Within First 24 Hours of Stroke Onset Predicts Poor Outcomes

TOPLINE

An increase in body temperature within the first 24 hours of stroke onset was significantly associated with higher odds of poor functional outcomes at 3 months in patients with ischaemic and haemorrhagic strokes.

METHODOLOGY

  • Using data from a prospective Spanish stroke registry, researchers conducted a retrospective study to assess how body temperature at admission, the maximum temperature within the first 24 hours, and temperature fluctuations affect functional outcomes at 3 months after stroke.
  • They included 5883 patients with stroke (mean age, 69.5 years; 44.5% women), comprising 4830 with ischaemic stroke and 1053 with haemorrhagic stroke, between 2008 and 2018.
  • To capture potential dynamic fluctuations, four temperature variables were evaluated: the temperature at admission, the maximum temperature within the first 24 hours, the difference between the maximum temperature and the temperature at admission, and the change in temperature during the first 24 hours.
  • Patients with a temperature of at least 37.5 °C upon admission or within the first 24 hours received oral paracetamol or intravenous metamizole every 8 hours until normothermia was achieved.
  • Functional stroke outcomes at 3 months were assessed using the modified Rankin scale (mRS), with good outcome defined as an mRS score of 2 or less and poor outcome defined as an mRS score of greater than 2.

TAKEAWAY

  • Temperature at admission did not predict the 3‑month functional outcomes after stroke.
  • The maximum temperature within the first 24 hours was associated with approximately fourfold increased odds of poor 3-month functional outcomes in ischaemic stroke (adjusted odds ratio [aOR], 4.68) and nearly threefold higher odds in haemorrhagic stroke (aOR, 2.96; P < .001 for both).
  • The early rise in temperature within the first 24 hours was significantly associated with approximately 10-fold and 17-fold increased odds of 3-month poor functional outcomes in ischaemic and haemorrhagic strokes, respectively (P < .001 for both).
  • Among treated patients, a temperature rise of at least 0 °C during the first 24 hours predicted poor outcomes, with a sensitivity of 89% and a specificity of 84% in those with ischaemic stroke and a sensitivity of 83% and a specificity of 71% in those with haemorrhagic stroke.

IN PRACTICE

"Monitoring temperature changes, specifically the rise in body temperature during the first 24 h after stroke onset, provides the most robust indicator for initiating antihyperthermic therapy. Targeting patients who exhibit a temperature increase over this period, rather than relying on a single admission measurement, may optimize treatment efficacy and improve functional outcomes," the authors wrote.

SOURCE

This study was led by Crhistian-Mario Oblitas, Neuroimaging and Biotechnology Laboratory, Clinical Neurosciences Research Laboratory, Health Research Institute of Santiago de Compostela, Hospital Clínico Universitario, Santiago de Compostela, Spain. It was published online on June 19, 2026, in the Journal of Clinical Medicine.

LIMITATIONS

The study relied on data from a prospective registry that was not specifically designed to assess temperature metrics. Detailed longitudinal analyses of temperature changes could not be performed due to methodological limitations. Although data on the infectious source of fever were taken into account in the analysis, data on the severity of infections and the spectrum of antimicrobial therapies were lacking, which may have introduced bias.

DISCLOSURES

This study received funding from the Spanish Ministry of Science and Innovation, Xunta de Galicia, Instituto de Salud Carlos III, and CIBERNED. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Sunday, May 31, 2026

Yawning May Help Flush Waste From Your Brain, Early Research Suggests

 Your competent? doctor already has created brain waste removal protocols, right? Only 5+ years and even your board of directors is so incompetent they don't know they are running an INCOMPETENT HOSPITAL?

Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and title(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHERE I'M WRONG.

Yawning May Help Flush Waste From Your Brain, Early Research Suggests

New research suggests yawning might help your ‘glymphatic system’—aka the brain’s waste clearance pathway.

In a small study of 22 participants who underwent MRI scans, yawning sent cerebrospinal fluid (or CSF) away from the brain. This suggests that it “reorganizes neurofluid flow,” per the researchers.

Experts suggest yawning might be a “potential backup system” for the brain, acting as a sort of backup pump to clear brain waste.

It can be hard to stop a yawn once the urge strikes, but now, new research suggests that going with it might be good for you. The latest study suggests that yawning might actually help “clean” your brain by facilitating fluid movement along brain waste-clearance pathways.

While yawning in the middle of your boss’s big work presentation might not ever be socially acceptable, you can at least console yourself with the knowledge that the yawn you just unleashed may help your brain.

Before you start yawning all day, every day in the name of health, know this: The study didn’t definitively prove that yawning is good for you—but it had some interesting findings that suggest a good yawn here and there might help more than hurt. Here’s the deal.

Tuesday, May 19, 2026

Stroke Awareness Month Highlights Emerging Therapies and Opportunities in Recovery Care

 

The key word signifying incompetence is 'CARE'; NOT RECOVERY!  You don't have to go any farther than the word 'care' to declare incompetence. See how simple it is to evaluate stroke. 'Awareness' never got anyone recovered!


Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and title(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHERE I'M WRONG. I want to hear your excuses for failure(not getting to 100% recovery IS FAILURE!) so I can demolish them! You aren't solving to 100% recovery protocols with NO EXCUSES! I've never received any communications from any stroke association. You'd think they would want to talk to their fiercest critic, but no, they are hiding under a rock someplace, probably don't even know I exist! Swearing at me is allowed, I'll return the favor. Don't even attempt to use the excuse that brain research is hard.

Stroke Awareness Month Highlights Emerging Therapies and Opportunities in Recovery Care

Stroke Awareness Month, observed each May, is intended to increase public and clinician awareness of stroke prevention, early recognition, and timely intervention for a condition that remains a leading cause of long-term disability and mortality.1,2 Campaigns during the month emphasize education around modifiable vascular risk factors, including hypertension, diabetes, smoking, obesity, and atrial fibrillation, as well as rapid identification of symptoms using the B.E. F.A.S.T. framework (Balance loss, Eye changes, Face drooping, Arm weakness, Speech difficulty, Time to call 911).2,3 The observance also highlights secondary prevention strategies, with estimates suggesting that up to 80% of strokes may be preventable through risk-factor modification and evidence-based cardiovascular care.1 Rehabilitation care is another key focus of the awareness month.

To highlight ongoing priorities in stroke awareness, prevention, and recovery, NeurologyLive® sat down with Andrew Abdou, DO, attending physician of neurorehabilitation at Burke Rehabilitation Hospital. The discussion revolved around the evolving landscape of stroke rehabilitation and emerging therapeutic innovations aimed at improving long-term outcomes for survivors.

In the conversation, Abdou highlighted the importance of raising awareness around stroke prevention, recurrent stroke risk, and the often-overlooked challenges patients and caregivers face after hospital discharge. He emphasized the critical role of neuroplasticity, continuity of care, and lifestyle interventions in optimizing recovery. Abdul also detailed several novel rehabilitation approaches, underscoring growing optimism around technologies that may help patients continue making functional gains even years after a stroke.

NeurologyLive: What is the importance of Stroke Awareness Month, and what significance does it hold for individuals at risk of stroke or those who have already experienced one?

Andrew Adbou, DO: This is an important time of year to recognize stroke survivors and the real day‑to‑day challenges they face, and to learn more about what the overall quality of life looks like for them. We want to raise awareness not only about those challenges, but also about prevention, especially reducing the risk of the first stroke and the risk of recurrent strokes among stroke survivors.

Beyond that, we want to highlight the importance of early treatment and ongoing rehab. Often, what we see with stroke survivors is feeling overwhelmed, feeling lost, and it’s important for them to know that there is a place they can go, a place where they can come to continue to heal, whether it be months after the stroke or years after the stroke. We also want to have a place for their caregivers, their families, their loved ones, to better understand how to support these survivors through this very critical time when they’re healing.

Are there any new therapeutic agents for stroke that clinicians should be aware of?

Especially here at Burke Rehab, there are a growing number of clinical trials that are focused specifically on stroke recovery. I'm a principal investigator on the Brain Q clinical trial (NCT06386874) which is a non‑invasive brain stimulation. In addition, there are our Vivistim options in the outpatient setting. It’s a program where patients have an implanted device to help with upper limb recovery through vagal nerve stimulation, and this is a great opportunity for patients in the chronic stroke phase to continue to recover even after they've been told they've plateaued or there will be limited to no recovery in those chronic years. There’s now a chance for them to continue to recover, whether it be through our current clinical trials or through their stim program as well.

In addition, there are advances in spasticity management that we're implementing. Often, the mainstay of intervention would be oral medications or botulinum toxin injections. We also have cryoneurolysis, which is one of the emerging treatment strategies for spasticity after stroke, with more immediate and longer‑lasting effects. There are a lot of exciting stuff that’s currently happening, and we really have options for those in the chronic phase to continue to recover and get stronger.

How can clinicians optimize stroke care or rehabilitation for some of these patients?

The core of recovery after stroke is neuroplasticity, and it's really about how we get more hours in the day or time in the week to continue with this repetition. We address this in the outpatient setting, but also with well-organized home exercise programs, and by having good continuity of care over the long term to ensure that patients are maintaining both repetition and continuity of their stroke recovery program in therapy.

What’s great is that because we have inpatient rehab and outpatient rehab, we can really track these patients. I see my patients from day one of their inpatient rehab all throughout their stay on inpatient, and then continue to see them in the outpatient setting. So, we’re monitoring these patients closely and maintaining continuity of care, because those first 3-, 6-, and 12-month windows are where the highest rate of recovery occurs, and we want to optimize that as much as we possibly can.

Ways we can optimize outside of direct therapy, in addition to some of the emerging technologies we mentioned, include lifestyle medicine. I myself am certified in lifestyle medicine. It’s an emerging field, but it relies on the core tenets of health: nutrition, exercise, sleep, avoiding risky substances, as well as mental health, and ensuring that patients have strong relationships with their family, friends, and community. If we can optimize all of these, it helps make for better recovery overall and a better quality of life.

What is your perspective on the role of exercise and broader lifestyle changes in supporting recovery after stroke?

There are many mechanisms as to why lifestyle changes support recovery. There is the overall health piece: having better cardiovascular health and minimizing other risk factors such as diabetes and high cholesterol. That in itself confers a better prognostic outcome and helps with stroke prevention.

That’s one pathway, but then you also have neuroplastic pathways that are enhanced. Exercise alone is known to release certain neurotrophic factors, such as brain‑derived neurotrophic factor, which can help enhance neurorecovery. The repetition of exercise improves plasticity as well, because that repetition of the exercise itself is a pathway of neurorecovery. Through all these different mechanisms, it amounts to improved function and overall health status.

Are there any new pathways to treat stroke that are currently being studied?

I want to talk a little bit more about some of the novel interventions, devices, and clinical trials that we're doing here at Burke. Again, I'm the principal investigator on Brain Q, which is our EMAGINE trial. It uses non‑invasive brain stimulation—Brain Q—for patients to recover. We're doing trials in both acute and chronic stroke. Patients wear a device that they’ll use about 45 minutes a day, 3 to 5 days a week, along with a tablet of guided exercises. The idea is that this will enhance their neurorecovery, even in the chronic phase. It's really exciting that we get to be part of this clinical trial, and we're really hoping for it to become more commonplace. Often, patients do their rounds of therapy, and when they’re in this chronic phase, the recovery slows down. We want to jumpstart that recovery and give them an opportunity to continue to make gains.

The other device I mentioned previously was Vivistim. This is a vagal nerve stimulation implanted device that patients can turn on and off while they’re in therapy, doing a structured program with our occupational therapists for upper limb recovery. We’re seeing patients who had not made gains in years start making gains again, and that is huge. You can think of it as sparking a match to get that recovery going again and reactivating those pathways. It’s exciting, both for stroke patients with ischemic strokes and for what we hope to continue with in future clinical trials.

What are some technological advances in the stroke field that are exciting to you?

What’s exciting to me is the field of non‑invasive brain stimulation with all the emerging technologies. Non‑invasive brain stimulation can range from transcranial magnetic stimulation to transcranial direct current stimulation.

In fact, there is another trial at Burke that we're doing for patients with aphasia, utilizing transcranial direct current stimulation. I think this is a field that’s really emerging in many different areas of rehab, whether it be stroke, brain injury, spinal cord injury, or pain management.

These non‑invasive approaches and the broader field of neuromodulation are very exciting. Patients are often overloaded with oral medications and have gone through many rounds of therapy. They’re really looking for something new, something novel, something different, ways to jumpstart their recovery after months or years of slow progress. I think this is a really exciting opportunity.

Beyond that, as I alluded to earlier with our other treatments for spasticity: the mainstay currently is chemo‑denervation with botulinum toxin or implanted baclofen pump devices. Cryoneurolysis is one of the newer, novel treatments that we provide here at Burke. It has immediate effects and lasts twice as long as botulinum, and for some patients that really opens up a lot of options for managing their spasticity.

What gives you the most optimism in the Stroke field?

Greater access to these innovative therapies and clinical trials for patients is really an exciting thing. I can't tell you how many times I have patients who have gone from facility to facility, looking for more. These are motivated people with simple goals. For example, patients with their Vivistim device, some patients all they want to do is hug their spouse again or hold their grandchild, and these devices can help them do that.

It’s also about our ability, as a community here, to increase empowerment and education for caregivers and patients alike and to let them know what opportunities they have. It doesn't just end after discharge from the hospital. There is a community. There is an opportunity for everyone here to make gains, to grow, and to improve their quality of life. That makes me proud to be at an institution like Burke, leading those advancements while maintaining patient‑centered care.

Transcript edited for clarity.