Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, March 4, 2026

Prediction of Stroke Outcomes in a Super-aged Society: Different Effects Among Predictive Variables

 If your doctor can't predict and deliver 100% recovery, FIND SOMEONE COMPETENT!

Prediction of Stroke Outcomes in a Super-aged Society: Different Effects Among Predictive Variables


Yoshihiro Kanata • Yuki Uchiyama • Satoko Matsushima • Mika Kanatani • Tetsuo Koyama • Kazuhisa Domen

Published: March 02, 2026

DOI: 10.7759/cureus.104580 

Peer-Reviewed

 





Cite this article as: Kanata Y, Uchiyama Y, Matsushima S, et al. (March 02, 2026) Prediction of Stroke Outcomes in a Super-aged Society: Different Effects Among Predictive Variables. Cureus 18(3): e104580. doi:10.7759/cureus.104580

Abstract

Background and objective: Population aging has progressed rapidly worldwide, particularly in developed countries such as Japan. Age is a well-established prognostic factor after stroke; however, its influence on functional outcomes may differ in increasingly older populations. This study aims to investigate whether the impact of age on post-stroke functional independence differs between patients aged ≥75 years (late elderly) and those aged <75 years.

Methods: This retrospective cohort study included 169 post-stroke patients admitted to a convalescent rehabilitation ward between 2018 and 2023. All patients were independent before stroke onset and received intensive multidisciplinary rehabilitation. Functional outcomes were assessed using the Functional Independence Measure (FIM), with the motor score at discharge as the primary endpoint. Patients were divided into a younger group referred to as the 'early elderly' (<75 years, n = 80) and an older group known as the 'late elderly' (≥75 years, n = 89). Multivariable linear regression analyses were performed for the entire cohort and separately for each age group, adjusting for demographic, clinical, and functional variables at admission.

Results: Baseline FIM motor and cognitive scores and trunk function were significantly poorer in the late elderly group; however, no significant age-related difference in FIM gain was observed. In the overall cohort, age, time from stroke onset to transfer, FIM cognitive score at admission, and trunk function independently predicted the FIM motor score at discharge. In subgroup analyses, age was not a significant predictor in the early elderly group but was a strong independent predictor in the late elderly group, along with cognitive function, motor impairment, trunk function, and time to rehabilitation.

Conclusions: The prognostic significance of age differs by age group in post-stroke rehabilitation. Age does not independently predict functional independence in patients aged <75 years, but plays a critical role among those aged ≥75 years. These findings highlight the need for age-specific prognostic models and rehabilitation planning in aging societies, particularly among patients undergoing intensive convalescent rehabilitation.

Introduction

Advances in public health and medical care have increased life expectancy worldwide, leading to rapid population aging. This demographic shift is particularly pronounced in developed countries. Japan is one of the most rapidly aging societies, with individuals aged ≥65 years accounting for more than 29% of the total population. In accordance with Japanese healthcare and social insurance policy, adults aged ≥65 years are classified as 'older,' those aged 65 to 74 years as 'early elderly,' and those aged ≥75 years as 'late elderly' [1]. This distinction reflects recognized differences in health status, functional reserve, and healthcare utilization between early and late elderly populations and provides a clinically meaningful framework for age-stratified analyses of functional outcomes.

Stroke is a leading cause of disability among older adults [2]. Residual hemiparesis and cognitive impairment are common after stroke and often result in substantial limitations in independence in activities of daily living (ADL) [3]. Early initiation of rehabilitation is essential for promoting functional recovery and independence [4]. Therefore, accurate prognostic prediction is critical for establishing appropriate rehabilitation strategies [5]. For example, when independent ambulation is unlikely, rehabilitation programs emphasize basic self-care activities such as eating, grooming, and dressing. In contrast, patients expected to regain ambulatory function may be assigned more advanced goals, including stair climbing. Numerous factors influence stroke outcomes, including initial stroke severity, lesion volume, and age, the latter of which has consistently been identified as a major determinant of prognosis [6].

However, the influence of age on stroke outcomes may differ from that reported in earlier studies, particularly in developed countries experiencing extreme population aging. Accordingly, this study investigated the impact of age on functional outcomes after stroke by comparing late elderly patients with their younger counterparts in a cohort from a rural region of Japan, where population aging is especially pronounced.

Materials & Methods

Study design and participants

This retrospective cohort study included post-stroke patients admitted to our convalescent rehabilitation ward between November 2018 and March 2023. During hospitalization, patients received up to 180 minutes per day of physical therapy, occupational therapy, and speech therapy, seven days per week, in accordance with the Japanese Guidelines for the Management of Stroke [7].

Eligibility criteria included a pre-stroke modified Rankin Scale (mRS) score of ≤2, indicating independence in ambulation and activities of daily living [8], and the absence of severe dementia. As in our previous studies [9-11], patients with subarachnoid hemorrhage or lesions involving the cerebellum or brainstem were excluded, as were those with medical complications requiring acute care (e.g., angina, gastrointestinal disease, or fractures). To minimize the influence of white matter lesions, only patients with a Fazekas score <2 were included [11,12]. The Fazekas scores were evaluated using MRI by an experienced physiatrist. The mRS was used solely as an eligibility criterion and is appropriately cited. No scale items, structured interview materials, or copyrighted content related to the mRS are reproduced in this manuscript.

Functional assessment

Functional status was assessed using the Functional Independence Measure (FIM) [13]. The FIM consists of 13 motor items and five cognitive items, each scored on a 7-point scale ranging from 1 (total assistance) to 7 (complete independence). Total scores range from 18 to 126, with motor subscale scores ranging from 13 to 91 and cognitive subscale scores from 5 to 35. Discharge was determined when the FIM motor score plateaued.

Functional improvement was quantified as FIM gain, defined as the change in the FIM motor score between admission and discharge, and was used as an indicator of rehabilitation effectiveness. The FIM was used solely for routine clinical scoring and outcome reporting. No copyrighted test forms, manuals, instructions, or item-level content are reproduced or described in this manuscript.

Assessment of motor and trunk function

Motor impairment was evaluated using the motor domain of the Stroke Impairment Assessment Set (SIAS), and trunk function was assessed using the SIAS trunk items [14]. Motor function for five components (upper limb, hand/fingers, hip, knee, and ankle) was scored on a 6-point scale (0-5). The sum of these components was calculated to assess the overall severity of motor impairment in the affected extremities (SIAS motor total).

Trunk function was scored from 0 to 6 based on vertical sitting balance and abdominal muscle strength (SIAS trunk), in accordance with the SIAS scoring system. The SIAS was used in accordance with standard academic practice; only summary scores were analyzed and reported, and no proprietary materials were reproduced.

Statistical analysis

Collected data included age, sex, type of stroke (ischemic (I) or hemorrhagic (H)), time from stroke onset to transfer, FIM and SIAS scores at admission and discharge, FIM gain, and total length of hospital stay (including the acute care period). The FIM motor score reflects functional performance [13], whereas SIAS scores assess neurological impairment [14]; therefore, these variables were considered complementary rather than redundant despite assessing related domains. Prior to age stratification, age was analyzed as a continuous variable in exploratory models to evaluate potential age-dependent changes in prognostic relationships.

Statistical analyses were performed in two steps. First, participants were divided into early elderly (<75 years) and late elderly (≥75 years) groups, and group differences were examined using Wilcoxon rank-sum tests or chi-squared tests, as appropriate. Continuous variables are presented as medians with interquartile ranges and were compared using the Wilcoxon rank-sum test due to non-normal distributions. Second, multiple linear regression analyses were conducted using the forced-entry method, with the FIM motor score at discharge as the dependent variable. Independent variables included age, type of stroke, time from onset to transfer, FIM motor and cognitive scores at admission, and SIAS motor total and SIAS trunk scores at admission.

Three regression models were constructed: one including all participants, one including only the early elderly group, and one including only the late elderly group. All statistical analyses were performed using the JMP software (SAS Institute Inc., Cary, NC, USA). A p-value <0.05 was considered statistically significant.

Results

Patient selection and baseline characteristics

The patient selection process is summarized in Figure 1. During the study period, 394 patients were admitted to the convalescent rehabilitation ward, of whom 169 met the eligibility criteria. Based on the predefined age cutoff of 75 years, 80 patients were assigned to the early elderly group and 89 to the late elderly group. Patient characteristics are presented in Table 1.

Flow-diagram-showing-the-patient-screening-process

First FDA-approved device to improve arm and hand function

 Massive incompetence there, was approved in The MicroTransponder Vivistim Paired VNS System received FDA Premarket Approval (PMA) on August 27, 2021

Or maybe you don't want surgery.

The latest here; just proving how fucking incompetent they are in getting interventions into their hospitals!

First FDA-approved device to improve arm and hand function

Contact:
Chelsey Kralicek
Sanford Health Media Relations
701-516-4903 / Chelsey.Kralicek@SanfordHealth.org

BISMARCK, N.D. —A breakthrough therapy for stroke survivors to help improve upper‑limb function through vagus nerve stimulation (VNS) paired with rehabilitation is now available at Sanford Bismarck. Mobia Medical Inc. and Sanford Health today announced the availability of the FDA‑approved Vivistim.

Vivistim is the first and only FDA‑approved device that uses VNS during therapy to help stroke survivors significantly improve arm and hand function—even years after their stroke. Clinical studies show patients using Vivistim achieve two to three times greater improvement than rehabilitation alone.

The system works by delivering gentle, precisely timed vagus‑nerve stimulation during therapist‑guided rehabilitation, strengthening neural pathways that support motor recovery. Vivistim is intended for chronic ischemic stroke survivors who continue to experience moderate to severe upper‑limb impairment six months or more after their stroke. The therapy includes a small, implanted device, therapist‑led sessions using a wireless remote, and at‑home exercises activated by a handheld magnet to support continued recovery in daily tasks.

“Our team is excited by the potential of Vivistim,” said Tiffany Skor, MOTR/L, CLT, therapy and rehabilitation manager, Sanford Bismarck. “As occupational therapists, we see firsthand how innovation can reshape the patient journey, and Vivistim represents a significant step forward. Its capabilities open new possibilities for personalized therapy, improved outcomes and more efficient care. We’re excited to bring this technology into our practice and confident it will make a meaningful difference for the patients and families we serve.”

For more information, visit vivistim.com.

The Sanford Health Bismarck Region provides health care to central and western North Dakota, eastern Montana and northern South Dakota. It includes 26 clinics in Bismarck, Mandan, Minot, Dickinson, Williston and Watford City, as well as a Level II trauma center located in Bismarck.

About Sanford Health
Sanford Health, the largest rural health system in the United States, is dedicated to transforming the health care experience and providing access to world-class health care in America’s heartland. Headquartered in Sioux Falls, South Dakota, the organization has 55,000 employees and serves more than 2 million patients and nearly 415,000 health plan members across the upper Midwest including South Dakota, North Dakota, Minnesota, Wyoming, Iowa, Wisconsin and the Upper Peninsula of Michigan. The integrated nonprofit health system includes a network of 58 hospitals, 289 clinic locations, 145 senior care communities, 4,500 physicians and advanced practice providers and 1,100 active clinical trials and studies. The organization’s transformational virtual care initiative brings patients closer to care with access to nearly 80 specialties. More than 400 residents and fellows are trained each year through graduate medical education with Sanford Health fully funding and supporting 29 of the 40 available programs. Sanford Health also includes Lewis Drug, a pharmacy and retail chain with 60 locations in three states and nearly 190 pharmacists. Learn more about Sanford Health’s commitment to shaping the future of rural health care across the lifespan at sanfordhealth.org or Sanford Health News.

Three Major Studies Tie Healthy Midlife Diet to Lower Risk of Cognitive Decline

 

None of them have any objective specifics(NO protocol!) so you can be sure you're following them properly. In my opinion, pretty much useless other than whitewashing your doctor's incompetence in not knowing anything specific to get you recovered!

Three Major Studies Tie Healthy Midlife Diet to Lower Risk of Cognitive Decline

Healthy eating in midlife was associated with better cognitive performance and lower risk of subjective cognitive decline (SCD) in three large prospective studies of US health professionals.

The analysis included participants from three long-running cohorts of US health professionals who were followed for years with repeated dietary assessments and cognitive evaluations. Individuals with the highest adherence to healthy eating patterns, particularly the Dietary Approaches to Stop Hypertension (DASH) diet, had significantly lower risk of SCD and performed better on objective cognitive testing

For example, participants in the 90th percentile of adherence to the DASH diet had a 41% lower risk of reporting SCD during follow up compared with peers in the 10th percentile.

Of note, the DASH diet was consistently associated with a lower risk of SCD even when measured up to 26 years before the SCD assessments and had robust protective associations at various ages, particularly in midlife (45-54 years). 

“These findings support the importance of healthy eating as part of midlife brain-health strategies and motivate pragmatic and implementation research to translate these findings into scalable programs,” investigators, led by Hui Chen, PhD, Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, wrote.

The research was published online February 23 in JAMA Neurology

Healthy Diet, Healthy Brain 

Dementia is projected to affect 150 million people worldwide by 2050. While healthy diets are widely believed to benefit brain health, prior evidence has been inconsistent, and few studies have compared multiple dietary patterns within the same population.

The new analysis focused on 159,347 participants in three long-running cohorts. These included the Nurses’ Health Study (NHS), NHSII, and the Health Professionals Follow-Up Study. The average age at baseline was 44.3 years, and 83% of participants were women. 

The researchers evaluated six established healthy dietary patterns in relation to both SCD — an early indicator of cognitive problems preceding detectable deficits — as well as objectively measured cognitive function.

Diet was assessed every 4 years using validated food frequency questionnaires, and cumulative average scores were calculated for six dietary patterns: the Alternate Healthy Eating Index 2010 (AHEI-2010), the DASH diet, the Healthful Plant-Based Diet Index (hPDI), the Planetary Health Diet Index (PHDI), and two data-driven patterns reflecting lower hyperinsulinemia (reverse Empirical Dietary Index for Hyperinsulinemia [rEDIH]) and lower inflammatory potential (reverse Empirical Dietary Inflammatory Pattern [rEDIP]).

SCD was measured using self-reported questions about memory and other cognitive changes, while objective cognition in older NHS participants (age 70+ years) was assessed by telephone using validated tests of global cognition, verbal memory, verbal fluency, and working memory.

Across all six healthy dietary patterns, higher adherence was associated with lower risk of global SCD, with the DASH diet showing the strongest magnitude of effect, the researchers found.

For instance, risk ratios for the increasing quintiles of the DASH score were 1.00, 0.91, 0.78, 0.74, and 0.59 in fully adjusted models.

Comparing participants at the 90th vs 10th percentile of adherence, the risk ratio for SCD was 0.59 for DASH; 0.76 for hPDI and rEDIH; 0.80 for PHDI; 0.84 for AHEI-2010; and 0.89 for rEDIP.

A higher DASH diet score in midlife (ages 45-54 years) showed the strongest association with lower risk of SCD, supporting the concept that midlife may represent a critical window for brain health.

Higher scores across most dietary patterns were also associated with better objectively measured global cognition, with the exception of the hPDI and PHDI patterns.

For instance — compared with those at the 10th percentile of the DASH score — on average, participants at the 90th percentile had a 0.05-higher global cognition z score (equivalent to 0.76 years younger in cognitive aging), a 0.04-higher verbal fluency z score (0.87 years younger), and a 0.05-higher working memory z score (1.37 years younger). 

Analyses of individual food groups suggested that higher intake of fish and leafy green, yellow, and other vegetables, as well as moderate wine consumption, was associated with better cognitive outcomes, while red and processed meats, fried potatoes, sweetened beverages, and sweets were linked to worse cognition.

“Our findings generally support the role of a healthy diet, manifested by six dietary patterns, in benefiting cognitive health,” the investigators concluded. 

“Further studies with larger sample sizes are needed to reveal modifiers of the diet-cognition association, and large-scale long-term clinical trials are needed to fully reveal the cognitive effects of the healthy diet,” they noted. 

The study had no commercial funding. The authors had no relevant disclosures. 


Turning Pathophysiologic Promise Into Evidence-Based Potential: Are Factor XIa Inhibitors Ready for Prime Time in Secondary Stroke Prevention?

 You'll have to ask your doctor.  Your doctor is already familiar with this earlier research, right! I'm not watching the 20 minute video.

Turning Pathophysiologic Promise Into Evidence-Based Potential: Are Factor XIa Inhibitors Ready for Prime Time in Secondary Stroke Prevention?

Novel plasma panel advances noninvasive detection of Alzheimer’s disease

 Because of your extra risk of dementia, you need this so your competent? doctor CAN DELIVER THOSE EXACT ALZHEIMER PREVENTION PROTOCOLS! 

With your risk of dementia, you need this.

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

But I bet your doctor has nothing! Good luck dealing with Alzheimer's on your own.

Novel plasma panel advances noninvasive detection of Alzheimer’s disease

In a study of 520 participants, researchers used mass spectrometry and machine learning to identify Alzheimer’s disease-specific structural changes in plasma proteins, developing a 3-marker panel that achieved 83% accuracy in distinguishing healthy individuals, mild cognitive impairment (MCI), and Alzheimer’s disease (AD), with area under the receiver operating characteristic curves (AUCs) exceeding 0.93 for key binary comparisons.

The findings, published in Nature Aging, suggest that plasma conformational biomarkers could offer a highly accurate, minimally invasive tool for early detection and disease monitoring, with important implications for clinical trial design and therapeutic intervention in AD.

“With this work, we established a potential new biomarker panel that reveals structural disruptions in proteins linked to Alzheimer’s disease that are invisible to traditional approaches,” said lead author John Yates, The Scripps Research Institute, La Jolla, California. “This approach accurately distinguishes stages of the disease, meaning that it could help enable earlier diagnosis.”

For the cross-sectional and longitudinal analysis, the researchers profiled plasma protein structural alterations in 520 participants using high-resolution mass spectrometry combined with machine learning algorithms. Participants included people with and without AD and MCI. 

The investigators examined conformational changes linked to ApoE variants and neuropsychiatric symptoms, ultimately identifying a 3-peptide diagnostic panel derived from C1QA, CLUS, and ApoB that captured AD-specific structural signatures.

The resulting multi-marker panel achieved 83.44% accuracy in 3-way classification among healthy, MCI, and AD groups, with AUCs of 0.9343 for healthy versus MCI and 0.9325 for MCI versus AD. 

Longitudinal samples were classified with 86% accuracy.

“This work introduces a fundamentally new, blood-based approach to detecting and staging Alzheimer’s disease,” commented Richard Hodes, National Institute on Aging, part of the National Institutes of Health, Bethesda, Maryland. “By revealing protein structural changes associated with genetic risk, symptom severity, and sex differences -- features not captured by existing biomarkers -- this research could enable earlier diagnosis and more effective clinical trials.”

Reference: https://www.nature.com/articles/s43587-026-01078-2

SOURCE: National Institutes of Health

Why the Brain and Breath Part Ways During Heavy Slumber

 One line in there interests us. Have your doctor and hospital ENSURE FURTHER RESEARCH OCCURS!

Why the Brain and Breath Part Ways During Heavy Slumber

Summary: Does your brain stop “listening” to your lungs when you fall into a deep sleep? According to a new study, the answer is yes. Researchers discovered that during the deepest stages of non-REM sleep (characterized by slow delta waves), the brain’s activity becomes increasingly independent of the rhythm of breathing.

By focusing on the substantia nigra—a deep-brain region that produces dopamine and controls movement—scientists found that the usual “coupling” between breath and brain waves seen during wakefulness and lighter sleep essentially dissolves during deep rest. This discovery offers vital clues into the mechanics of anesthesia and could lead to new treatments for Parkinson’s disease, where both sleep and breathing are often severely disrupted.

Key Facts

  • The “Disconnect”: While brain waves and breathing patterns are usually synchronized during quiet wakefulness and light sleep, they become mostly independent during the “slow delta” activity of the deepest non-REM sleep.
  • Focus on the Substantia Nigra: This is the first study to detail how breathing affects this critical deep-brain region, which is responsible for dopamine production and motor control.
  • Parkinson’s Link: Because the substantia nigra is the primary area damaged in Parkinson’s disease, understanding its “rhythm” during sleep could explain why Parkinson’s patients suffer from both sleep apnea and insomnia.
  • Anesthesia Insights: The study also compared sleep states to ketamine anesthesia, finding that different states of “unconsciousness” have unique ways of linking (or unlinking) the brain to peripheral rhythms like breathing.
  • The Primary Motor Cortex: In addition to the deep brain, researchers tracked the motor cortex, showing that this “breath-brain decoupling” is a widespread phenomenon during deep restorative sleep.

Source: HMH

Could the deepest parts of the brain hold some of the secrets of sleep that still remain elusive to science?

A team from Hackensack Meridian Health and its Center for Discovery and Innovation (CDI) have produced a new in-depth study penetrating into the brain, finding that during the deepest sleep, breathing patterns and brain activity become more independent from one another – unlike lighter sleep or quiet wakefulness.

This shows a woman sleeping.
Scientists have discovered that during the deepest stages of sleep, the brain’s neural activity operates independently from the rhythm of respiration. Credit: Neuroscience News

The study was published in The Journal of Neuroscience in January, with the team led by CDI author Bon-Mi Gu, Ph.D., also of the Hackensack Meridian School of Medicine. The research team includes Kolsoum Dehdar, Ph.D., and Elliot Neuberg, and recently relocated from the Neuroscience Institute at Hackensack Meridian JFK University Medical Center to the CDI.

The paper focuses on the basal ganglia, clusters of neurons responsible for motor control and other roles. Of prime interest to the scientists is the tiny region called the substantia nigra, which controls movements and produces dopamine, among other functions.

The relation between these structures and sleep – and how they relate to each other’s rhythm has not heretofore been widely studied, according to the scientists.

“In this study, we provide the first detailed characterization of respiration-neural coupling across multiple states – including quiet wakefulness, non-REM sleep, REM sleep, and anesthesia – in the substantia nigra and the primary motor cortex, two regions not previously studied in this context,” write the authors.

The team measured the sleep cycles of mice, comparing electrical brain activity and breathing and how the two timed off one another. They also assessed the mice during wakefulness, as well as under ketamine anesthesia.

The scientists found nuances and variations in all states. But one consistent thread was that the deepest non-REM sleep had breathing mostly independent of the brain waves, especially with the “slow delta” activity during the deepest part of slumber.

“The strength of respiration-neural coupling varied across multiple states, including NREM sleep, REM sleep, quiet wakefulness, and anesthesia, and was directly related to the delta power, a hallmark of NREM sleep,” write the authors.

The conclusions could pave the way into better understanding of how sleep works – and could help with some disease states, they find.

“These findings provide new insights into how internal brain states interact with peripheral rhythms like respiration, with important functional implications for both sleep and anesthesia,” write the scientists.

“Furthermore,” they add, “elucidating the mechanisms underlying respiration-neural coupling, especially within basal ganglia circuits, will shed light on the pathophysiology of conditions such as Parkinson’s disease, where both sleep and respiration are commonly disrupted.”

Key Questions Answered:

Q: If my brain and breath “disconnect,” is that dangerous?

A: Not at all—it’s actually a hallmark of restorative sleep. During wakefulness, your brain is highly responsive to the world (and your own body). In deep sleep, the brain essentially “closes the curtains” to focus on internal maintenance and memory consolidation, allowing its waves to flow independently of your physical breathing rhythm.

Q: Why does this study focus on the “Substantia Nigra”?

A: This region is the brain’s “dopamine factory.” We already know it’s vital for movement, but we didn’t know how it behaved during sleep. If this region fails to “decouple” or “sync up” correctly, it might be the reason why people with Parkinson’s experience such restless, low-quality sleep.

Q: Could this lead to better anesthesia?

A: Yes. By understanding how breathing and brain waves interact under anesthesia versus natural sleep, doctors can develop more precise ways to monitor patients, ensuring they stay at the perfect level of unconsciousness without disrupting their vital rhythms.

Editorial Notes:

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

About this sleep and neuroscience research news

Author: Seth Augenstein
Source: HMH
Contact: Seth Augenstein – HMH
Image: The image is credited to Neuroscience News

Sending Positive Signals: Could Exercise Mimetics Help Treat Depression?

 Don't let your incompetent? doctor give you this instead of preventing depression the CORRECT WAY OF EXACT 100% RECOVERY PROTOCOLS!

Let's see how long your doctor has known about and working on preventing post stroke depression. I think a decade is plenty of time to come up with the correct solution, at least for those actually trying to solve the problem! Is your competent? doctor trying to solve the problem, or just regurgitating nonsolutions from medical school?

Didn't your competent? doctor prescribe this years ago?

  • 'Exercise-in-a-pill' (7 posts to May 2017)
  • Sending Positive Signals: Could Exercise Mimetics Help Treat Depression?

    University of Ottawa researchers have been studying a concept that might one day allow functionally limited patients with depression to enjoy the mood-boosting benefits of exercise. Their focus is exercise mimetics, which are compounds that appear to reproduce the effects of endurance exercise on skeletal muscle by activating key signaling pathways important for muscle metabolism. 

    photo of Nicholas Fabiano
    Nicholas Fabiano, PhD

    “I saw that there was a discrepancy in how we treated patients with medication and therapy, but we disregarded other treatment measures like exercise, which has a lot of emerging evidence,” lead author Nicholas Fabiano, PhD, a researcher and psychiatry resident at the University of Ottawa, told Medscape News Canada. 

    “With the increasing interest in exercise for depression, it only made sense to look into what’s happening on the muscle-brain level,” he said. 

    The researchers’ findings were published February 19 in Molecular Psychiatry.

    Sending Positive Signals 

    During exercise, muscles contract and release myokines, which mediate communication between the muscles and other organs, including the brain. Low cerebral levels of myokines (eg, brain-derived neurotrophic factor and interleukin-6 and -14) have been associated with impaired quality of life and depression, as well as depression-related inflammation and slowed metabolism. 

    Exercise mimetics include natural substances (eg, omega-3 fatty acids and resveratrol) and synthetic drugs (eg, metformin). The researchers’ theory is that chronic administration of exercise mimetics might cause skeletal muscle fibers to alter their metabolic and contractile activity, thus providing antidepressive benefits like those seen with endurance training. 

    Data are limited, however. In mice, ingesting exercise mimetics appeared to improve depressive-like behaviors, and the observed mechanisms (eg, enhanced muscle-brain axis, amplified signaling across membranes, and increased myokine secretion) resembled those observed in humans, Fabiano explained.

    “There’s not even a whole lot of research at this preclinical level, looking mechanistically in mice or different organisms at what these compounds may do from a mental health perspective,” he said. 

    The same is true of human studies. A systematic review and meta-analysis highlighted a small, randomized controlled trial in which metformin was associated with significant reductions in depressive symptoms in patients with comorbid depression and diabetes at 24-week follow-up. The underlying mechanism is related to metformin’s effect on AMP-activated protein kinase, which regulates metabolism and energy. 

    A second systematic meta-review in heterogeneous populations identified four studies in 226 patients without depression. The findings demonstrated a relationship between resveratrol and nonsignificant mood improvements

    A Future Clinical Role? 

    Each year in Canada, 1 in 10 adults experiences major depression. Various guidelines mention low-to-moderate intensity exercise as a first-line strategy to prevent and treat depression. 

    photo of Guy Faulkner
    Guy Faulkner, PhD

    But biological pathways may not be critical for the observed antidepressant effect of exercise, Guy Faulkner, PhD, endowed chair in applied public health at the University of British Columbia in Vancouver, told Medscape News Canada. Faulkner’s research focuses on the implementation gap between recommendations and practice. 

    “What I think is more important is the process of being physically active, which makes people feel better,” he said. “Essentially, it’s the feelings of competence, autonomy, and relatedness that can be generated through a physical activity intervention and experience. It’s much more than these biological or psychological pathways or mechanisms. That’s not to say they’re not occurring, but they don’t seem to be essential for mental health benefits.” 

    “It’s not an either/or question,” said Johny Bozdarov, MD, staff psychiatrist at the Centre for Addiction and Mental Health and assistant professor of psychiatry at the University of Toronto. Bozdarov’s work focuses on how the effect of exercise on the brain’s networks can be translated into psychiatric care pathways and structure-based exercise interventions for marginalized populations. 

    photo of Johny Bozdarov
    Johny Bozdarov, MD

    “Depression clearly has a biological correlation that research is showing, like inflammation, neuroplasticity, stress hormones, et cetera. But people don’t experience, to our knowledge, depression at the level of cytokines or synapses.” 

    Whether exercise mimetics will have a future role in clinical practice is uncertain. “It’s scientifically compelling and exciting. But without robust human clinical trials, it’s too early to be thinking about it in clinical translation,” said Bozdarov. “I’m wondering, if the evidence comes out, if it could be as an adjunct, potentially with therapeutic interventions, or to get people started as a first step. Maybe they’d experience a boost in energy or muscle to motivate them to engage in exercise programming.” 

    When asked about future applications, Fabiano gave a measured response. “Exercise mimetics will probably have a lower efficacy than exercising itself,” said Fabiano. “I don’t think it completely replaces the whole biopsychosocial part of depression.” 

    “If we could only roll all the benefits of exercise into a pill, it would be prescribed for everyone,” said Faulkner. 

    Fabiano, Faulkner, and Bozdarov reported no relevant financial relationships.

    Vagus nerve non-surgical therapy

     Don't do this, only your competent? doctor knows of medically approved ways to accomplish this. Oh, your doctor doesn't know and has nothing? Then find a better doctor.

     Here's all the info on vagus nerve your doctor is very familiar with!

    vagus nerve (65 posts to July 2012

    The latest here:

    Truvaga vagus nerve stimulation

    AI system spots Parkinson’s signs in voice, walking and drawings

    Have your competent? doctor EXPLAIN EXACTLY HOW THEY ARE GOING TO PREVENT Parkinsons! They've known of the problem for years! Are they still incompetent in having done nothing? And the incompetent board of directors hasn't fired them yet?

    Parkinson’s Disease May Have Link to Stroke March 2017 

    The latest here:

     AI system spots Parkinson’s signs in voice, walking and drawings

    By merging voice instability, gait asymmetry, and tremor-driven handwriting changes into a single explainable AI framework, researchers show how digital biomarkers can move Parkinson’s detection closer to reliable real-world screening.

    Doctor going through results on computer tablet with older adult patientStudy: Explainable multimodal feature fusion networks for Parkinson's disease prediction. Image credit: goodluz/Shutterstock.com

    Recent advances in computing, especially the use of artificial intelligence, hold promise for increased accuracy and efficiency of medical diagnosis. A recent study published in the journal Frontiers in Digital Health presents a deep learning approach that uses multiple modalities of input data to improve the detection of Parkinson’s disease.

    Digital biomarkers aim to catch early Parkinson's Disease

     Parkinson’s disease (PD) is a progressive neurodegenerative disorder. It manifests as motor impairments, including tremor, rigidity, gait abnormalities, handwriting difficulties, and slowed movement. It also presents with impaired cognition, problems with speech, and sleep issues. PD diagnosis is primarily clinical, based on neurological examination. The subjective nature of this process may increase the risk of misdiagnosis or of missed diagnosis, especially in early disease.

    Artificial intelligence (AI) can help overcome these limitations by analyzing handwriting, gait, and speech for telltale signs of early dysfunction. These objectively measured digital biomarkers can help detect PD at early stages. AI-driven speech analysis has achieved up to 99 % accuracy in controlled datasets. Similarly, gait-based analytics can discriminate between PD patients and healthy controls with up to 97 % accuracy. Handwriting analysis has also achieved nearly 98 % accuracy.

    Despite this, each of these has significant problems when applied to the clinical context. For instance, speech analysis may be confounded by differences in accent, language, or background noise. Similar quality issues plague gait-based and handwriting-based detection systems. The former relies heavily on the proper use of high-quality sensors, whereas handwriting analysis is often based on experiments performed in controlled rather than real-world conditions. Thus, these unimodal systems are poorly generalizable and cannot be easily scaled.

    AI models are also often poorly interpretable; they offer predictions but do not explain the reasoning that drives how and why decisions are made. This has led to the introduction of explainability mechanisms, exemplified in this case by SHapley Additive exPlanations (SHAP), Gradient-weighted Class Activation Mapping (Grad-CAM), and Integrated Gradients (IG). When integrated into PD models, these allow clinicians to understand which attributes influenced the decision-making process. Their relatively limited use has slowed the growth of clinical support for AI-based detection systems.

    The current study sought to overcome these obstacles by using a multimodal deep learning framework that incorporates three modalities: gait, handwriting, and speech. This approach integrates complementary findings from multiple modalities, representative of the wide range of PD clinical features, into a single prediction. If one modality is unreliable or noisy, the other two may help strengthen overall classification performance.

    Even so, explainability has lagged behind in multimodal frameworks, making them unpopular in clinical practice. In view of this gap, the researchers present a static early-feature fusion system. The model combines modality-specific features via feature concatenation, followed by XGBoost classification, thereby optimizing overall prediction performance. In addition, the model includes SHAP, Grad-CAM, and Integrated Gradients to ensure interpretability.

    Inside the trimodal early fusion architecture

    In this model, deep neural networks were used to process individual modalities via dedicated feature-extraction pipelines. For speech, log-Mel spectrograms were analyzed using EfficientNet-B0; for gait, temporal convolutional networks and autoencoders were used to extract vertical ground reaction force features; and for handwriting, spiral drawings were processed using ResNet-50. This was followed by static feature concatenation and classification with an XGBoost model. Explainable AI techniques were employed to make the model interpretable at both modality and feature levels.

    For speech analysis, log-Mel spectrogram representations were used to capture vocal instability, pitch variation, and spectral features associated with PD. Using multiple vocal parameters improved prediction performance. Similarly, wearable sensor–derived gait signals, specifically vertical ground reaction force data from a public PhysioNet dataset, were analyzed to capture stride irregularities, asymmetry, and temporal instability.

    For handwriting analysis, digitized spiral drawings were used to detect tremor-induced deviations, curvature changes, and micrographia. Grad-CAM visualizations highlighted regions of the spiral most influential in classification decisions.

    Importantly, unlike several studies cited in the literature review, this framework did not incorporate cerebrospinal fluid biomarkers, neuroimaging, olfactory testing, sleep data, facial movement analysis, or finger-tapping assessments. The proposed system relied exclusively on speech, gait, and handwriting datasets.

     

    Benchmark datasets validate multimodal performance

     The system was evaluated using publicly available benchmark datasets: a spiral handwriting dataset (3,264 samples), the MDVR-KCL speech dataset (approximately 73 subjects), and the GAITPDB gait dataset (approximately 168 subjects). Fivefold stratified cross-validation was employed to ensure robust evaluation.

    The trimodal fusion model achieved an accuracy of 92 %, outperforming unimodal handwriting (91 %), gait (90 %), and speech (74 %) models. It achieved a macro F1-score of 0.89, an area under the ROC curve (AUC) of 0.95, and an average precision of 0.96, with balanced sensitivity and specificity of approximately 90 % and 89 %, respectively.

    In simpler terms, the combined model correctly classified roughly nine out of ten cases while maintaining a good balance between identifying people with Parkinson’s disease and avoiding false alarms.

    Bootstrapped confidence intervals further supported the statistical robustness of these results. External validation experiments demonstrated similar classification patterns, although with slight performance variation attributable to dataset differences.

    The model performed better than unimodal systems and provided an interpretable AI-assisted framework. However, the fusion mechanism involved static concatenation rather than adaptive or reliability-based dynamic weighting, and the study did not experimentally simulate missing-modality scenarios. The authors also emphasize that while multimodal fusion improved robustness, performance was evaluated retrospectively on benchmark datasets rather than in prospective clinical trials.

     

    Explainable AI strengthens Parkinson’s screening potential

     The study presents a diagnostic system based on multimodal feature fusion modeling, using AI, demonstrating solid performance and interpretability on benchmark datasets. However, the authors acknowledge important limitations. The framework has not yet undergone prospective clinical validation, was evaluated only for binary classification (PD versus healthy controls), and did not include clinician-guided assessment of the explainability of its outputs. Additionally, modality-specific generalizability challenges remain, particularly for speech and gait data collected under different real-world conditions.

    Future studies should involve neurologists and longitudinal analyses to establish the clinical validity of this framework, build trust, and ensure regulatory readiness. Lighter, deployment-oriented versions of the model, along with more adaptive multimodal fusion strategies, may further enhance real-world applicability.

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