Brain Waves During Sleep Predict Dementia Risk

 With your extra risk of dementia post stroke will your competent? doctor use this to validate that their EXACT DEMENTIA PREVENTION PROTOCOLS WILL BE USED?

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this! Is s/he willing to prevent this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

Brain Waves During Sleep Predict Dementia Risk

Key Takeaways

• An EEG-derived brain age index predicted dementia risk across five cohorts.
• Each 10-year increase in the brain age index was linked with a 39% higher dementia risk.
• The findings indicate that the predictive value of the index should be further assessed, the researchers said.

A brain age index based on microstructures of sleep electroencephalography (EEG) data predicted dementia risk, a meta-analysis showed.

Across five cohorts and 7,105 participants, each 10-year increase in the EEG-derived index was tied to a 39% higher risk of dementia (HR 1.39, 95% CI 1.21-1.59, P<0.001) after adjusting for covariates, reported Yue Leng, PhD, of the University of California San Francisco, and co-authors.

The relationship remained significant after adjusting for comorbidities and apnea-hypopnea index scores (HR 1.31, P<0.001) and APOE4 gene status (HR 1.22, P=0.03), the researchers wrote in JAMA Network Open. Links were consistent across sex and age groups.

"Sleep gives us a unique window into the brain. This study shows that we can use brain activity during sleep to estimate how the brain is aging," Leng told MedPage Today.

"Sleep isn't just rest; it reflects how well the brain is functioning and maintaining itself," she said. "By turning sleep EEG into a measure of 'brain age,' we may be able to detect risk of dementia earlier and more easily."

The brain age index captures the difference between sleep EEG-based brain age and chronological age, Leng and colleagues noted, with negative values indicating a younger brain age and positive values reflecting an older one. The index incorporated 13 microstructural features of brain waves from EEG recordings of overnight, home-based polysomnography.

Earlier work has linked sleep macrostructure -- like sleep efficiency or time spent in certain sleep stages -- to dementia risk, but results have been inconsistent.

This study "advances the field by shifting attention from macrostructure to EEG microstructure (i.e., spectral power in specific bands, spindle and slow oscillation characteristics, and waveform properties across sleep stages)," observed Omonigho Bubu, MD, PhD, MPH, of the NYU Grossman School of Medicine in New York City, in an accompanying editorial.

"What makes this work particularly compelling is that brain age index is a general marker of neurophysiologic aging, developed in an independent cohort and then tested, prospectively, against dementia outcomes," Bubu wrote. "That design enhances its plausibility as a robust marker of accelerated brain aging, rather than an overfitted prediction tool."

Dementia research is moving toward combining genetic information, blood biomarkers, imaging, and cognitive testing into integrated risk assessments, Bubu pointed out. "Within this landscape, sleep EEG-based brain age index occupies a distinctive niche as it reflects real-time brain physiology, relies on widely used clinical technology, and condenses complex neural information into an interpretable brain age," he added.

For their individual participant data meta-analysis, Leng and co-authors pooled information from five community-based longitudinal cohorts: the Multi-Ethnic Study of Atherosclerosis (MESA; 1,802 participants), the Atherosclerosis Risk in Communities (ARIC; 1,796 participants) study, the Framingham Heart Study-Offspring Study (FHS-OS; 617 participants), the Osteoporotic Fractures in Men Study (MrOS; 2,639 participants), and the Study of Osteoporotic Fractures (SOF; 251 participants).

Participants' average ages at the time of the sleep study ranged from 59.5 to 82.7 years, and more than 90% were cognitively normal. The primary outcome for the pooled analysis was incident dementia, with death treated as a competing risk.

Over follow-up, 1,088 people developed dementia, with a median time to dementia ranging from 3.6 to 16.9 years.

The findings highlight the need to evaluate the predictive value of the brain age index as a digital marker for early dementia detection in community settings, the researchers said.

The five cohorts included in the study differed in population characteristics, data collection methods, dementia ascertainment, and follow-up times, which may have introduced heterogeneity and potential bias, they acknowledged. Only death was used as a competing risk, but other life events may affect follow-up or dementia ascertainment, they added. The analysis is observational and a causal relationship between brain age index and dementia can't be inferred.

"Moreover, as a composite measure, brain age index itself is not a plausible therapeutic target," Leng and colleagues wrote. "Rather, brain age index should be viewed as a prognostic marker for future dementia risk."

Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Connect:

Disclosures

This work was supported by grants from the National Institute on Aging.

Leng reported receiving grants from the NIH and serving on the advisory board of ResMed.

Co-authors reported relationships with GLG Councils, Guidepoint, MyCardio, the Alliance of Sleep Apnea Partners, Sleep Health, the NIH, Google, Axsome, Eli Lilly, and Beacon Biosignals.

Bubu reported relationships with the ResMed medical advisory board, the NIH, the Alzheimer's Association, the Michael J. Fox Foundation, CurePSP, and the BrightFocus Foundation.

Primary Source

JAMA Network Open

Source Reference: Sun H, et al "Machine learning-based sleep electroencephalographic brain age index and dementia risk: an individual participant data meta-analysis" JAMA Netw Open 2026; DOI: 10.1001/jamanetworkopen.2026.1521.

Secondary Source

JAMA Network Open

Source Reference: Bubu OM "Sleep electroencephalography brain age -- a window into incident dementia risk" JAMA Netw Open 2026; DOI: 10.1001/jamanetworkopen.2026.1494.

Advancing Stroke Equity Globally: From Recognition to Strategic Action

 More useless blathering from our fucking failures of stroke associations. Until 100% recovery is the only thing talked about, why don't you retreat to the locker room and let real leaders solve stroke? NOTHING ON 100% RECOVERY! Get back to survivors when you've actually left stroke! Because you are absolute pieces of shit! You're not 'in the arena', so get the hell out!

Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name(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 WHY you aren't solving to 100% recovery protocols with NO EXCUSES! I've never received any communications from any stroke association(This is you; ASA and WSO). 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.

Advancing Stroke Equity Globally: From Recognition to Strategic Action

Aidan R. Lindgren https://orcid.org/0009-0009-8110-9211 RolandFaigleMD https://orcid.org/0000-0002-9074-1915, and Amytis Towfighi MD https://orcid.org/0000-0002-9565-6787 towfighi@usc.edu Author Info & Affiliations Stroke Volume 57 Number 4 https://doi.org/10.1161/STROKEAHA.125.049864

An Alzheimer's Revolution Is Coming, Experts Say

 Ask your competent? doctor if anything here will guarantee not getting Alzheimers

An Alzheimer's Revolution Is Coming, Experts Say

Research roundtable highlights early detection, biomarkers, interventions

An earlier diagnosis and intervention strategy for Alzheimer's disease is on the horizon, signaling a need to overhaul current detection methods and patient care protocols, experts at the Alzheimer's Association Research Roundtable (AARR) said.

"Advances in biomarker technology, digital cognitive assessments, and amyloid-targeting therapies have redefined the opportunities for accurate and early diagnosis and care of Alzheimer's disease," reported Christopher Weber, PhD, of the Alzheimer's Association in Chicago, and co-authors in Alzheimer's & Dementia: Translational Research & Clinical Interventions.

These advances create new possibilities to intervene before the onset of cognitive impairment, Weber and colleagues wrote. Targeting the earliest stages of Alzheimer's, Weber said, "is similar to how doctors treat other diseases like heart disease and some cancers, where early detection and prevention are key parts of care."

Alzheimer's disease often remains undiagnosed until significant memory loss and functional decline have occurred, observed co-author Suzanne Schindler, MD, PhD, of Washington University School of Medicine in St. Louis. "This means that patients and care partners don't get a diagnosis until later in the disease, after the window when interventions are most helpful and patients can make truly independent decisions," she told MedPage Today.

In 2024, an Alzheimer's Association workgroup established new biologically-based criteria for Alzheimer's, incorporating biomarker classifications and a revamped disease staging system. This approach recognized Alzheimer's disease as a process detectable by abnormal biomarkers, even without cognitive symptoms.

The shift wasn't without controversy. A diagnosis based on biomarkers without symptoms sparked debate among clinicians, some of whom argued there may be potential harms to redefining Alzheimer's disease.

In spring of 2025, the AARR convened academic, industry, clinical, and government experts to discuss how to identify and treat people in Alzheimer's earliest stages. "This meeting and paper reviewed the state of the field and areas that need further work, especially if treatments for asymptomatic Alzheimer's are approved in the near future," Schindler said.

Earlier detection brings a set of complex issues, from identifying who's at highest risk and navigating treatment decisions to clear, compassionate communication with patients and families, the AARR said. Stigma and ethical concerns will need to be addressed. Economic, social, and policy factors will need to be considered.

While plasma biomarkers offer hope for broad applications in the clinic, tests must be rigorously validated, the AARR emphasized. Primary care clinicians, who will be on the front lines, will need enhanced tools, training, and support.

Two anti-amyloid therapies currently are approved to treat Alzheimer's patients with mild symptoms -- lecanemab (Leqembi) and donanemab (Kisunla). The AHEAD 3-45 trial of lecanemab and the TRAILBLAZER-ALZ 3 study of donanemab are now testing these drugs in people with biomarker evidence of Alzheimer's who are cognitively intact. "If these studies are successful, it could change how doctors manage the disease," Weber said.

If the trials are successful, it also may create new challenges, noted Eric Widera, MD, of the University of California San Francisco, who was not part of the AARR.

"We struggle currently for people diagnosed with mild cognitive impairment and mild dementia, whether the current treatments equate to a meaningful difference when we see a small but statistically significant difference in the Clinical Dementia Rating-Sum of Boxes," Widera told MedPage Today. "It will be so much more complicated in cognitively unimpaired individuals as it's such a larger population that it will apply to, the measures being studied are not generally outcomes patients truly care about, and it's unclear what a meaningful difference is in these measures."

The consensus that Alzheimer's starts years before symptoms appear has refocused dementia prevention strategies, the AARR pointed out. "Doctors need to learn more about how Alzheimer's disease starts many years before symptoms begin, and also about preventive interventions -- from exercise to hearing aids -- that may reduce the risk of cognitive impairment," Schindler said.

"Research studies, including the U.S. POINTER trial, show that healthy habits with structure and accountability can improve thinking and support brain health in older adults at risk for cognitive decline," Weber added.

Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Connect:

Disclosures

This report was supported by the Alzheimer's Association and other groups.

Weber is an employee of the Alzheimer's Association.

Schindler reported serving on scientific advisory boards of biomarker testing and clinical care pathways for Eisai and Novo Nordisk and receiving consultancy/speaking fees for biomarker testing presentations from Eisai, Eli Lilly, and Novo Nordisk.

Co-authors disclosed relationships with nonprofit groups and industry; several were employed full time by pharmaceutical companies.

Widera had no conflicts of interest.

Primary Source

Alzheimer's & Dementia: Translational Research & Clinical Interventions

Source Reference: Schindler SE, et al "Alzheimer's disease stage 1 and 2: biology, diagnostics, and treatment" Alzheimer's Dement 2026; DOI: 10.1002/trc2.70216.

No evidence to suggest medicinal cannabis is effective for depression, anxiety or PTSD: research

 This contradicts a lot of previous research, so have your competent? doctor DETAIL EXACTLY WHY! 

• PTSD, (98 posts to July 2012)
• Post stroke depression(33% chance).

• Post stroke anxiety(20% chance).  
• marijuana (163 posts to February 2011)

One line in there is interesting; medical cannabis may be beneficial for spasticity in multiple sclerosis(Ask your doctor if this would work for spasticity in stroke. NO answer, your doctor is FUCKING INCOMPETENT!)

No evidence to suggest medicinal cannabis is effective for depression, anxiety or PTSD: research

30 Minutes Of This Form Of Exercise Can Boost Your Brain Health by mindbodygreen

 Your competent? doctor did tell you all the benefits of BDNF and EXACT PROTOCOLS TO GET IT, right? Oh NO, failure on both points!

And your board of directors is so incompetent they don't have any method of measuring doctor competence!

• BDNF (203 posts to April 2011)

30 Minutes Of This Form Of Exercise Can Boost Your Brain Health

You might have a laundry list of things you can do to make your muscles stronger and your stomach feel better–drinking hot water in the morning, strength training, eating whole foods, taking an evening walk. However, it is easy to feel like your brain health is out of control. You might feel like names slipping your mind and a foggy feeling when you're staring at your laptop are inevitable as you get older.

But, you have more control over your brain health than you might think. A recent study found that aerobic exercise strengthens your brain1, in addition to your heart and muscles. It triggers the release of brain-derived neurotrophic factor (BDNF), a protein that supports your prefrontal cortex, the brain region responsible for attention, decision-making, and executive function. And the more participants worked out as the 12 weeks went on, the more their bodies produced BDNF in response to exercise.

What is BDNF, and why does it matter?

BDNF is essentially fertilizer for your brain cells. This protein supports the growth of new neurons, strengthens the connections between existing brain cells, and plays a key role in learning and memory.

BDNF is particularly important for your prefrontal cortex, the region responsible for executive functions like attention, decision-making, and impulse control. This protein also supports neuroplasticity, the foundation of learning, memory, and mental flexibility. Higher levels of BDNF better equip our brains to form new connections and adapt to new challenges.

BDNF levels naturally decline with age, but here's where exercise comes in.

The exercise-BDNF connection

When you engage in aerobic exercise, your body responds by ramping up BDNF production.

Previous studies have shown that 30-minute bouts of moderate-intensity walking significantly increased serum BDNF levels2 compared to prolonged sitting. Another showed that even a single session3 of high-intensity interval training (HIIT) was enough to elevate BDNF.

A new study published in Brain Research examined how the benefits of exercise on BDNF levels1 compound over time. 30 participants, with a baseline of little exercise, participated in a twelve week program consisting of six weeks of light cycling each day followed by six weeks of moderate-vigorous cycling each day. Researchers assessed VO2 max and BDNF levels before and after each of these six week blocks, in addition to conducting cognitive tests to measure changes in the prefrontal cortex.

The data showed that as participants improved their cardiovascular fitness, their BDNF response to exercise grew stronger. Even more compelling, higher BDNF levels correlated with changes in prefrontal cortex function during tasks requiring attention and inhibition.

In other words, the fitter these participants became, the more their brains benefitted from each workout.

How much exercise benefits your brain?

The research points to a surprisingly accessible threshold–just 30 minutes of moderate-to-vigorous aerobic exercise is enough to trigger BDNF release.

What counts as moderate-to-vigorous? Think:

• A brisk walk where you can talk on the phone, but not sing along with your headphones
• Cycling at a pace that gets your heart rate up
• A HIIT session with short bursts of intense effort
• Doing laps in a swimming pool

The most important part of this exercise is that it is something you enjoy and can do commit to on a routine basis. You need to consistently get your heart pumping to see these brain benefits.

The takeaway

This research offers a hopeful message for anyone concerned about keeping their mind sharp as they age. Regular aerobic exercise isn't just good for your heart—it's actively supporting your brain's ability to adapt, learn, and stay resilient.

By boosting BDNF through consistent movement, you're investing in your brain's neuroplasticity—its capacity to form new neural pathways and maintain cognitive function. Think of each workout as a deposit in your long-term brain health savings account.

And don't worry if you're thinking, "I should have started this years ago." Research suggests it's never too late to see benefits. Your brain remains capable of change at any age. So the next time you're feeling foggy or stuck, consider hitting the treadmill.

Doing This In Your Free Time Can Increase Dementia Risk: 5 Better Alternatives by mindbodygreen

 My TV watching is maybe 2-3 hours a day, after 6-7 hours of computer time keeping this blog going. 

Doing This In Your Free Time Can Increase Dementia Risk: 5 Better Alternatives

Are you a die-hard Bravoholic? On your 12th rewatch of The Office in its entirety? Ever been confronted with your TV streamer's judgmental "Are you still watching?" notice? It's no secret that we're living in the golden age of television, and it's easier to get hooked on the best of old and new than ever. But science may have found a reason to consider pumping the brakes on your TV consumption—even if means trading it in for another form of screentime. The link between TV and computer time and dementia rates For a study published in the journa Proceedings of the National Academy of Sciences, researchers set out to explore the relationship between sedentary activities and dementia. Namely, they looked at both TV watching and computer use and their correlation to the onset of all-cause dementia.

The bad news? Increased TV watching was related to increased rates of dementia. But interestingly enough, increased computer use was actually observed to decrease dementia rates. This relationship was observed regardless of physical activity level. It's important to note that this research was done on UK biobank participants, with the authors pointing out that the group studied lacked diversity in terms of race and ethnicity. They also note that the study relied on self-reported behaviors, which can always lead to imperfect data. There is no evidence to suggest watching TV in moderation is related to dementia risk. But while the study found compelling data on the overall trends of TV watchers, it does not propose a magic number of TV episodes that should be safe for cognitive health.

If watching TV is something you enjoy, there is no need to give it up cold turkey. But when it comes to TV time, this study suggests that moderation is key for healthy aging. Opt for a handful of shows you really enjoy, and consider swapping out hours of mindless watching for something more mentally stimulating. Here are a few habits to help you maximize leisure time in support of brain health: Go on a walk and put on a podcast or audiobook: Exercise is undeniably great for your health, and it helps protect the brain against cognitive decline. Educational podcasts can also get your mental wheels turning as you move. (Pssstt...if you need a good rec,the mindbodygreen podcast is full of health nuggets.) Pick up a page-turner: A long-standing leisure pastime, reading is a wonderful way to get lost in a story, learn new things, and flex your imagination. Plus, it's got tons of proven health benefits, including improving our memory and brain health as we age. Eat to protect your brain: In addition to spending your leisure time wisely, consider arming your brain with protective foods and supplements. Ingredients like citicoline all have impressive neuroprotective properties. Meditate: If you haven't picked up a meditation practice yet, this might be your sign. Even a short daily practice can work wonders for your brain and overall mental health

Milk Consumption Linked to Higher Parkinson Disease Risk, Especially in Men

 Ask your competent? doctor to quantify that risk, because dairy fat is good for you and you need to weigh the pros vs. the cons!

• dairy fat (45 posts to April 2016)
• milk (16 posts to February 2013)

 And then ask how much coffee you need to drink to negate that risk.

How coffee protects against Parkinson’s Aug. 2014 

If your doctor can't answer those simple questions, FIND A BETTER ONE! 

My milk consumption has declined dramatically by skipping breakfasts of cereal.

Milk Consumption Linked to Higher Parkinson Disease Risk, Especially in Men

Higher total dairy and milk intake were associated with increased Parkinson disease risk, with stronger effects observed in men, while yogurt, cheese, butter, and ice cream were not associated with risk. Parkinson disease (PD) risk is higher among individuals with greater dairy intake, particularly milk consumption, according to a systematic review and meta-analysis published in Public Health. Dietary intake has been hypothesized to influence PD risk through mechanisms involving the gut microbiome and the gut–brain axis. Researchers conducted a systematic review and meta-analysis of observational studies in adult populations examining associations between dairy consumption and PD risk and reporting corresponding risk estimates. The potential mechanisms, which span the gut microbiome, uric acid biology, contaminant exposure, and immunogenetic interactions, warrant further investigation to inform targeted dietary guidance and prevention strategies. A total of 9 studies were included, comprising 8 cohort studies and 1 case-control study conducted across the United States, Europe, and Asia. The combined cohort studies included 634,327 participants with 4285 incident PD cases. The case-control study included 617 individuals, of whom 368 were in the control group and 249 had PD. Most studies included middle-aged to older adults and had follow-up periods ranging from approximately 8 to 41 years. Higher total dairy intake was associated with increased PD risk (Relative risk [RR], 1.211; 95% CI, 1.071-1.37; P=.002). This association was not significant in women (RR, 1.019; 95% CI, 0.814-1.276 P=.868) but was significant in men (RR, 1.282; 95% CI, 1.049-1.567; P=.015). Milk consumption was also associated with increased PD risk (RR, 1.13; 95% CI, 1.079-1.20; P<.001). For milk intake, the association remained significant in women (RR, 1.094; 95% CI, 1.028-1.16; P=.004) but was more pronounced in men (RR, 1.265; 95% CI, 1.089-1.47; P=.002).

No significant associations were observed for yogurt or fermented milk, cheese, butter, or ice cream. Study limitations include the reliance on self-reported dietary data and the use of baseline-only dietary assessments, which may not reflect changes over time. “The potential mechanisms, which span the gut microbiome, uric acid biology, contaminant exposure, and immunogenetic interactions, warrant further investigation to inform targeted dietary guidance and prevention strategies,” the authors concluded. References: Yang D, Nepal G, Ojha R, Tu Z.  Association between dairy consumption and Parkinson’s disease: a systematic review and meta-analysis Public Health. 2026;252:106143.

Stroke Rehabilitation: Which is the Main Functional Outcome to Reach?

 If you have to ask, YOU DON'T BELONG IN STROKE! It's 100% RECOVERY, you blithering idiots!

Stroke Rehabilitation: Which is the Main Functional Outcome to Reach?

Loredana Cavalli*, Andrea Guazzini, Bruno Rossi and Carmelo Chisari University of Florence, Italy 

Abstract 

Background: 

Stroke rehabilitation targets range from treatment of spasticity to pain reduction, gait speed gain, or autonomy amelioration. A correct evaluation of individual residual capabilities is essential to select the most appropriate rehabilitative programme; furthermore the observation of rehabilitative outcomes can provide information about gait training effects and possible compensation mechanisms. 

Aim: 

To investigate the main outcome to reach in stroke rehabilitation. 

Methods: 

We examined retrospectively a heterogeneous sample of 119 subjects recovered for the treatment of stroke outcomes. Functional parameters were assessed before and after rehabilitative treatment, such as upper limbs motility impairment, lower limb sensitiveness, muscle trophism or tone, necessity of auxilium, Berg and Fugl-Meyer scale. 

Results: 

A consistent improvement of standing equilibrium was reported, regardless of gender, stroke nature, hemiparetic side, type of rehabilitation performed, botulin toxin use and initial conditions, with an average increase of Berg and Fugl-Meyer scales score of 14% and 21%, respectively. The variation of equilibrium and motility across treatment resulted directly proportional and negatively correlated to lower limbs sensitivity impairment. On the contrary, initial equilibrium resulted inversely correlated with the variation of motility and vice versa. Interestingly, older subjects seem to better increase equilibrium and sensitivity as measured by Fugl-Meyer scale. 

Conclusion: 

In stroke subjects any type of rehabilitation leads to a consistent improvement of standing balance. While proportional to motility and sensitivity increase, this result is inversely correlated to initial motility score, suggesting that an appropriate evaluation of the stroke patient’s functional parameters at admission contributes to select the main rehabilitation targets and the best therapeutic strategy. 

The Role of Muscle Ultrasound in Stroke Rehabilitation: A Review of Calf Muscle Alterations and Clinical Implications

 Useless! You tell us nothing about the efficacy of recovery AND PROVIDE NO PROTOCOLS! Your mentors and senior researchers should be ashamed of allowing  such useless research to be produced

The Role of Muscle Ultrasound in Stroke Rehabilitation: A Review of Calf Muscle Alterations and Clinical Implications

• 

  Ying Shi

• 

  Chuanxiong Li

• The Affiliated Hospital of Yunnan University, Kunming, China

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Abstract

Background: 

Post-stroke morphological alterations in lower-leg muscles contribute to gait impairment. Conventional assessments are subjective and cannot quantify intramuscular changes. Musculoskeletal ultrasound offers a non-invasive, quantitative tool for evaluating these alterations. 

Objective: 

This systematic review synthesizes the past five years of literature on musculoskeletal ultrasound (B-mode, elastography, dynamic, and quantitative ultrasound) for assessing lower-leg muscle changes in stroke patients, exploring correlations with clinical outcomes and utility in guiding rehabilitation. 

Methods: 

PubMed, CNKI, and Wanfang Data were searched (January 2020–December 2025) following PRISMA guidelines. Included were original studies involving stroke patients, using ultrasound to assess lower-leg muscles, and reporting morphological or functional parameters. Results: Eight studies were included. The gastrocnemius and tibialis anterior were most assessed. Paretic muscles showed reduced thickness and cross-sectional area, altered pennation angle, shortened fascicle length, increased echo intensity (fat infiltration/fibrosis), and elevated shear wave velocity/Young's modulus (increased stiffness). These parameters correlated with spasticity, motor function, and muscle strength. Ultrasound effectively monitored treatment responses. 

Conclusion: 

Musculoskeletal ultrasound objectively assesses post-stroke lower-leg muscle changes, correlates with functional outcomes, and aids personalized rehabilitation. Standardized protocols are needed for broader clinical application.