Endovascular Thrombectomy Boosts Outcomes in Medium-Vessel Ischemic Stroke

 So, still a failure since 100% recovery was not achieved!

Here is your business101 requirements. Not measuring 100% recovery is the height of incompetence!

“What's measured, improves.” So said management legend and author Peter F. Drucker ) 

Endovascular Thrombectomy Boosts Outcomes in Medium-Vessel Ischemic Stroke

Chinese randomized trial shows "meaningful improvement" in functional outcomes(NOT GOOD ENOUGH! Survivors do want 100% recovery, they don't accept your tyranny of low expectations.)

Key Takeaways

• Endovascular thrombectomy is indicated for acute ischemic stroke due to a large vessel occlusion in the anterior circulation within 24 hours of the time last known to be well.
• The ORIENTAL-MeVO randomized trial from China found that mechanical thrombectomy also improved outcomes for acute middle-vessel occlusion stroke.
• The findings might help expand patient selection for this treatment, although further trials in a Western population might be needed to confirm the benefit.

For patients with moderate-to-severe deficits from an acute middle-vessel occlusion stroke, endovascular treatment within 24 hours of onset improved functional independence, the Chinese ORIENTAL-MeVO trial found.

Survival without more than mild disability at 90 days (modified Rankin Scale score of 0-2 on the 6-point scale) was 24% more likely with randomization to thrombectomy compared with medical treatment alone (58.6% vs 46.6%, adjusted RR 1.24, 95% CI 1.07-1.44, P=0.004), Wei Hu, MD, of the First Affiliated Hospital of the University of Science and Technology of China in Hefei, and colleagues reported in the New England Journal of Medicine.The impact on functional outcomes was clinically meaningful, the group wrote, with a number needed to treat of 8.2 to observe a functional-independence outcome -- "a magnitude similar to that reported for established reperfusion therapies in acute ischemic stroke and consistent with meaningful improvement in patient-centered functional outcomes."

The procedure led to numerically more symptomatic intracranial hemorrhage (4.7% vs 2.2% at 24-72 hours) and 90-day mortality (11.1% and 10.2%), although neither was statistically significant.

"These findings highlight the importance of careful patient selection(You're failing at the goal of leaving no survivor behind!), particularly given the smaller infarct burden that is typically associated with strokes due to medium-vessel occlusion," Hu and colleagues wrote.

Indeed, in an accompanying editorial, Johanna M. Ospel, MD, PhD, and Michael D. Hill, MD, both of the University of Calgary in Canada, cautioned "[m]ost patients with stroke due to medium-vessel occlusion will not benefit from endovascular thrombectomy."

"The neutral results of the ESCAPE-MeVO and DISTAL trials, taught us that although we can technically open medium-vessel occlusions, many patients with less severe stroke simply did not benefit," they wrote.

"The ORIENTAL-MeVO trial now provides evidence from a randomized trial that a subset of patients with more severe stroke at a younger age and in earlier time windows has important characteristics with regard to the selection of treatment candidates," Ospel and Hill added. "This result is concordant with the ESCAPE-MeVO and DISTAL trials, in which post hoc analyses suggest that favorable baseline imaging (good collaterals [pial-vessel filling] or a favorable mismatch profile on CT perfusion imaging) and faster treatment are likely to be important."

Not being sequentially or concurrently treated with thrombolysis likely predicts greater benefit from mechanical thrombectomy for middle-vessel occlusion as well, they suggested.

ORIENTAL-MeVO included 563 adults who presented at 48 centers in China within 24 hours after the onset of a moderate-to-severe stroke (National Institutes of Health Stroke Scale score ≥6, median 10 on the 42-point scale) due to occlusion of a medium vessel. Median age was 71 years, 42.8% were women, and 36.6% received IV thrombolysis.

Patients were randomly assigned to open-label treatment with medical management alone or together with thrombectomy of the neurointerventionalist's choice. Standard medical treatment followed clinical guidelines and included one or two antiplatelet agents (at the discretion of the treating physician) and IV thrombolysis (when patients met established eligibility criteria). Overall, 361 of the patients presented within 4.5 hours of stroke onset, and median time from onset to arterial access in the thrombectomy group was 5.3 hours.

Enrollment exclusively in China, where the incidence of embolic stroke is lower than that in Western populations, might limit the generalizability of the findings, according to Hu and colleagues. They noted that the DUSK trial is underway in the U.S. to test thrombectomy for medium-vessel strokes.

Imaging criteria for enrollment included less than 50% ischemic involvement of the clinically estimated at-risk territory on noncontrast CT or diffusion MRI or a penumbra-to-core mismatch ratio greater than 1.4 with a volume of at least 10 mL on CT perfusion or MR perfusion imaging. Key exclusion criteria were multiterritory occlusions, intracranial hemorrhage, or contraindications to MRI or CT angiography.

"The imaging criteria that were based on physician judgment will be essential to unpack," the editorialists wrote. "Well-evolved infarcts may be readily recognized in everyday clinical practice but are hard to define precisely. Patients with well-evolved infarcts simply do not benefit, and a small proportion may be harmed with reperfusion therapies."

They pointed to studies planned or under way that should help further refine the procedure and the target population.

Crystal Phend is a contributing editor at MedPage Today. Connect:

Disclosures

The trial was funded by the National Natural Science Foundation of China and the Noncommunicable Chronic Diseases–National Science and Technology Major Project.

Hu disclosed no conflicts of interest.

Hill disclosed relationships with Basking Bioscience, Boehringer Ingelheim, BrainsGate, the Canadian Institutes of Health Research, Medtronic, and NoNO.

Ospel disclosed grant funds paid to her institution from Medtronic.

Primary Source

New England Journal of Medicine

Source Reference: Hu W, et al "Endovascular treatment of medium-vessel-occlusion strokes" N Engl J Med 2026; DOI: 10.1056/NEJMoa2514120.

Secondary Source

New England Journal of Medicine

Source Reference: Ospel JM, Hill MD "Endovascular therapy for medium-vessel occlusion stroke -- narrowing the target population" N Engl J Med 2026; DOI: 10.1056/NEJMe2601852.

Do predictors of motor recovery differ between robotic and conventional post-stroke rehabilitation?

 

You're supposed to solve problems, NOT just predict them you blithering idiots. Hoping comeuppance hits you really hard when you are the 1 in 4 per WHO that has a stroke! 

Why are you incompetently? predicting failure to recover than delivering recovery?

Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem!

Do predictors of motor recovery differ between robotic and conventional post-stroke rehabilitation?

• Silvia Campagnini,
• Piergiuseppe Liuzzi,
• Marco Germanotta,
• Arianna Pavan,
• Alessio Fasano,
• Francesca Cecchi,
• Irene Giovanna Aprile &
• Andrea Mannini 

We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Abstract

Background

While research on robotic rehabilitation has largely focused on evaluating device effectiveness, there remains a clear need to investigate patient characteristics that predict response to robot-assisted therapy. Recent advancements in machine learning (ML) techniques support such investigations by enabling the development of data-driven tools to assist in selecting appropriate rehabilitation treatments. This study aimed to develop two ML models, predicting two motor outcomes each, following either robot-assisted or conventional upper limb rehabilitation in post-stroke patients. It further sought to compare how baseline predictors contributed differently across the two treatment modalities.

Methods

We conducted a retrospective analysis of data from a previous randomized controlled trial evaluating robotic upper limb rehabilitation in post-stroke patients. Four ML algorithms were trained and validated using a nested cross-validation framework, with models developed separately for robotic and conventional treatment subgroups. Baseline predictors were used to estimate two post-treatment motor outcomes: Fugl-Meyer Assessment (FMA) and Action Research Arm Test (ARAT). SHAP analyses were performed to assess the contribution of each predictor to the models.

Results

After data cleaning, 99 patients in the conventional group and 91 in the robotic group were included. Prediction errors for ARAT score after training (expressed in median and absolute error) were 5.0 [6.0] in the robotic group and 3.0 [6.0] in the conventional group. For FMA prediction, results were 5.0 [5.0] and 5.0 [7.0], respectively. Baseline FMA was a strong predictor of ARAT outcomes in both groups. For FMA prediction, the presence of neglect emerged as more influential in the robotic group. Age was a key predictor of both outcomes, but only in the conventional group.

Conclusions

The differing contributions of baseline predictors across treatment types provide clinically meaningful insights and support the development of clinical decision support systems aimed at optimizing rehabilitation strategies based on individual patient characteristics.

Slowing Parkinson’s by Blocking a Key Protein

 Your competent? doctor needs to know about this because of your risk of Parkinsons post stroke. 

Parkinson’s Disease May Have Link to Stroke March 2017 

Slowing Parkinson’s by Blocking a Key Protein

Summary: Researchers identified a promising new target for slowing the progression of Parkinson’s disease (PD). The study demonstrates that a protein called GPNMB (glycoprotein nonmetastatic melanoma B) acts as a catalyst for the spread of toxic alpha-synuclein clumps between neurons.

By using monoclonal antibodies to block this protein, scientists were able to interrupt the cycle of damage in preclinical models, offering a potential path toward the first disease-modifying therapy for PD.

Key Research Findings

• The Alpha-Synuclein Driver: Parkinson’s progresses as abnormal clumps of alpha-synuclein move from affected neurons to healthy ones, leading to cell death and worsening symptoms like tremors.
• The Role of Microglia: The brain’s immune cells, microglia, are a major source of GPNMB. When neurons are injured, microglia increase GPNMB production; enzymes then release the protein, allowing it to move freely and accelerate the spread of pathology.
• A Self-Reinforcing Cycle: The study suggests PD is driven by a feedback loop: alpha-synuclein damages neurons, which triggers the release of GPNMB, which in turn speeds up the spread of alpha-synuclein to more neurons.
• Human Evidence: Analysis of 1,675 brains from the Penn Brain Bank showed that individuals with genetic variants for high GPNMB production had more extensive alpha-synuclein pathology.
• Specificity: Elevated GPNMB levels were specifically linked to Parkinson’s and were not associated with markers for other neurodegenerative conditions like Alzheimer’s disease.
  

Source: University of Pennsylvania

Monoclonal antibodies can block a key immune‑related protein that drives the spread of brain cell damage in Parkinson’s disease (PD). 

This protein, called glycoprotein nonmetastatic melanoma B (GPNMB), might be part of a promising strategy for developing a treatment that slows disease progression at its earliest stages, according to a new study published today in Neuron, from researchers at the Perelman School of Medicine at the University of Pennsylvania.  

Interruption of the self-reinforcing GPNMB cycle could potentially slow or stop the neurodegeneration that follows the spread of alpha-synuclein through the brain. Credit: Neuroscience News“Many patients with Parkinson’s disease are diagnosed in the early stages, when symptoms are relatively mild, but there is currently no treatment that slows the progression,” said lead author, Alice Chen‑Plotkin, MD, Parker Family Professor of Neurology.

“These early results are a promising step towards developing this type of treatment.” 

How Parkinson’s disease spreads through the brain

PD affects more than one million people in the United States, with roughly 90,000 new diagnoses each year. While the exact cause of the disease remains unclear, scientists have long known that PD spreads through the brain in stages. 

This progression is driven by abnormal clumps of a neuronal protein called alpha‑synuclein. These clumps accumulate inside affected neurons, contributing to their dysfunction and death, and are then released and taken up by nearby healthy neurons.

As this pathology moves through different brain regions, patients experience the worsening symptoms that characterize PD, like tremors and difficulty walking or swallowing. 

While there are a number of medications and therapies that can help improve the symptoms of PD—ranging from a drug called levodopa to deep-brain stimulation delivered through an implanted electrode—there is no existing treatment that slows the progression of PD.  

Identifying immune cells as an unexpected therapy  

In earlier work published in 2022, Chen‑Plotkin and colleagues identified GPNMB as a key molecule involved in the neuron‑to‑neuron spread of alpha‑synuclein pathology, making it a compelling therapeutic target. 

In this new study, the researchers discovered that microglia, the brain’s resident immune cells, are a major source of GPNMB related to Parkinson’s disease. When microglia are near injured or dying neurons, they produce increased amounts of GPNMB. Enzymes then separate the protein from the cell surface, releasing part of it to move freely between cells. 

In preclinical experiments using cultured neurons, Chen-Plotkin developed antibodies that block GPNMB prevented the spread of alpha‑synuclein pathology from cell to cell.

“These results suggest Parkinson’s disease may be driven by a self reinforcing cycle—alpha-synuclein accumulates in neurons, damaging the neurons. The injury to the neurons initiates the release of GPNMB, which accelerates the spread of alpha-synuclein, leading to further damage,” Chen‑Plotkin said.

“Interrupting this cycle would hopefully slow, or even stop, the spread of alpha-synuclein through the brain and the neurodegeneration that follows.”  

Charting a potential path toward disease modifying therapy 

To assess the relevance of these findings in people, the team analyzed tissue from 1,675 brains in the Penn Brain Bank. Individuals with genetic variants associated with higher GPNMB production showed more extensive alpha‑synuclein pathology, providing strong human evidence that the protein plays a central role in disease progression. What’s more, elevated levels of GPNMB were not associated with the markers of other neurodegenerative diseases like Alzheimer’s disease. 

“These results are promising for laboratory models and human brain tissue analysis, but we still have a lot of work to do before we can translate this therapy into humans,” said Chen-Plotkin. “That being said, these results are encouraging as we continue to work towards a novel treatment for PD.” Funding: This study was supported by the National Institutes of Health (R37 NS115139, P30 AG010124, U19 AG062418, P01 AG084497), SPARK‑NS, the Parker Family Chair, and the Lipman Family Fund. 

Key Questions Answered:

Q: Why is this different from current Parkinson’s medications?

A: Current treatments, like levodopa, only manage symptoms, they don’t stop the underlying brain damage. This antibody therapy aims to be “disease-modifying,” meaning it could actually slow or stop the physical spread of the disease through the brain.

Q: How do antibodies “block” the damage?

A: The monoclonal antibodies developed by the researchers bind to the GPNMB protein. By latching onto GPNMB, they prevent it from interacting with neurons and spreading the toxic alpha-synuclein “seeds” to healthy cells.

Q: Is this treatment available for patients now?

A: Not yet. While the results in laboratory models and human tissue analysis are highly encouraging, the researchers emphasize that more work is needed before this can be translated into human clinical trials.Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this Parkinson’s disease research news

Author: Eric Horvath
Source: University of Pennsylvania
Contact: Eric Horvath – University of Pennsylvania
Image: The image is credited to Neuroscience NewsOriginal Research: Open access.

“Secreted GPNMB enhances uptake of fibrillar alpha-synuclein in a non-cell-autonomous process that can be blocked by anti-GPNMB antibodies” by Marc Carceles-Cordon, Eliza M. Brody, Masen L. Boucher, Michael D. Gallagher, Robert T. Skrinak, Travis L. Unger, Cooper K. Penner, Adama J. Berndt, Sromona Das, Katie Lam, Rudolf Jaenisch, Vivianna Van Deerlin, Edward B. Lee, Kurt Brunden, Kelvin C. Luk, and Alice S. Chen-Plotkin. Neuron
DOI:10.1016/j.neuron.2026.04.033

Rewiring Your Brain: The Science of Neuroplasticity and Practical Applications

 

Nothing here will guarantee survivor recovery, right?

You haven't identified the EXACT signals between neurons that tell one neuron to drop their use and take on a neighboring neuron's use! That could then make neuroplasticity repeatable on demand.  Until that occurs ALL OF THIS SUPPOSED NEUROPLASTICITY RESEARCH IS ALMOST COMPLETELY FUCKING USELESS! 

Rewiring Your Brain: The Science of Neuroplasticity and Practical Applications

See article at link.

What Brain Imaging Reveals About The Effects Of Light Alcohol Use by mindbodygreen

 But totally ignoring the social connections part which is going to prevent dementia. 

My social connections are Sunday night jazz; Tuesday night jazz; Thursday night trivia. All at bars so some alcohol is involved and since preventing dementia is vastly more important for me that anything negative here. 

If you're worried about lower blood flow there are solutions which your doctor won't know about.

• cerebral blood flow (47 posts to July 2016)
• cortical oxygenation (1 post to November 2020)
• oxygen delivery (20 posts to January 2020)

chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers. August 2017

But this: 

Pot Smoking Baby Boomers Are On The Rise, Why Are Scientists So Happy For Them? Hint: Benefits For The Aging Brain 

The latest here:

What Brain Imaging Reveals About The Effects Of Light Alcohol Use

For decades, there's been a rather surprising amount of positive research on alcohol. A glass of wine was framed as something beneficial. Red wine was supposed to be good for your heart, thanks to polyphenols and so on. Somewhere along the way, a daily drink started to feel not just normal, but harmless.

That perspective has been shifting. Over the past several years, research has taken a closer look at how alcohol actually interacts with the body, linking even moderate intake to higher cancer risk, changes in metabolic health, and more fragmented sleep than people tend to realize. The picture has become less about isolated benefits and more about cumulative effects.

Now, a new study¹ adds another layer to that conversation, suggesting alcohol may be influencing brain health in ways that are hard to ignore.

Alcohol’s impact on brain blood flow

To get a clearer picture, researchers focused on a group of healthy adults between the ages of 22 and 70 who all drank within what’s currently considered “low-risk” limits. None had a history of alcohol use disorder, and their intake stayed within standard guidelines, up to about one drink per day for women and two for men.

Instead of grouping people into categories like “light” or “moderate” drinkers, the researchers treated alcohol intake as a continuous variable. This captures more nuance. Someone having three drinks per week and someone having ten are both technically “moderate,” but their exposure isn’t the same.

Participants underwent MRI scans that measured two key markers of brain health. The first was cerebral blood flow, often referred to as perfusion. This reflects how efficiently blood delivers oxygen and nutrients to brain tissue. The second was cortical thickness, which looks at the structure of the brain’s outer layer, an area tied to functions like memory, language, and decision-making.

They also looked at lifetime alcohol intake, not just recent habits, to understand how long-term patterns might interact with age.

RELATED READ: These Are The 16 Best Supplements For Memory & Cognition

The brain changes linked to moderate drinking

The most consistent pattern was that higher alcohol intake, even within “low-risk” ranges, was associated with lower brain blood flow.

This showed up across multiple regions, including areas involved in thinking, memory, and attention. Blood flow is one of those markers that doesn’t get much attention day to day, but it plays a central role in how well the brain functions. Less efficient circulation means fewer resources reaching the cells that rely on them.

The second layer of the finding adds more context. Age amplified the effect. Older adults who had higher lifetime alcohol intake showed more widespread reductions in blood flow, along with thinner cortical regions. This points to a gradual shift in both how the brain is functioning and how it’s structured.

Researchers suggest that mechanisms like oxidative stress, a process that can damage cells over time, may help explain how repeated exposure adds up.

Rethinking “moderation”

This study doesn’t ask you to swear off a glass of wine with friends or skip the toast at a celebration. But it does shift the perspective. What feels moderate on a random Tuesday night can look different when you stack those nights over months and years. The more useful question becomes less about whether you’re within a daily guideline and more about your overall pattern. How often is alcohol showing up, and is it adding something meaningful when it does?

For some people, that shift is small. Maybe you space out drinking days a bit more or save it for moments that actually feel worth it. Maybe you mix in alcohol-free options during the week. The point isn’t restriction. It’s awareness. When you start paying attention to frequency instead of just quantity, your habits tend to shift.

Plus, these findings highlight that the effect of alcohol may not just be about sleep or hydration. It could reflect changes in how the brain is being supported at a more fundamental level.

RELATED READ: How To Cut Back On Alcohol Without Sacrificing Your Social Life

The takeaway

This study emphasizes that consistent alcohol intake (even if it's considered moderate or low-risk) can still have negative cognitive effects.

Your brain is always responding to what you give it, from the food you eat to how you sleep to how often certain exposures show up in your routine. Blood flow and brain structure aren’t static. They reflect patterns, repeated over time, often in ways you don’t notice in the moment.

Both Caffeinated & Decaf Coffee Improved Mood, Memory, & Stress by mindbodygreen

 Will your competent? doctor ever get a 24 hour coffee station installed in the stroke department and accessible to survivors? 

And your doctor wasn't familiar with this early research? A fireable offense!

How Coffee May Protect Brain Health: A New Study Suggests The Benefits Aren't Just From Caffeine December 2018 

The latest here: 

Both Caffeinated & Decaf Coffee Improved Mood, Memory, & Stress

Most coffee drinkers have made their peace with caffeine dependency. You know the science on longevity, the data on Parkinson's and Alzheimer's disease risk reduction, the cardiovascular benefits. You've already defended your habit at dinner parties. 

Testing coffee’s effects on mood, cognition, & the gut

To get a clearer answer, researchers designed a randomized crossover trial, which is a way of testing the same people under different conditions so each person essentially acts as their own control. It’s one of the more reliable ways to tease apart subtle effects like mood or cognition.

They worked with healthy adults and tracked what happened across three phases: a period of regular coffee consumption, a washout phase where participants stopped drinking coffee altogether, and then a reintroduction phase where they were given either caffeinated or decaffeinated coffee.

Throughout the study, they measured more than just how people felt. Participants completed cognitive tasks that tested things like attention, memory, and mental flexibility. They also reported on mood, stress, and emotional reactivity. At the same time, researchers analyzed the gut microbiome using advanced sequencing techniques and tracked metabolites, which are small molecules produced during digestion that can influence brain function.

The goal wasn’t just to see if coffee “worked.” It was to understand how it might be working, especially through the gut-brain axis, the communication network that links your digestive system and your brain.

RELATED READ: This Type Of Coffee Bean Delivers Superior Flavor & Health Benefits

Both regular & decaf coffee shift mood, stress, & brain function

When participants reintroduced coffee after the washout period, both caffeinated and decaffeinated versions led to improvements in mood. People reported lower stress, fewer symptoms of depression, and less impulsivity. That alone suggests caffeine isn’t the whole story.

Caffeinated coffee did have some unique effects. It was more strongly linked to reduced anxiety and better attention and vigilance, which aligns with what we already know about caffeine’s role as a stimulant. But decaf held its own in other areas. It was associated with better sleep, improved memory and learning, and even higher levels of physical activity.

So instead of one single effect, coffee seems to be doing multiple things at once, depending on what’s in it and how your body responds.

Coffee & gut health

Then there’s the gut piece, which adds another layer. Coffee intake changed the composition of the gut microbiome, increasing certain bacterial species and shifting the production of metabolites linked to brain health and inflammation. Some of these compounds are involved in regulating mood and cognitive function, which helps explain why the effects showed up even without caffeine.

This is because of the gut-brain axis. The microbes in your gut help produce and regulate neurotransmitters, immune signals, and metabolic compounds that your brain relies on. When coffee changes that environment, it can indirectly shape how you feel and think.

RELATED READ: Coffee Always Made Me Anxious & Jittery — Until I Tried This Type

The takeaway

This research broadens the definition of what coffee is doing. It’s not just a stimulant. It’s a complex mix of compounds, including polyphenols, which are plant-based molecules that can act like fuel for beneficial gut bacteria. Those downstream effects may be part of why coffee has been consistently linked to better long-term brain and metabolic health.

It also takes some of the pressure off caffeine itself. If you’re sensitive to caffeine or trying to cut back, decaf isn’t a “downgrade” in the way people often assume. You’re still getting many of the same gut and mood-related benefits, just without the stimulant effect.

Arterial widening emerges as key driver of small vessel stroke

 How will this change your competent? doctors' protocols on treating stroke? Oh, nothing will happen because there are NO protocols, since your doctor is guessing every step of the way, Hope the guesses are correct because your doctor gets paid regardless!

Arterial widening emerges as key driver of small vessel stroke

A prospective study of 229 patients with lacunar or mild non-lacunar stroke found that large-artery stenosis was not associated with cerebral small-vessel disease (cSVD) or incident infarcts, whereas arterial widening and basilar artery dolichoectasia were strongly linked to lacunar stroke, higher cSVD burden, and progression of brain lesions over 1 year.

The findings, published in Circulation, challenge traditional atherosclerotic paradigms and suggest that intrinsic microvascular pathology plays a central role in cSVD, underscoring the need for mechanism-specific diagnostic and therapeutic strategies in stroke care.

“This study provides strong evidence that lacunar stroke is not caused by fatty blockage of larger arteries, but by disease of the small vessels within the brain itself,” said Joanna Wardlaw, University of Edinburgh’s Institute for Neuroscience and Cardiovascular Disease, Edinburgh, United Kingdom. “Recognising this distinction is crucial, because it explains why conventional treatments like antiplatelet drugs are not as effective for this type of stroke and highlights the urgent need to develop new therapies that target the underlying microvascular damage.”

For the study, the researchers followed 229 patients (mean age, 65.9 years; 57% with lacunar stroke) with serial clinical and MRI assessments over 1 year to evaluate the impact of large-artery stenosis and arterial widening on stroke subtype and cSVD. Large-artery stenosis (≥50%) was present in 20.5% of patients and basilar artery dolichoectasia in 15.7%, with multivariable analyses adjusting for demographic and vascular risk factors.

Results showed that large-artery stenosis was not associated with cSVD markers or incident infarcts and was instead linked to lower odds of lacunar versus non-lacunar stroke (odds ratio [OR] = 0.49), whereas basilar artery dolichoectasia was strongly associated with lacunar stroke (OR = 4.67), higher small-vessel disease burden (OR = 2.57), increased risk of incident infarcts (OR = 2.29; 75% subcortical), and greater progression of white matter hyperintensities over 1 year (β 0.15 per log10 volume increase).

The researchers said that future treatments should target the underlying small vessel damage. Trials such as LACI-3 are now testing whether existing drugs, including cilostazol and isosorbide mononitrate, can protect the brain, reduce further strokes, and help prevent problems with memory, mobility, and dementia after lacunar stroke.

Reference: https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.126.079493

SOURCE: University of Edinburgh

Researchers develop ‘breakthrough’ nasay[sic] spray for stroke

 Ask your competent? doctor EXACTLY what this contains and the method of action.  This said absolutely nothing useful!

So quiz your doctor on all this other nasal research! NO knowledge is grounds for termination!

•  nasal delivery (10 posts to December 2017)
• intranasal delivery (8 posts to June 2022)
• dihydroergotamine nasal powder (2 posts to May 2025)
• /,13 nasal delivery options (6 posts to April 2014)

Researchers develop ‘breakthrough’ nasay[sic] spray for stroke

A nasal spray designed to protect brain cells after stroke could offer a new prehospital emergency option, researchers say.

Researchers say the approach could help slow brain cell death and buy time for clot-removing or clot-busting treatment.

The spray has been developed by scientists at the University of Hong Kong, who describe it as the world’s first nasal spray designed to protect brain cells immediately after stroke.

Stroke is a leading cause of death and disability, with researchers citing an annual global healthcare burden of more than US$890bn.

Current stroke treatment usually begins after hospital admission and can involve clot-breaking drugs or reperfusion therapies, which aim to restore blood flow through arteries going to the brain.

The window for effective treatment is narrow, meaning more than 85 per cent of patients are unable to receive treatment quickly enough.

Researchers said many brain-targeting drugs also fail in trials because they cannot cross the blood-brain barrier.

The blood-brain barrier is the brain’s protective filter. It helps keep harmful substances out of the brain, but can also stop medicines reaching the area where they are needed.

Aviva Chow Shing-fung, from the University of Hong Kong, said: “The failure rate of drug candidates targeting the central nervous system in clinical trials exceeds 90 per cent, largely because these drugs cannot cross the blood-brain barrier, and thus fail to reach the brain to exert their therapeutic effects.”

To address this, the team developed a “Nanopowder” nasal spray containing brain-protective drugs(What are they?) in ultra-small inhalable powders.

The spray is inhaled into the nasal cavity, where it settles in the target area and separates into nanoparticles.

These tiny particles then travel through the nose-to-brain pathway, bypassing the blood-brain barrier.

Researchers said this could deliver the drug directly to the brain and provide early protection while a patient is being taken to hospital.

They reported that giving the nasal spray within 30 minutes of stroke onset reduced brain tissue death by more than 80 per cent in their tests.

They also said the spray protected neurological and body movement functions, reduced inflammation, helped prevent cell death and supported the integrity of the blood-brain barrier.

Neurological functions are abilities controlled by the brain and nervous system, such as movement, speech, memory and coordination.

Shao Zitong, a postdoctoral fellow at the University of Hong Kong, said: “After a stroke, every second matters.

“Even an additional 10 minutes of brain protection might determine whether a patient can walk or speak in the future.

“The key breakthrough of this technology lies in shifting stroke treatment from the ‘in-hospital’ setting to the ‘prehospital’ stage, enabling neuroprotection rather than merely clot dissolution or thrombectomy.”