Wednesday, May 20, 2026
Neuroplex Tracks Nine Separate Brain Circuits in Real Time
I can't imagine this ever getting to human testing.
Neuroplex Tracks Nine Separate Brain Circuits in Real Time
Summary: A major technological leap has shattered a long-standing limitation in behavioral neuroimaging. Researchers introduced Neuroplex, an imaging pipeline capable of simultaneously tracking the real-time functional activity of up to nine distinct neuronal populations in freely moving mice.
By integrating lightweight, head-mounted miniscopes with high-end spectral confocal microscopy and a custom Python-based alignment tool, the pipeline maps specific genetic or circuit identities directly onto functional brain records. This open-source framework transforms how scientists analyze complex neural computations, offering an unprecedented tool for longitudinal studies of learning, aging, and neurodegenerative disease progression.
Key Facts
- Overcoming the Two-Color Limit: Traditional head-mounted miniscopes can record neural activity in behaving animals but lack the spectral capability to differentiate more than two color-coded cell types at a time, forcing slow, animal-to-animal iterative testing.
- The Neuroplex In-Vivo Solution: The new pipeline leaves the animal’s brain tissue intact. It records broad neural activity via a miniscope during behavior, removes the scope, and immediately uses a specialized confocal microscope (ZEISS LSM 980) to decode up to nine fluorescent tags through the exact same implanted lens.
- Automated Spatial Co-Registration: Developed alongside MetaCell data scientists, Neuroplex uses anatomical landmarks and a custom Python-based alignment script to seamlessly match and overlay the functional miniscope footage with the multicolor confocal identity map.
- High-Throughput Validation: As a proof of principle, the team targeted nine distinct projection circuits branching out from the medial prefrontal cortex during social behavior. The automated program successfully assigned roughly 75% of active neurons to their specific circuit identity with 90% accuracy.
- Longitudinal Tracking Power: Because the entire alignment procedure is performed non-destructively within the living animal, researchers can identify cell populations and monitor the exact same neurons across weeks or months to see how circuits warp during learning or disease.Source: MPI Florida
Scientists at the Max Planck Florida Institute for Neuroscience (MPFI), in collaboration with ZEISS and MetaCell, have developed a powerful new imaging pipeline called Neuroplex.
Published in eLife, the technique allows simultaneous monitoring of the activity of up to nine distinct neuronal populations in freely moving mice, dramatically accelerating the pace of scientific exploration into how the brain controls behavior.
For years, neuroscientists linking brain activity to behavior have faced a fundamental limitation: miniscopes, the tiny head-mounted microscopes used to observe neural activity in behaving animals, could capture neural activity, but couldn’t reliably distinguish more than two different types of brain cells at a time.
“To understand the brain, we need to link patterns of activity in specific neurons to behavior,” stated lead author Dr. Mary Phillips.
“We can readily use labels to color-code different populations of neurons, but when using miniscopes to correlate neural activity to behavior, we couldn’t distinguish more than two of these populations. This made it difficult to compare the activity across multiple cell types and circuits to understand how specific circuits regulate behavior.”
To work around this, researchers were forced to test one cell type at a time, repeating the same behavioral experiments, but labeling distinct neuron types each time. This iterative process, however, was slow and costly. It also prevented direct comparison of different neuron types within the same animal, muddying conclusions due to differences among individual animals.
As an alternative, scientists delineated different neuron types after the behavioral experiment by removing and slicing brain tissue, color-coding different neuron types, then imaging the processed brain tissue using microscopes that can distinguish multiple colors.
However, matching the cells imaged with a miniscope in a living animal to those in post-mortem, processed brain tissue was challenging and low-throughput, resulting in significant data loss. Additionally, this approach destroyed the ability to track the activity of identified cell types over time to determine how their activity changes with learning, aging, or during disease progression.
The Solution: Neuroplex
To overcome these challenges, the MPFI team, together with collaborators at ZEISS and MetaCell, developed Neuroplex, an imaging pipeline that combines the two complementary imaging approaches in the same living animal. Researchers first label up to nine different neural circuits or cell types using a spectrum of differently-colored fluorescent tags.
They then use a tiny lens and a head-mounted miniscope to record the neural activity of the entire labeled population in freely moving, behaving mice. After miniscope imaging, which cannot distinguish among the fluorescent tags, the miniscope is gently removed, and the mouse is positioned under a confocal microscope capable of distinguishing many different colors.
In this case, scientists used the ZEISS LSM 980, a confocal microscope with spectral detection capabilities to distinguish each of the different color tags. With the confocal microscope, the same neurons visualized with the miniscope are imaged through the same lens, but this time the color-coded tags are visualized, identifying which neurons belong to which specific type.
Finally, the images from the miniscope and the confocal are co-registered using anatomical landmarks and a custom Python-based alignment tool that the scientists developed with MetaCell. The result is that the team can map each neuron’s color identity directly onto its functional activity record.
“As part of MetaCell’s contribution to this project, we helped take the complex data collected and turn it into a practical computational workflow that enables imaging, registration, and analysis with greater accuracy, reproducibility, and confidence.“Neuroplex shows how carefully designed computational tools can help researchers make sense of complex biological imaging data and study multiple neuronal populations at once and over time,” says Dr. Zhe Dong, co-author and Data Scientist at MetaCell.
As proof-of-principle, the researchers retrogradely targeted nine brain regions that receive projections from the medial prefrontal cortex, a brain area important for decision making. This allowed them to use a distinct fluorescent marker to distinguish neurons projecting from the prefrontal cortex to nine other brain regions.
They recorded the activity of the neurons across all nine circuits simultaneously as animals interacted socially, sniffing, approaching and following.
“Neuroplex allowed direct comparison of neural activity patterns across cell circuits during social behavior, overcoming long-standing challenges in miniscope recordings and dramatically expanding the efficiency and reproducibility of data collection,” explains senior author Dr. Ryohei Yasuda.
The scientists found that approximately 75% of active neurons could be assigned to one of the nine specific cell types, and the automated program built to assign a neuron to a specific group performed with 90% accuracy and few false positives.
“Because Neuroplex is performed entirely in the living animal through the same implanted lens, it enables scientists to measure how different populations of neurons change their activity over time.
“Researchers can identify cell populations prior to behavior and monitor the same neurons over weeks or months, enabling studies of learning, aging, and disease progression over time,” described Dr. Phillips.
What Comes Next
The team is already working on even more improvements to the technique to increase the accuracy of color code identification. Additionally, they hope to make Neuroplex accessible to all labs, including those that may not have access to high-end spectral confocal systems.
Their goal is to disseminate this approach widely to the neuroscience community by using standard filter-based widefield microscopes, bring the core benefits of the approach to the entire research community.
“The increase in data collection efficiency for cell-type- or circuit-specific functional data will accelerate our understanding of the neural computations underlying behavior,” says Phillips.
“Beyond basic research, we expect this approach to accelerate understanding of circuit-specific functional changes in disease models, particularly in neurodevelopmental or neurodegenerative disease models, which benefit from longitudinal studies examining disease progression.”
To disseminate the approach, the team has also developed tutorials for scientists who wish to use Neuroplex in their own research. In addition, the approach will be featured in a ZEISS webinar with first author Dr. Mary Philips on July 14th to share the technique and resources with the scientific community. Register here for more details.
Funding:This research was funded by National Institutes of Health Grants R35-NS-116804 (RY) and F32MH120872 (M.L.P.) This content is solely the authors’ responsibility and does not necessarily represent the official views of the funders.
Key Questions Answered:
Q: Why couldn’t scientists just use colored lights to see multiple cell types before this invention?
A: The issue wasn’t the colors themselves; it was the physics of the microscopes. To watch a mouse navigate a social environment, the microscope must be tiny and light enough to sit on its head. These miniature scopes are incredible at capturing fast flashes of neural activity, but they are color-blind, they simply cannot distinguish between five, six, or nine different shades of glowing cells. Scientists could color-code the brain, but the live miniscope video just showed a monochrome blur of firing neurons, masking which cell belonged to which circuit.
Q: How does Neuroplex match the color of a cell to its actual behavioral recording?
A: The pipeline treats the problem like an automated puzzle. First, the miniscope records the un-colored, flashing activity of all neurons while the mouse interacts socially. Then, the miniscope is detached, and the mouse is placed under a powerful ZEISS confocal microscope that can read the full spectrum of colors through the exact same lens. Finally, an automated Python program created with MetaCell maps anatomical landmarks to align the two images perfectly, matching each cell’s color identity to its behavioral record.
Q: How does this pipeline help us understand complex brain conditions like Alzheimer’s?
A: Many brain disorders don’t just damage one type of cell; they slowly disrupt communication across vast, interconnected networks of multiple cell types over time. Previously, because identifying cell types required killing the model and slicing the brain tissue, tracking disease progression in a single animal over time was impossible. Because Neuroplex is completely non-destructive, scientists can track how nine different circuits in the exact same brain gradually degrade or adapt over weeks and months of aging or disease.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this neurotech and neuroscience research news
Author: Lesley Colgan
Source: MPI Florida
Contact: Lesley Colgan – MPI Florida
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Functional imaging of nine distinct neuronal populations under a miniscope in freely behaving animals” by Mary L. Phillips, Nicolai T. Urban, Taddeo Salemi, Zhe Dong, and Ryohei Yasuda. eLife
DOI:10.7554/eLife.110277.3
Longitudinal Trajectories of Global and Domain-Specific Cognition After Stroke Using the Oxford Cognitive Screen
USELESS! You tell us nothing on how to get cognitive recovery! Ph. D.s and still no brains at all!
You're supposed to solve problems, NOT just describe them you blithering idiots. Hoping comeuppance hits you really hard when you are the 1 in 4 per WHO that has a stroke!
Longitudinal Trajectories of Global and Domain-Specific Cognition After Stroke Using the Oxford Cognitive Screen
Abstract
BACKGROUND:
Cognitive impairment is common after stroke and linked to poor outcomes, yet long-term recovery or decline, particularly across specific cognitive domains, remains unclear. Most studies use brief global screeners with short follow-up, limiting insight into recovery patterns. This study aimed to characterize domain-specific cognitive trajectories over ≥2 years poststroke and identify predictors of persistent impairment.
METHODS:
Participants were recruited at a regional acute stroke unit (John Radcliffe Hospital, Oxford, United Kingdom; 2012–2019) and assessed acutely, at 6 months, and ≥2 years poststroke. The Oxford Cognitive Screen was administered at all timepoints. Global impairment severity was quantified by the proportion of Oxford Cognitive Screen subtasks impaired. Logistic mixed-effects models examined longitudinal change and predictors of domain-specific impairments (language, memory, attention, executive function, and number processing). Latent class growth analysis identified distinct cognitive trajectories. Models were adjusted for acute cognitive impairment severity and time.
RESULTS:
Of 866 patients assessed acutely, 105 were followed up at ≥2 years (98 with complete Oxford Cognitive Screen data; median, 4.1 [interquartile range, 3.3] years; mean age, 69 years, 41% female). Cognitive impairment severity improved substantially by 6 months (β=−0.11; P<0.001) and further long-term (β=−0.15; P<0.001). Acute impairment severity strongly predicted long-term outcomes (β=0.50; P<0.001), while demographic and vascular factors explained minimal variance. Latent class growth analysis identified 4 overall trajectories: no or mild acute impairment with stability (47.6%), moderate-improving (32.3%), large improvement (15.2%), and decline (4.8%). Domain-specific improvements were greatest in memory (odds ratio, 16.40 [95% CI, 5.52–48.7]) and language (odds ratio, 8.17 [95% CI, 3.17–21.1]), more limited in attention (odds ratio, 5.41 [95% CI, 2.52–11.6]) and executive function (odds ratio, 4.14 [95% CI, 1.96–8.75]). Domain models revealed additional classes of persistent or delayed recovery, particularly in executive function and attention.
CONCLUSIONS:
Cognitive recovery is most pronounced within 6 months and continues across domains though executive dysfunction often persists. Acute impairment severity best predicted long-term outcomes, while vascular and demographic factors were less informative. Distinct trajectory classes highlight the need for individualized, long-term cognitive monitoring to guide rehabilitation and prognostication. These findings underscore the importance of long-term cognitive follow-up in stroke care and provide empirical benchmarks for recovery across domains.
Graphical Abstract
Cognitive impairment is common following stroke1,2 and frequently contributes to poor functional outcomes,3,4 increased dependency,5 and reduced quality of life.4 While many individuals experience some degree of cognitive recovery, others may show persistent impairment or delayed decline.3,6 However, the long-term trajectories of change across different cognitive domains remain poorly understood.7 This is partly due to cognitive deficits often being overlooked beyond the immediate postacute period unless dementia develops, which is not an inevitable outcome.6,8,9
Dozens of stroke units lose ‘A’ ratings
'A' ratings should only be given if stroke units show good progress in getting patients to 100% recovery. Your current rating system is completely flawed, ignoring what survivors want to focus on what little you can actually deliver!
Dozens of stroke units lose ‘A’ ratings
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MMP-9 Levels Linked to Hemorrhagic Transformation Risk in Ischemic Stroke
The earliest report I have of MMP-9 being useful for stroke was way back in 2005. And 21 years later we still have no translational use for it. We keep doing studies but never seem to get anywhere useful with it. A great stroke leader would get something accomplished.
In 2005, the scientist(Mr Gu) had previously played the role of lead author on a study published in the Journal of Neuroscience that had revealed MMP-9 could be a promising area that therapeutic medicines for stroke patients could target.
But while you wait for researchers to actually solve stroke you can read up on MMP-9. I like the red wine molecule solving Alzheimer's symptoms.
MMP-9 (24 posts to May 2012)
MMP-9 Levels Linked to Hemorrhagic Transformation Risk in Ischemic Stroke
Matrix metalloproteinase-9 showed moderate diagnostic accuracy for hemorrhagic transformation after acute ischemic stroke, supporting its potential role in risk stratification.
Elevated matrix metalloproteinase-9 (MMP-9) levels are associated with an increased risk for hemorrhagic transformation (HT) following acute ischemic stroke, according to study findings published in Neurology Open Access.Researchers conducted a systematic review and meta-analysis to evaluate the association between MMP levels and hemorrhagic complications after ischemic stroke. Eligible studies included primary research evaluating MMP levels in relation to HT outcomes, with cohort and case-control studies included.
The primary outcome was the association between MMP levels and HT occurrence, while secondary analyses evaluated diagnostic performance measures, including sensitivity and specificity. Statistical analyses included pooled mean differences for continuous outcomes and diagnostic test accuracy modeling.
These findings support the biological relevance of MMP-9 as a marker of [blood-brain barrier] disruption and vascular injury.
The meta-analysis included 9 studies encompassing 1051 patients. Among these, 274 patients experienced HT and 777 did not. Across studies, patient ages ranged from 60 to 90 years overall, and study populations included patients receiving thrombolysis, anticoagulation, and endovascular therapies. MMP-9 levels were measured at varying time points, including at admission, baseline, within 24 to 36 hours after admission, and before or after endovascular thrombectomy procedures.
MMP-9 levels were significantly higher among patients who developed HT compared with those who did not, with a pooled mean difference of 70.51 ng/mL (95% CI, 35.47-105.5). Although this analysis demonstrated substantial heterogeneity across studies (I² =93%), diagnostic accuracy analyses showed more consistent performance. Pooled sensitivity and specificity for MMPs were 0.79 (95% CI, 0.79-0.84) and 0.796 (95% CI, 0.67-0.88), respectively. The positive likelihood ratio was 3.88 (95% CI, 2.35-6.40), and the negative likelihood ratio was 0.26 (95% CI, 0.20-0.35), corresponding to a diagnostic odds ratio of 14.75 (95% CI, 7.62-28.58).
Across individual studies, sensitivity estimates ranged from approximately 0.72 to 0.87, while specificity values varied from 0.75 to 0.90. The pooled diagnostic accuracy estimates demonstrated consistent performance across studies, supporting the potential role of MMP-9 in risk stratification for hemorrhagic complications after ischemic stroke.
The biological role of MMP-9 in degrading extracellular matrix components and disrupting the blood-brain barrier may explain its association with HT, as elevated levels reflect ongoing vascular injury and inflammation.Study limitations include variability in MMP-9 measurement timing, lack of standardized cutoff thresholds, differences in treatment protocols, heterogeneous study designs, variability in HT classification methods, and limited reporting on symptomatic vs asymptomatic HT, all of which may affect generalizability and clinical implementation.
“These findings support the biological relevance of MMP-9 as a marker of [blood-brain barrier] disruption and vascular injury,” the study authors concluded.
B Vitamins and Stroke: How B Vitamins Can Support Stroke Recovery and Help Prevent Another Stroke by Fint rehab
Have your competent? doctor give you EXACT SPECIFICS ON THIS. Unable to do so, then find someone competent!
B Vitamins and Stroke: How B Vitamins Can Support Stroke Recovery and Help Prevent Another Stroke
How Exercise & Creatine Protect Muscle & Metabolic Health As You Age by mindbodygreen
Have your competent? doctor give you EXACT PROTOCOLS on creatine and exercise so you get the best benefits! If not possible you'll have to scour the world for competence.
How Exercise & Creatine Protect Muscle & Metabolic Health As You Age
20 year anniversary
I had my stroke 20 years ago at age 50, got tPA in 90 minutes and still ended up with a fair amount of disability. I see NOTHING in those 20 years that even remotely suggests that stroke survivors now will now get any closer to 100% recovery. If fact I can guarantee that the next 20 years will do nothing either. NO one has ever contacted me for insight into stroke survivors! All because there is NO STRATEGY AND NO LEADERSHIP in stroke!
Tuesday, May 19, 2026
Defining Social and Cultural Barriers to Global Stroke Care: A SVIN–Mission Thrombectomy Initiative
The first barrier to break down is changing the word 'care' to RECOVERY!
UNTIL THAT OCCURS YOU'RE NOT WORTH LISTENING TO!
Defining Social and Cultural Barriers to Global Stroke Care: A SVIN–Mission Thrombectomy Initiative
Abstract
Stroke has become the single leading neurological illness that results in neurological disability and is the second most common cause of death worldwide. Approximately 85% of strokes are ischemic, whereas the remaining 15% are hemorrhagic. With the advent of increasingly effective(Not true, you are not delivering 100% recovery! And that IS MASSIVE FAILURE BY THE STROKE MEDICAL WORLD! You all need to be keel hauled!) treatment modalities, such as intravenous thrombolytics and endovascular mechanical thrombectomy, there has been a growing disparity in the ability to provide standard of care(NOT RECOVERY!), despite substantial efforts made in lower- and middle-income countries. substantial effort in high-income countries to provide the current standard of care(NOT RECOVERY!) to patients with stroke, with the hope of improving outcomes. Extensive research has shown that the disparities in treatment among various countries stem from multiple sociocultural barriers and the lack of robust healthcare infrastructure.(WRONG! It's because you haven't delivered 100% recovery protocols regardless of time to hospital!
Pedro Bach-y-Rita recovered fully back in 1958 with only a partial brain! Aren't you smart enough to duplicate that?)
The societal influences in play include the lack of knowledge of stroke symptoms, cultural beliefs, health, and spiritual fatalism, which are then associated with delayed healthcare-seeking behaviors. As a result, it is imperative to increase access to treatment for patients with stroke to address inequities in stroke care(NOT RECOVERY!) and diminish the global burden of stroke. This narrative review highlights causes of major gaps in stroke treatment infrastructure in several global communities and examines the pertinent sociocultural factors that impede progress in stroke treatment.
Graphical Abstract
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.
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