3D Exoskeleton Therapy Boosts Upper Limb Outcomes After Subacute Stroke

 'Boosts' is NOT GOOD ENOUGH! What will it take to get to 100% recovery? The only goal in stroke! Send these researchers back to the drawing board. 

3D Exoskeleton Therapy Boosts Upper Limb Outcomes After Subacute Stroke

Upper limb robot-assisted therapy using a 3-dimensional exoskeleton significantly improves motor recovery in patients with moderate-to-severe subacute stroke.

Upper limb robot-assisted therapy (UL-RAT) with a 3-dimensional (3D) exoskeleton significantly improves upper limb motor recovery when administered within the first month after a stroke, according to study findings published in Stroke.The multicenter randomized controlled trial evaluated the efficacy of RAT using a 3D exoskeleton to improve upper limb motor recovery in inpatients with subacute stroke and moderate-to-severe arm deficits.

Inpatients were enrolled from 8 stroke neurorehabilitation units between December 2020 and March 2024. The participants were aged 18 to 85 years and had a first-ever ischemic stroke confirmed with brain imaging. They were assigned to the robotic group, receiving UL-RAT, or the control group, which received conventional upper limb rehabilitation.

The patients were evaluated at baseline, end of treatment, and at 6 months after stroke onset. The primary outcome was the motor component of the Fugl-Meyer Assessment for Upper Limb (FM-UL), with a minimal clinically important difference (MCID) of 10.

 

These findings underscore the importance of early intensive intervention in the subacute phase and support the integration of exoskeleton-assisted therapy into rehabilitation programs…

A total of 94 patients with subacute stroke were enrolled, and 82 completed the treatment. The robotic group had 38 participants (mean age, 62 years; 31% women), and the control group had 44 participants (mean age, 63 years; 36% women). At 6 months, 49 participants were available for reassessment. A significant difference was observed in the FM-UL motor part, with higher values in the robotic group at the end of treatment (P <.001), in the between-group analysis.

Sensory score was significantly increased at the end of treatment compared with baseline in the robotic and control groups (P <.001). The joint passive range of motion did not significantly vary in the robotic group (P =.888), although it did in the control group (P =.005).

The proportion of patients who overcame the MCID of the FM score was 68.4% in the robotic group, which was more than double that occurring in the control group (31.8%), and this difference was statistically significant (P <.001). The relevant odds ratio was 4.64 (95% CI, 1.83-11.8).The interaction between time onset (≤30 and >30 days) and the participants’ severity in the robotic group compared with the control group was evaluated in a Kruskal-Wallis analysis, which did not find any statistically significant differences at baseline (P =.338) among the groups. Significant differences were found at the end of treatment (P =.008).

Limitations of the study include a relatively high dropout rate, especially at 6 months (52%), and baseline imbalances in the groups may have affected the results.

“These findings underscore the importance of early intensive intervention in the subacute phase and support the integration of exoskeleton-assisted therapy into rehabilitation programs, particularly for individuals with moderate-to-severe impairments,” the study authors concluded.

St. Vincent’s Joins the Nation’s Top Hospitals with Comprehensive Stroke Certification

 

 I wouldn't go there for stroke; they refer to 'care; NOT RECOVERY! Survivors want 100% recovery; this center does nothing of the sort! YOU are going to have to scream at them for not showing these three results:

There is no quality here if you don't measure the right things.

1. tPA full recovery? Better than 12%?
2. 30 day deaths? Better than competitors?
3. rehab full recovery? Better than 10%?

 

You'll want to know results so call that hospital president(whomever that is) RESULTS are; tPA efficacy, 30 day deaths, 100% recovery. Because there is no point in going to that hospital if they are not willing to publish results.

St. Vincent’s Joins the Nation’s Top Hospitals with Comprehensive Stroke Certification

 St. Vincent’s Medical Center has earned The Joint Commission’s Gold Seal of Approval® and the American Heart Association/American Stroke Association’s Heart-Check mark for Comprehensive Stroke Center Certification. St. Vincent’s underwent a rigorous, onsite review. During the visit, a team of Joint Commission reviewers evaluated compliance with program standards. The Joint Commission’s standards are developed in consultation with health care experts and providers, measurement experts and patients. They are informed by scientific literature and expert consensus to help health care organizations measure, assess and improve performance. “Comprehensive Stroke Center Certification recognizes healthcare organizations committed to striving for excellence and fostering continuous improvement in patient safety and quality of care(NOT RECOVERY!),” says Ken Grubbs, DNP, MBA, RN, executive vice president of Accreditation and Certification Operations and chief nursing officer, The Joint Commission. “We commend St. Vincent’s Medical Center for using The Joint Commission certification process to reduce variation in clinical processes and to strengthen its clinical program to drive safer, higher quality and more compassionate care(NOT RECOVERY!) for individuals served.” “We congratulate St. Vincent’s Medical Center for this outstanding achievement,” says Nancy Brown, chief executive officer, the American Stroke Association. “This certification reflects its commitment to providing the highest quality ofcare(NOT RECOVERY!) for stroke patients.” “We are proud to achieve this designation, which reflects the dedication of our multidisciplinary stroke team and our commitment to providing the highest level of care(NOT RECOVERY!) for our community,” said Stroke Director Jeremy Wells, MD, at St. Vincent’s Medical Center. “This certification affirms our ability to deliver world-class, rapid, evidence-based treatment for the most complex stroke patients.” To prepare for the certification, St. Vincent’s Medical Center strengthened its stroke program by enhancing standardized protocols, expanding advanced neuroimaging, and improving coordination across care(NOT RECOVERY!) teams. The hospital also enhanced staff training to support rapid stroke recognition and treatment, while ensuring 24/7 access to specialized services, including neurosurgery and interventional care(NOT RECOVERY!)—delivering timely, comprehensive treatment when every second counts. Comprehensive Stroke Center Certification is the highest level of stroke certification awarded by The Joint Commission and recognizes organizations with the infrastructure, staff, and training to receive and treat the most complex stroke cases. This designation positions St. Vincent’s Medical Center as a regional leader in stroke care(NOT RECOVERY!), improving access to life-saving treatment for patients across the community and statewide. This achievement is yet another example of how Hartford HealthCare’s acquisition of St. Vincent’s Medical Center has expanded access to high-quality, advanced care(NOT RECOVERY!) close to home for the community.

Malpractice Risks in Neurology: Lessons From a $4.5 Million Stroke Verdict

 Get the neurologist, CT and MRI scans out of the picture.

Why would you want to do slow CT/MRI scans when much faster methods are available? You do know; 'Time is Brain!'

 The answers are already out there, AND YOU'RE SO FUCKING INCOMPETENT YOU DON'T KNOW THAT!

These people must not have any working brains at all!

Like maybe these fast diagnosis options?

Hats off to Helmet of Hope - stroke diagnosis in 30 seconds; February 2017 

Smart Brain-Wave Cap Recognises Stroke Before the Patient Reaches the Hospital

 October 2023

And then this to rule out a bleeder.

New Device Quickly Assesses Brain Bleeding in Head Injuries - 5-10 minutes April 2017 

The latest here: They deserved to lose the suit.

Malpractice Risks in Neurology: Lessons From a $4.5 Million Stroke Verdict

Author’s Note: This periodic feature will focus on legal issues faced by neurologists and other health care practitioners. It will use case studies to illustrate topics such as the elements of medical malpractice, HIPAA, informed consent, delayed diagnosis, and other issues. We hope you will find it informative and useful in your practice.Medical malpractice claims in neurology often arise from diagnostic errors, particularly missed or delayed identification of conditions such as stroke, intracranial aneurysm, or subdural hematoma, which can result in severe patient harm. As with many medical specialties, communication breakdowns and inadequate documentation are also common contributing factors. The case discussed here highlights several of these issues, including delayed diagnosis as well as deficiencies in communication and documentation.

 

During an acute stroke, every second counts.

Facts of the Case

Mr B was a 57-year-old White man with no significant medical history. He worked as a master electrician and owned his own company. One morning, he woke up with a headache, noticed a slight weakness in his left arm, and his speech was a bit slurred. While speaking to him, his girlfriend noticed that he seemed confused and had a tremor in his left arm. Concerned, his girlfriend convinced him to go to the emergency department (ED) of the local hospital to get examined.

In the ED, Mr B was seen by Dr E, the attending emergency physician, who recognized that the patient’s symptoms were consistent with a stroke. Dr E ordered a non-contrast head CT at around noon, which showed no acute abnormalities. He assigned the patient a National Institutes of Health (NIH) Stroke Scale score of 2.

This 'Too Good to Treat' crapola caused the whole problem, Debunked over a decade ago:

VIDEO: "Too good to treat" stroke patients may benefit from tPA

 February 2015

Dr N was the on-call neurologist at the hospital that day. Dr E contacted the neurologist after examining the patient to discuss whether to administer tissue plasminogen activator (tPA). After the 2 physicians spoke, it was decided that Mr B was outside the time frame for tPA, and that he was not a candidate for intervention at that point due to his symptoms, duration of onset, and low NIH Stroke Scale score. Instead, Dr E started the patient on aspirin, admitted him for observation, and asked Dr N to evaluate the patient.

Dr N eventually arrived to evaluate the patient several hours after admission. Dr N noted acute gait instability, ataxia, headache, right mouth droop, impaired repetition, and a left arm tremor. The physician ordered a magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) to assess for infarct or vascular occlusion; however, he failed to write ‘stat’ on the order to note the urgency and instead gave it routine priority. Dr N was also unaware that the hospital’s MRI/MRA machine was currently not working and the hospital was waiting for a service call. Hours passed without the tests being performed. In all that time, Dr N did not follow up to find out why the MRI/MRA had not been completed. The rest of the day and night passed without Mr B receiving the MRI/MRA.

The next morning, approximately 24 hours after the onset of symptoms, Mr B was found unresponsive, with labored breathing and significant neurologic decline. His NIH Stroke Scale score had risen to 13. A repeat CT revealed a basilar artery thrombus. Mr B was transferred to another hospital, where an MRI revealed acute infarcts in both cerebellar hemispheres, the left mesial temporal lobe, bilateral thalami, and thrombi in the basilar and left posterior cerebral arteries. Although he underwent a mechanical thrombectomy at the second hospital, the intervention came too late to reverse the damage. As a result, the patient suffered “locked-in syndrome,” where he was aware but unable to speak or move for 5 days before he finally died from the damage caused by the severe stroke.

The Trial

After Mr B’s death, his family consulted with a plaintiff’s attorney, who reviewed the medical records and agreed to take the case. The attorney filed a lawsuit against Dr N, alleging that his failure to order the imaging on a ‘stat’ basis, failure to follow up on the order, and failure to send the patient to another hospital with a working MRI machine resulted in Mr B’s severe and life-ending stroke.

Dr N was assigned an attorney from his malpractice insurance company. After several years, the case went to trial. At trial, the defense attorney argued that the severe stroke that occurred the morning after Mr B was admitted was an entirely new and unpredictable event. The plaintiff’s attorney argued that the original stroke did exactly what it was at risk of doing: causing significant harm. The plaintiff’s attorney described the horror of “locked-in syndrome” and elicited testimony from the defense’s expert that he had previously described it as “a terrifying experience for the patient” and “a fate worse than death.”

The testimony lasted for 2 weeks, and the jury deliberated for 5 hours before returning a verdict for the plaintiff and awarding his family over $4.5 million.

Protecting Yourself

We all know that time is of the essence when diagnosing a stroke, which makes it all the more shocking that Dr N did not order the test ‘stat’. Worse still, when the test wasn’t done in the ensuing hours, Dr N did not follow up to find out why. Had the physician known that the MRI machine was down, he could have had the patient transferred to another hospital where the tests could have been conducted. With the information gained from an MRI/MRA, Mr B could have been treated.

The jury’s high monetary award indicated that they were sympathetic to the patient, were swayed by the expert’s description of “locked-in syndrome” as a “fate worse than death,” and found fault with the neurologist for failing to order tests with the proper urgency and to follow up on his own orders.

During an acute stroke, every second counts. Quick diagnosis and treatment are vital to a good outcome. Rapid intervention is essential, and tests and imaging should always be ordered on a stat basis to protect your patient… and yourself.

Psychological Distress Linked to Increased Risk for Dementia

 All stroke patients are under massive distress because your incompetent? doctor doesn't have 100% RECOVERY PROTOCOLS. Your doctor has known since medical school that stroke recovery is a complete shitshow and done nothing to fix that!

Psychological Distress Linked to Increased Risk for Dementia

Psychological distress in midlife was associated with an increased risk for dementia, highlighting its value as a clinical marker for identifying high-risk groups.

Psychological distress is associated with poorer later-life cognitive performance and increased risk for dementia, though not with cognitive decline over time, according to results of a study published in Alzheimer’s & Dementia.

In a multi-cohort study, researchers examined associations between psychological distress and subsequent cognitive outcomes and dementia risk. They pooled data from 5 longitudinal studies: the Caerphilly Prospective Study (CAPS), English Longitudinal Study of Ageing (ELSA), National Child Development Study (NCDS), National Survey of Health and Development (NSHD), and Whitehall II (WHII).

The analysis included 24,564 participants. Across cohorts, baseline sample sizes ranged from 1180 to 9022 participants. Cohorts comprised 44.7% to 100% men, with mean baseline ages ranging from 23 to 64.1 years, and 3.3% to 25.5% of participants reporting long-term health conditions. Between 7.6% and 27.7% of participants reported clinically significant psychological distress at baseline.

 

Findings highlight the relevance of psychological distress in later cognitive outcomes, with potential future implications for dementia prevention and identifying high-risk groups.

Greater baseline psychological distress was associated with worse subsequent fluid cognitive performance at a mean age of 62 to 72 years (adjusted b, -0.03; 95% CI, -0.06 to -0.01; I2=70%). Similar associations were observed for clinically significant distress (b, -0.1; 95% CI, -0.1 to 0.0; I2=62%), intermittent distress (b, -0.1; 95% CI, -0.2 to -0.02; I2=83%), and persistent distress (b, -0.1; 95% CI, -0.1 to -0.1; I2=0%).

In analyses of cognitive trajectories, psychological distress was not associated with overall cognitive decline in pooled models. Although cohort-specific analyses showed decline in ELSA (b, -0.04; 95% CI, -0.04 to -0.04), NSHD (b, -0.01; 95% CI, -0.01 to 0.004), and WHII (b, -0.01; 95% CI, -0.01 to 0.01), these findings were not consistent across studies.

Baseline psychological distress was also associated with increased odds of dementia at follow-up (adjusted odds ratio [aOR], 1.1; 95% CI, 1.0-1.2; I2=0%). Increased dementia risk was observed for clinically significant distress (aOR, 1.3; 95% CI, 1.1-1.5; I2=0%), intermittent distress (odds ratio [OR], 1.3; 95% CI, 1.0-1.7; I2=40%), and persistent distress (OR, 1.4; 95% CI, 1.0-2.0; I2=44%).

Age-stratified analyses showed that psychological distress was associated with dementia when assessed at ages 55 to 64 years (OR, 1.3; 95% CI, 1.2-1.4; I2=0%) and 65 to 75 years (OR, 1.3; 95% CI, 1.2-1.4; I2=14%), but not at ages 45 to 54 years (OR, 1.1; 95% CI, 0.9-1.3; I2=34%).Study limitations included heterogeneity across cohorts in population characteristics, measurement of psychological distress, and outcome assessment.

The researchers concluded, “Findings highlight the relevance of psychological distress in later cognitive outcomes, with potential future implications for dementia prevention and identifying high-risk groups.”

Socioeconomic Vulnerability Linked to Loss to Follow-Up After Acute Stroke

 You wouldn't need to worry about this loss to follow-up if you delivered EXACT 100% RECOVERY PROTOCOLS upon discharge, because you know they would be fully recovered! Can't you people think at all?

Socioeconomic Vulnerability Linked to Loss Self-pay insurance and high functional impairment at discharge are significantly associated with increased odds of loss to follow-up within 12 months of acute stroke.

 Clinical and socioeconomic factors, including functional disability and insurance status, are associated with loss to follow-up after hospitalization for acute stroke, according to a study published in Journal of Clinical Neuroscience. Patients discharged after hospitalization for acute stroke require multidisciplinary care to reduce risk for functional decline, stroke recurrence, and death. However, many health systems lack the infrastructure to support long-term care coordination following stroke. Researchers conducted a retrospective cohort analysis of patients admitted with acute stroke to Mount Sinai Hospital in New York City between January 1, 2016, and December 31, 2020. The primary outcome was loss to follow-up (LTFU) within 12 months of discharge, defined as the absence of any post-discharge encounters within the Mount Sinai Health System. Variable selection was performed using least absolute shrinkage and selection operator (LASSO) regression, followed by multivariable logistic regression to evaluate associations with LTFU.[T]his study demonstrated that patients with post-stroke LTFU were more likely to have increased medical complexity, markers of social vulnerability, and high functional impairment that may have prevented them from seeking follow-up care. Among 2597 patients included in the analysis, the mean (SD) age was 65.5 (15.6) years, and 50.8% were women. A total of 33.8% of patients were LTFU within 12 months of discharge. Compared with patients who maintained follow-up, patients who were LTFU were more likely to be men (52.9% vs 47.4%; P =.009), have intracerebral hemorrhage (12.1% vs 8.9%; P =.005), undergo endovascular treatment (12.8% vs 10.0%; P =.030), be transferred from another hospital (48.0% vs 40.7%; P =.003), and be discharged to an acute care facility (4.0% vs 0.87%; P <.001). They also had greater functional impairment, including modified Rankin Scale (mRS) scores of 4 to 5 at discharge (35.2% vs 30.2%; P =.006) and higher discharge National Institutes of Health Stroke Scale (NIHSS) scores (6.1 vs 4.9; P <.001).

In multivariable analysis, self-pay insurance (adjusted odds ratio [aOR], 3.8; 95% CI, 1.3–11.4; P =.016), discharge to an acute care facility (aOR, 5.3; 95% CI, 1.5–18.4; P =.009), and discharge mRS score of 5 (aOR, 2.4; 95% CI, 1.0–5.7; P =.045) were associated with increased odds of LTFU.

In contrast, Medicare coverage (aOR, 0.60; 95% CI, 0.40–0.92; P =.018), discharge to inpatient rehabilitation (aOR, 0.54; 95% CI, 0.34–0.86; P =.009), family history of stroke (aOR, 0.37; 95% CI, 0.18–0.76; P =.007), obesity (aOR, 0.40; 95% CI, 0.19–0.81; P =.012), renal insufficiency (aOR, 0.43; 95% CI, 0.23–0.81; P =.009), and depression (aOR, 0.27; 95% CI, 0.11–0.64; P =.003) were associated with decreased odds of LTFU, potentially reflecting greater baseline engagement with the healthcare system.

 Study limitations include the single-center retrospective design, limited capture of social determinants of health, inability to account for follow-up outside the health system, and lack of post-discharge mortality data. “[T]his study demonstrated that patients with post-stroke LTFU were more likely to have increased medical complexity, markers of social vulnerability, and high functional impairment that may have prevented them from seeking follow-up care,” the study authors concluded.  Disclosures: Some study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of disclosures. References:

Kummer BR, Hwang SA, Agarwal P, et al. Exploring key risk factors for loss to follow-up after hospitalization for acute stroke. J Clin Neurosci. Published online February 26, 2026. doi:10.1016/j.jocn.2026.111951

Treating Hearing Loss Could Halt Dementia

Let's see how long your competent? doctor has known about this and created a protocol for testing and implementation. OH NO, NOTHING EXISTS BECAUSE INCOMPETENCE! And yet your doctor still gets paid.

• hearing loss (19 posts to February 2013) Impressive incompetence there; 13 plus years!

 

Treating Hearing Loss Could Halt Dementia

Summary: Can a simple ear surgery protect your memory? A major new study suggests the answer is yes.

By analyzing data from over 363,000 participants in the NIH’s All of Us Research Program, researchers discovered that two treatable middle ear conditions, eardrum perforations and cholesteatoma (abnormal skin growth), are linked to nearly double the odds of developing dementia. Crucially, the study found that when these conditions were treated with surgery or hearing aids, the elevated dementia risk significantly decreased or disappeared entirely.

Key Findings

• The Risk Factor: Participants with a perforated eardrum had twice the odds of dementia, while those with cholesteatoma had nearly double the risk compared to those with healthy hearing.
• The “Cure” for Cognitive Risk: For those with cholesteatoma, surgical treatment made the association with dementia nonsignificant, effectively “resetting” the risk profile to that of a healthy individual.
• Hearing Aids as a Shield: Using hearing aids also reduced the dementia link for both conditions, reinforcing the theory that keeping the brain “plugged in” to sound is vital for cognitive health.
• A Targeted Exception: Otosclerosis (a bone-related middle ear condition) was not significantly linked to dementia in this specific study, suggesting that certain types of hearing loss may impact the brain differently.

Source: AAO

A new study published in Otolaryngology–Head and Neck Surgery, the official peer-reviewed publication of the American Academy of Otolaryngology–Head and Neck Surgery Foundation (AAO-HNSF), finds that two common and treatable causes of conductive hearing loss—eardrum perforations and cholesteatoma, a type of abnormal skin growth in the middle ear—are associated with higher odds of dementia.

Notably, the study also found that treatment, whether through surgery or hearing aids, was associated with a reduction in that elevated risk.

The findings, first presented at the AAO-HNSF 2025 Annual Meeting & OTO EXPO in Indianapolis, Indiana, add to a growing body of evidence linking hearing loss to cognitive decline and raise an important question: if the underlying cause of hearing loss is treatable, could treating it help protect the brain?

“We have known for some time that untreated hearing loss is related to worse cognition in adults. This study shows that specific forms of surgically addressable hearing loss are also adversely related to cognition.

“But what is most exciting is that treatment with routine surgery may improve both the hearing and possibly reduce the risk of dementia,” said Justin S. Golub, MD, MS, corresponding author on the paper from the Department of Otolaryngology–Head and Neck Surgery, Columbia University Vagelos College of Physicians and Surgeons, NewYork-Presbyterian/Columbia University Irving Medical Center.

Researchers at Columbia University and the University of Utah analyzed data from more than 363,000 participants in the All of Us Research Program, a large and diverse national health dataset sponsored by the National Institutes of Health.

They found that participants with eardrum perforations had more than twice the odds of dementia compared to those without, and those with cholesteatoma had nearly twice the odds. Otosclerosis, a condition affecting the bones of the middle ear, was not significantly associated with dementia in this study.

Importantly, when surgical treatment was accounted for in the analysis, the association between cholesteatoma and dementia became nonsignificant. Treatment with hearing aids also reduced the association for both conditions, suggesting that restoring hearing, whether through surgery or devices, may play a meaningful role in lowering dementia risk.

Key Questions Answered:

Q: How can a hole in my eardrum possibly affect my brain?

A: It’s all about “cognitive load.” When you have conductive hearing loss, your brain has to work much harder to decode sound. This extra effort “steals” resources from other functions like memory. Additionally, social isolation caused by poor hearing can lead to brain atrophy.

Q: If I get surgery to fix my hearing, is the dementia risk gone?

A: The study found that for cholesteatoma, surgery made the dementia risk “nonsignificant.” While it’s not a 100% guarantee, restoring the physical pathway for sound appears to be one of the most effective ways to lower the biological risk associated with hearing loss.

Q: What if I have hearing loss but don’t want surgery?

A: Good news: the study found that hearing aids were also associated with a reduction in dementia risk. The key is simply restoring the flow of auditory information to the brain, whether through a device or a surgical fix.

Editorial Notes:

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

About this dementia and auditory neuroscience research news

Author: Tina Maggio
Source: AAO
Contact: Tina Maggio – AAO
Image: The image is credited to Neuroscience News

Original Research: Closed access.
“Conductive Hearing Loss Pathologies are Associated With Dementia in the All of Us Research Program” by Powell, S.D., Weinstein, H.N.W., Tucker, L.H., Denham, M.W., Gurgel, R.K. and Golub, J.S. Otolaryngology – Head and Neck Surgery
DOI:10.1002/ohn.70152

Complete failure of tearing tissue into small wads with one hand for plugging my running nose

 Impossible to plug both nostrils at the same time with tissue with one hand! Try it sometime.

My therapists and doctors completely failed at getting my left hand recovered and informing me of the consequences of having spasticity. Probably because they believed in the stupid and incorrect opinions of Dr. William M. Landau. 

Of course the infamous Dr. William M. Landau thinks spasticity is not worth treating. 

Do you believe in the do nothingism of Dr. William M. Landau on spasticity?  

His statement from here:

Spasticity After Stroke: Why Bother? Aug. 2004

Wonder if he will be singing the same tune after he becomes the 1 in 4 per WHO that has a stroke, will he be satisfied with not getting recovered?

KU neurology professor persistent in push for more understanding of stroke rehabilitation

 You're a damn professor with access to lots of brain power! JUST SOLVE THE PROBLEM OF STROKE RECOVERY!

You can be a great professor if you can solve that simple problem!  Leaders solve problems; you're NO leader yet!

You're also pushing HIT, which I would never do!

High Intensity Training (46 posts to April 2017)

Oops, I'm not playing by the polite rules of Dale Carnegie,  'How to Win Friends and Influence People'. 

Telling your supposedly smart stroke medical 'professionals' they know nothing about stroke is a no-no even if it is true. 

Politeness will never solve anything in stroke. Yes, I'm a bomb thrower and proud of it. Someday a stroke 'leader' will try to ream me out for making them look bad by being truthful, I look forward to that day.

KU neurology professor persistent in push for more understanding of stroke rehabilitation

Sandra Billinger’s research has resulted in widely adopted protocols in stroke recovery and exercise testing.March 26, 2026 | Dustin Vann

Sandra Billinger, Ph.D., professor of neurology at KU School of MedicineWhen Sandra Billinger, Ph.D., isn’t in a research lab, uncovering the latest breakthroughs in stroke recovery and exercise science, one might find her at work on another project: tending to her home garden. “It’s something I really enjoy,” Billinger said of her gardening hobby. “I like to build things, and I see gardening as a project you’re building on and see through to a finished product. That kind of thing is very exciting to me. Billinger, a professor in the Department of Neurology at the University of Kansas School of Medicine, has seen many significant scientific discoveries to the finish line during hercareer as a researcher. Her most widely recognized contribution is the development of the recumbent stepper submaximal exercise test, which predicts a person’s peak oxygen consumption or aerobic fitness. Nearly 15 years after its publication, it remains a widely adopted protocol for research and practical, clinic-based fitness assessment. “I’ve always had this curiosity that makes me ask questions, and finding ways to do things better,” Billinger said. “If you leave things the way they are, how do you grow? In the last year alone, she has co-authored a paper on high-intensity gait training, been named the principal investigator for a multi-site clinical tria investigating home-based stroke telerehabilitation and, alongside colleagues at KU Medical Center, received a patent related to a novel system for monitoring a patient’s response to exercise. 

“She is a visionary,” Michael Abraham, M.D., a professor in the Department of Neurology, said of his colleague and frequent collaborator.  “She thinks years into the future and has a good eye for the big picture.” 

A generous collaborator 

Billinger’s forward-thinking mindset doesn’t happen in a vacuum. For an innovative idea to reach its potential, Billinger believes that multiple perspectives are essential. (But, you're obviously missing the stroke survivor perspective; contact me at oc1dean@gmail.com and I'll give you my unfiltered perspective on all the failures in stroke! 32,000+ posts on that for my take)

“Collaboration has always been critical to me,” Billinger said. “It pushes me to think about things differently, explore new avenues of research or to see data from a different viewpoint.” 

Billinger’s collaborative approach has proved inspiring to colleagues such as Sarah Eickmeyer, M.D., professor and chair of the Department of Physical Medicine and Rehabilitation.  

“She’s very generous with her time and open to multiple new team members at a given time,” Eickmeyer said.  

As a physician also interested in stroke recovery, Eickmeyer appreciates the dynamic Billinger brings to the field. 

“As a researcher, she really tries to understand where a busy clinician is coming from and seeks to integrate her research team into the clinical work,” Eickmeyer said. “That approach makes it seamless and easy to collaborate.” 

Billinger has undertaken multiple stroke studies to discover the
most effective therapy protocols.(Stroke recovery therapy has only a 10% chance of full recovery. Should be working on solving the 5 causes of the neuronal cascade of death in the first week and thus saving hundreds of million to billions of neurons!)

That integration of perspectives has also shaped the scientific direction of Billinger’s laboratory. In her work with transcranial Doppler ultrasound, a noninvasive test that uses sound waves to measure blood flow in the brain’s major arteries, she sought to move beyond simple associations and examine how multiple physiologic systems interact during exercise. In an integrative study published in the Journal of Applied Physiology, Billinger and her team investigated how heart rate, blood pressure, carbon dioxide and cerebral blood flow influence one another during exercise. To answer those questions, she partnered with statisticians at the University of Washington. The collaboration generated first-of-its-kind data clarifying the relationships underlying cerebrovascular responses to exercise.

An attentive mentor 

The qualities that make Billinger a respected colleague are also the ones that make her a sought-after mentor for younger medical professionals. 

“Dr. Billinger is highly invested in the success of her trainees,” said Bria Bartsch, a student in KU’s rehabilitation science doctoral program who works in the Research in Exercise and Cardiovascular Health laboratory where Billinger serves as director. “She always makes time for updates and research questions despite being a very busy and accomplished researcher in the field of stroke recovery.” 

Billinger’s dedication to her trainees is something that many have carried into their own careers. 

“What stands out most to me is her combination of practical efficiency with genuine generosity in mentorship,” said Jacqueline Palmer, DPT, Ph.D., who worked alongside Billinger during her postdoctoral fellowship and is now an assistant professor at the University of Minnesota. “Sandy created an environment where I felt genuinely valued as a colleague and instilled in me a foundational principle I now carry in my own lab: that research participants and their experience come first.”  

For Billinger, mentorship always begins with a conversation. 

“To be a good mentor, I have to understand [my mentee’s] goals,” Billinger said. “When a mentee can articulate what exactly they want to do, then I try to position them with projects and connect them with others who can help them reach that goal.” 

A future of innovation 

In early February, Billinger traveled to New Orleans for this year’s International Stroke Conference, delivering a talk on high-intensity interval training, part of her ongoing effort to refine how intensity is defined and implemented in stroke recovery. This year will also mark the release of Billinger’s stepper submaximal exercise test as a smartphone app, translating years of research into a tool designed to increase access to precision-guided exercise. There’s also her home garden, which she’ll continue to cultivate. 

Whether advancing stroke recovery or tending to new growth at home, Billinger remains focused on building systems that endure.

“Persistence, I think, is part of innovation,” Billinger said. “You’ve got to keep pushing for it.” 

Cardiovascular imaging reveals pathways linking cardiovascular risk factors to brain aging and cognition

 I'm not worrying about any of this stuff, too busy having fun. 

Cardiovascular imaging reveals pathways linking cardiovascular risk factors to brain aging and cognition

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https://doi.org/10.1016/j.neurobiolaging.2026.04.002Get rights and content

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Open access

Highlights

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  Cardiovascular risk influences brain aging and cognitive performance.
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  Vascular structures mediate the effect of cardiovascular risk on brain aging.
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  Elevated total cholesterol level accelerates brain aging through vascular pathways.

Abstract

Cardiovascular risk (CVR) factors exert effects that extend beyond the vascular system, influencing brain structure, neural function, and cognitive performance. The mechanisms by which CVR factors exert these effects remain unclear. Here, we specifically investigate the impact of CVR factors on brain aging, testing whether quantitative measures of the heart and major arteries mediate the CVR-brain-age relationship. Using longitudinal UK Biobank data, we infer individual brain age estimates based on neuroimaging-derived measures and apply pathway analysis to quantify whether cardiovascular imaging phenotypes mediate the impact of eight established CVR factors on brain aging. Our findings reveal that structural characteristics of the aorta and carotid arteries, specifically the ascending and descending aortic areas and carotid thickness, mediate the effects of the Framingham risk score, a cumulative measure of CVR factors, on the rate of brain aging and cognitive decline. When examining individual CVR factors separately, elevated total cholesterol level was found to accelerate brain aging by affecting the aorta and carotid structures. Our findings highlight the cardiovascular characteristics, particularly vascular structure, as a potential target for early intervention to prevent or delay brain aging and cognitive decline.

Keywords

Brain-heart

Brain age

Cardiovascular risk factors

Cognition

MRI

1. Introduction

Cardiovascular risk (CVR) factors including age, elevated total circulating cholesterol, hypertension, diabetes mellitus, smoking and high body mass index (BMI), are associated with increased risk of brain disorders, including Alzheimer’s disease, other dementias, and age-related cognitive decline (Qiu and Fratiglioni, 2015), suggesting a link between the cardiovascular system and brain health. For example, hypertension and diabetes mellitus are associated with lower total brain volume as well as localized changes in grey mater volume (Lamar et al., 2020). Although cognitive abilities naturally decline with age (Nyberg et al., 2012), exposure to CVR factors might accelerate the pace of aging-related brain changes and cognitive decline (Randhawa and Varghese, 2025, Song et al., 2020).

Biological age can provide a reliable indicator of heart and brain aging (Cole and Franke, 2017). Previous research shows that CVR factors, including anthropometric measurements such as BMI and waist circumference, blood lipids, smoking and blood pressure are associated with the biological age of the brain (Beck et al., 2022). Likewise, the Framingham risk score (FRS) (D’Agostino et al., 2008), an aggregate of CVR factors estimating the risk of future cardiovascular disease, is associated with alterations in brain structure (Marrie et al., 2021, Song et al., 2020) and cognitive performance (Dregan et al., 2013, Kaffashian et al., 2011, Laughlin et al., 2011, Song et al., 2020). Specifically, higher FRS is associated with reduced volumes in the hippocampus, total grey matter, cortical, cerebellar, and subcortical grey matter, and total brain volume, as well as an increase in white matter hyperintensity volume (Song et al., 2020). Moreover, poorer cardiovascular health (Huang et al., 2024) and higher FRS (Wagen et al., 2022) are associated with older brain age. Associations between the biological age of the brain and cardiovascular system have also been reported (Amirmoezzi et al., 2024, Tian et al., 2023) and these studies suggest that advanced cardiovascular aging may contribute to accelerated brain aging. These findings underscore the importance of understanding how age, along with other modifiable CVR factors, influence brain aging, and the pathways through which these effects occur.

The adult brain relies on 15–20% of cardiac output (Xing et al., 2017), making it especially susceptible to disruptions in blood flow. Several factors, such as vascular pathology, cardiac dysfunction, and CVR factors, can impair cerebral circulation (Carmichael, 2014, Moore and Jefferson, 2021, Ovsenik et al., 2021) and impact brain health (van der Velpen et al., 2017). For example, vascular pathology (Moore and Jefferson, 2021) and cardiac dysfunction (Ovsenik et al., 2021) affect hemodynamic status and disrupt cerebral autoregulation, reducing cerebral blood flow and contributing to cognitive decline in the older adults. Similarly, CVR factors such as hypertension, older age, and elevated cholesterol level promote arterial stiffness and damage cerebral vasculature as well as drive the formation of atherosclerotic plaques, leading to restricted blood flow dynamics through stenotic cerebral vessels (Carmichael, 2014). These links motivate our investigation into the specific cardiovascular pathways through which CVR factors may influence brain aging. Given that CVR factors contribute to changes in the structure and function of the cardiovascular system (Petersen et al., 2017, Ren et al., 2015), we hypothesise that these changes reduce cerebral blood flow, which in turn may accelerate brain aging. We also hypothesise that the impact of CVR factors on brain aging is most prominently mediated by specific cardiovascular characteristics, particularly those related to vessels and left ventricular functional capacity, given that cardiac output results from the systolic contraction of the left ventricle and arteries deliver blood to the brain tissue. In contrast, right ventricular measures primarily influence pulmonary circulation and would therefore be less likely to directly mediate the association between CVR factors and brain aging (Bernal-Ramirez et al., 2021, Chandra et al., 2017).

Building on the physiological insights linking cardiovascular health and brain function, emerging imaging research has identified various brain-heart connections (Markousis-Mavrogenis et al., 2022, Zhao et al., 2023). Brain grey matter, white matter and functional connectivity are associated with the morphology and function of the aorta and cardiac chambers (Zhao et al., 2023). Moreover, different heart and brain imaging features are linked to both elevated cardiovascular risk and reduced cognitive function, including myocardial intensity (a proxy for myocardial size), total and grey matter volumes, white matter tract integrity, and white matter hyperintensity volume (Jaggi et al., 2024). These findings suggest that the brain-heart link may underlie the relationship between CVR factors and changes in brain structure and function, as well as cognitive decline. However, previous findings are based on cross-sectional analyses. Longitudinal studies are needed to investigate the potential mediating role of the heart in the relationship between cardiovascular risk and brain health.

Additionally, we explore the potential role of cognitive decline as a terminal point in the pathway linking cardiovascular risk and brain aging. Previous studies establish links between the cardiovascular system and cognition. Better cognitive performance is associated with larger left and right ventricular volumes, higher left and right ventricular stroke volumes, greater left ventricular mass, and greater aortic distensibility (Raisi-Estabragh et al., 2022), whereas cognitive impairment is associated with narrower carotid arteries (Frazier et al., 2014, Yue et al., 2016). More interestingly, a recent study shows that individual variation in grey matter volume can only partially explain the association between myocardial intensity and cognitive function, which suggests that heart structural variations may influence cognitive function through mechanisms independent of brain structural changes (Jaggi et al., 2024). These findings underscore the role of the cardiovascular system in cognitive function, suggesting that cognitive performance is influenced not only by CVR factors but also by cardiac structure and function. Further work is needed to elucidate pathways that may explain the complex interrelationships between CVR factors, heart and brain health and cognition, particularly in aging populations with a high comorbidity of brain and cardiovascular diseases (Eggermont et al., 2012). Exploring the link between cognitive impairment and the structural and functional phenotypes of the cardiovascular system may identify potential targets for early intervention strategies aimed at delaying brain aging and preventing cognitive decline.

In this study, we utilized longitudinal, multiorgan, and multimodal imaging data from the UK Biobank i) to examine the impact of CVR factors on brain aging and cognitive performance; and ii) to assess whether this impact is mediated by the structural integrity and functional capacity of the cardiovascular system (Figure 1). To this end, pathway analysis was conducted to explore the mediating role of different regions of the cardiovascular system, including the cardiac chambers and large arteries. Our work yields new physiological knowledge of how CVR factors lead to brain aging and cognitive decline. We also provide new leads into cardiovascular therapeutic targets for aging-related cognitive decline.

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Fig. 1

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