Deans' stroke musings
Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,134 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
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.
Tuesday, May 19, 2026
Defining Social and Cultural Barriers to Global Stroke Care: A SVIN–Mission Thrombectomy Initiative
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.
SSRI vs NDRI: Which Is Better for Post-Stroke Depression?
Your competent? doctor has already summarized this research right? I've got nothing on NDRIs. If your doctor is talking depression meds IT MEANS THEY ARE FUCKING INCOMPETENT IN GETTING YOU 100% RECOVERED!
- SSRIs
(31 posts to January 2013) Benefits and problems in here.
SSRI vs NDRI: Which Is Better for Post-Stroke Depression?
SAN FRANCISCO — The selective serotonin reuptake inhibitor (SSRI) fluoxetine and the norepinephrine-dopamine reuptake inhibitor (NDRI) bupropion are each effective for different psychiatric symptoms of post-stroke depression (PSD), new research suggests.
In a large retrospective cohort study with data for more than 100,000 patients with PSD, bupropion was associated with a significantly lower risk for suicidal ideation — the primary outcome — compared to treatment with fluoxetine.
However, for the secondary outcome of decreased demoralization and apathy, fluoxetine was the winner. (No 100% recovery protocols is the cause of demoralization! GET THERE!)
The results highlight the importance of customizing PSD treatment to the patient, said investigator Jaime Villa, an incoming first-year medical student at Reading Hospital, Tower Health System.
“For clinicians, the take-away message is that each of these antidepressants have a different effect on transmitters in the body,” Villa told Medscape Medical News. “So I’d say: focus on the symptoms and just treat each with the appropriate antidepressant.” The findings were presented May 17 at the American Psychiatric Association (APA) 2026 Annual Meeting.
Large Cohort
Depression is a common complication of stroke, affecting about 1 in 3 survivors, and is associated with poor recovery and increased morbidity. Most PSD cases occur within the first year post-stroke.
Fluoxetine is considered a first-line treatment for PSD, with both SSRIs and serotonin-norepinephrine reuptake inhibitors often prescribed for the condition. Caution has been urged for bupropion use in this population because it lowers the seizure threshold, and some studies have suggested a slightly higher risk for bleeding events.
The new retrospective cohort study aimed to address the lack of head-to-head data for secondary psychiatric outcomes between antidepressant classes.
“We wanted to look at the effect SSRIs and NDRIs had on the body for specific symptoms of depression,” Villa noted.
For the analysis, investigators included 2005-2025 data for 108,664 adult patients (mean age, 64 years; 59% women; 73% White) from the TriNetX Research Network database. All had been diagnosed with PSD within a year previously, with half receiving treatment with fluoxetine and the other half receiving bupropion.
Individualized Treatment Needed
Results showed a significantly lower suicidal ideation risk for the bupropion-treated group compared to the fluoxetine group (odds ratio [OR], 0.76; P < .05), as well as a lower percentage of recurrence (2.04% vs 2.66%, respectively).
However, bupropion was linked to greater increased risk for demoralization and apathy vs fluoxetine (OR, 1.54; P < .05), with a higher percentage of recurrence (0.13% vs 0.08%).
NDRIs increase the concentration of dopamine and norepinephrine and are known to regulate energy, motivation, and reward pathways, which Villa said could account for its efficacy for suicidal ideation prevention in patients with PSD.
Fluoxetine acts as a mood stabilizer and stress reliever, which makes it effective for such symptoms as apathy. However, it has a lower likelihood of affecting other neurotransmitters, including dopamine and norepinephrine, which may explain why it was less effective at preventing suicidal ideation, Villa added.
“These findings highlight differential psychiatric effects across antidepressant classes and underscore the importance of individualized treatment selection in PSD management,” he said.
The findings also underscore that clinicians have options depending on their patient's symptoms, he added.
Potentially Practice Changing?
The results offer some unexpected findings, said Charles S. Nguyen, MD, clinical professor of psychiatry at the University of California, Riverside, who was not part of the study.
“I always thought with bupropion, because it can lower the seizure threshold, maybe there’s a higher risk for seizures post-stroke. So I would not have thought that it would be a good choice to make” for this patient population, Nguyen told Medscape Medical News.
“We all knew that it could potentially be helpful, and after I look at this data showing it can help, I may be more inclined to consider it in my own practice in the future,” Nguyen added.
One question the research doesn’t answer, he noted, is whether there was an increased risk of stroke recurrence in the study participants.
Asked later about this concern, Villa said that while that outcome was not assessed in the current study, it would be an important topic to look into in the future.
Towards precision medicine for brain arteriovenous malformations
If you have one it will be good to train your doctor on this. I wouldn't take any chances that your doctor actually keeps up with stroke research.
Towards precision medicine for brain arteriovenous malformations
Andrew T. Hale,1,2 Adam J. Kundishora,3 Pazhanichamy Kalailingam,4 Tanyeri Barak,5 Phan Q. Duy,6 Christopher M. Ramundo,6 Baojian Fan,6 Qiang Li,6 Priscilla K. Brastianos,7 Ganesh M. Shankar,6 Seth L. Alper,7,8,9 Benjamin P. Kleinstiver,4,10,11 Patricia L. Musolino,4,12 and Kristopher T. Kahle6,9,13,14
Published May 15, 2026 - More info
View PDF- Abstract
Recent advances in cerebrovascular genomics, single-cell biology, pharmacology, and gene editing technology are transforming our understanding of brain arteriovenous malformations (bAVMs) — a leading cause of pediatric hemorrhagic stroke. Once considered static anatomical defects, bAVMs are now recognized as dynamic, genetically driven lesions resulting from somatic mutations in KRAS, BRAF, and pathways involved in arteriovenous specification, angiogenesis, and vascular remodeling. By integrating human genetics, animal models, and endovascular innovations, researchers have uncovered convergent mechanisms that link endothelial Ras/MAPK hyperactivation to abnormal vessel growth and higher rupture risk. These insights provide a foundation for precision medicine approaches that combine molecular diagnostics — such as liquid or endoluminal biopsies — with mutation-specific pharmacotherapies and emerging CRISPR-based gene editing strategies. We suggest that genotype-guided interventions, tailored by spatial and developmental cerebrovascular context, could ultimately reclassify bAVMs from surgically incurable malformations to treatable molecular conditions.
More at link.
Astrocytes in Brain Aging and Neurodegeneration: Cellular Mechanisms and Interventional Strategies
You'll have to ask your competent? doctor to get those emerging therapeutic strategies aimed at modulating astrocyte function, so your astrocytes don't deteriorate.
Astrocytes in Brain Aging and Neurodegeneration: Cellular Mechanisms and Interventional Strategies
ABSTRACT
Effect of Constrained Weight Shift With and Without Trunk Stabilization Training on Balance in Chronic Stroke Patients
With NO EXACT protocol written and distributed to all 10 million yearly survivors you did fucking useless work!
Effect of Constrained Weight Shift With and Without Trunk Stabilization Training on Balance in Chronic Stroke Patients
Abstract
Background
Stroke survivors often exhibit impaired postural control and balance due to trunk weakness and asymmetrical weight-bearing, increasing the risk of falls and limiting functional independence. Targeted rehabilitation strategies are essential to improve static and dynamic balance in chronic stroke patients.
Purpose
This study aimed to compare the effectiveness of constrained weight shift (CWS) training with trunk stabilization versus CWS training alone on static and dynamic balance in chronic stroke patients.
Methods
Thirty chronic stroke patients were randomly assigned to Group A (CWS + trunk stabilization) or Group B (CWS only). Both groups underwent 45-60-minute sessions, five days per week for six weeks, totaling 26 supervised sessions. Training involved weight-shifting exercises, functional tasks, and core strengthening exercises for the experimental group. Balance outcomes were assessed using the Berg Balance Scale (BBS) and Trunk Impairment Scale (TIS) pre- and post-intervention.
Results
Both groups demonstrated improvements in static and dynamic balance; however, Group A showed significantly greater gains in BBS and TIS scores (p < 0.05).
Conclusion
Adding trunk stabilization to CWS training enhances static and dynamic balance recovery in chronic stroke patients.
Stroke Awareness Month highlights recovery, rehabilitation
The real highlight is the complete fucking failure to get anywhere close to 100% recovery! You are totally fucking screwed if you have a stroke right now. No one in the world is competent at getting you fully recovered!
Here let's prove incompetency! You'll want 100% recovery, but won't get it!
There is no quality here if you don't measure the right things.
- tPA full recovery? Better than 12%?
- 30 day deaths? Better than competitors?
- rehab full recovery? Better than 10%?
Stroke Awareness Month highlights recovery, rehabilitation
SHREVEPORT, La. -- As part of Stroke Awareness Month, Willis-Knighton Health is partnering with KTBS to educate the community on prevention, symptoms, and recovery after a stroke.
Medical experts say stroke symptoms can include weakness, vision problems, and balance or coordination issues, often requiring immediate care. But recovery does not stop at the hospital. Physical therapy plays a critical role in helping patients regain mobility, rebuild strength, and return to daily life.
Therapists evaluate impairments early and create personalized plans to improve function and independence. Ongoing exercise is also key, supporting both physical recovery and mental health. Research shows many stroke patients experience depression, and staying active can help improve outlook and overall well-being.
Health leaders emphasize that recognizing symptoms quickly and committing to rehabilitation can significantly improve recovery outcomes.(You're completely lying right there by pushing your tyranny of low expectations; NOT DELIVERING 100% RECOVERY!)
Role of Hyperbaric Oxygen Therapy in Rehabilitation of Stroke Patients: A Randomized Controlled Pilot Study
Why HBOT? There are much faster and easier ways to get extra oxygen to stroke patients. But I guess your incompetent? doctor doesn't know of them!
Why do HBOT when there are vastly simpler, cheaper and less risky ways to increase oxygen uptake?
I can't see any use for HBOT unless it's delivered in the first week and there are vastly easier options for delivering oxygen than that.
Google this for risks: hyperbaric oxygen therapy deaths.
Here are 43 posts on HBOT for your edification
- Metformin (19 posts to July 2012)
Well, since this has been around for years why the hell doesn't someone actually do human testing and create protocols on stroke recovery?
Earlier research has this line:The drug, which is cheaply available for just $0.16 a day, works by boosting the number of oxygen molecules released into a cell, which in turn seems to benefit the robustness and longevity of the body’s basic building blocks. (This would seem to be much easier and faster than HBOT. I'm requesting this at my next stroke, my doctor won't know what hit her when I tell her how to treat me.)
If your doctor doesn't know about this s/he IS COMPLETELY FUCKING INCOMPETENT? And not creating protocols is even worse, allowing millions to billions of neurons to die because of lack of oxygen during the neuronal cascade of death!
What other protocols is your doctor using to significantly improve oxygen delivery immediately post stroke? The first hours and days? NOTHING? Then you DON'T have a functioning stroke doctor, do you?
Maybe these, why isn't your incompetent doctor already delivering these to you?
cerebral blood flow (29 posts to July 2016)
Cerebral blood flow autoregulation
(1 post to July 2021)
Cerebral Blood Flow Velocity (1 post to Febraury 2020)
cortical oxygenation (1 post to November 2020)
oxygen delivery (20 posts to January 2020)
oxygen uptake (5 posts to August 2013)
Normobaric oxygen (10 posts to January 2020)
Oh, your incompetent doctor doesn't have any and doesn't fucking care about learning better ways to get you recovered! Well, fire them!
The latest here:
Role of Hyperbaric Oxygen Therapy in Rehabilitation of Stroke Patients: A Randomized Controlled Pilot Study
- Ramakant Yadav
- Usha Shukla1
- Urvashi Yadav1
- Shipra Verma1,
- Sushil Kumar Shukla2
Background:
Improvement in neurological function has been reported in stroke patients after hyperbaric oxygen therapy (HBOT) administration. Although the majority of spontaneous neurological recovery occurs within the first 90 days poststroke, HBOT may further augment this recovery process. This study aimed to evaluate the role of HBOT in improving neurological function and quality of life (QoL) in stroke patients.
Materials and Methods:
This randomized controlled pilot study involved 30 patients who experienced an ischemic stroke 3–6 months before enrollment, randomly assigned to two groups: Group H (n = 15), which received 24 sessions of HBOT along with conventional physiotherapy and Group C (n = 15), which received only conventional physiotherapy. The primary outcome was the change in motor function, assessed using the National Institutes of Health Stroke Scale (NIHSS). The secondary outcomes included the changes in cognitive function, evaluated with the Mini-Mental State Examination (MMSE), and QoL, measured using the Short Form-36 questionnaire.
Results:
Following HBOT, there was a significant improvement in the NIHSS score from a baseline of (7.27 ± 2.71) to (5.46 ± 2.47) and in the MMSE from a baseline of (24.8 ± 2.98) to (26.73 ± 1.90). Similar improvements were also observed in Group C after the intervention compared to baseline. Group H showed significant improvement in the SF-36 questionnaire except for bodily pain and vitality, while Group C showed no significant change.
Conclusion:
Although clinical improvement in motor and cognitive function was better after giving HBOT in the 3–6 months poststroke period, the between-group comparisons postintervention were not statistically significant.