Daily Life Upper Limb Activity for Patients with Match and Mismatch between Observed Function and Perceived Activity in the Chronic Phase Post Stroke

 This is so fucking simple to explain! You didn't get them 100% recovered including stopping spasticity!

Daily Life Upper Limb Activity for Patients with Match and Mismatch between Observed Function and Perceived Activity in the Chronic Phase Post Stroke

Daily Life Upper Limb Activity for Patients with Match and Mismatch between Observed Function and Perceived Activity in the Chronic Phase Post Stroke Bea Essers 1, * , Marjan Coremans 1 , Janne Veerbeek 2 , Andreas Luft 3,4 and Geert Verheyden 1   Citation: Essers, B.; Coremans, M.; Veerbeek, J.; Luft, A.; Verheyden, G. Daily Life Upper Limb Activity for Patients with Match and Mismatch between Observed Function and Perceived Activity in the Chronic Phase Post Stroke. Sensors 2021, 21, 5917. https://doi.org/10.3390/ s21175917 Academic Editor: James F. Rusling Received: 26 July 2021 Accepted: 28 August 2021 Published: 2 September 2021 Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/). 1 Department of Rehabilitation Sciences, KU Leuven, 3001 Leuven, Belgium; marjan.coremans@kuleuven.be (M.C.); geert.verheyden@kuleuven.be (G.V.) 2 Luzerner Kantonsspital, Neurocenter, 6000 Lucerne, Switzerland; janne.veerbeek@luks.ch 3 Division of Vascular Neurology and Neurorehabilitation, Department of Neurology and Clinical Neuroscience Center, University of Zurich and University Hospital Zurich, 8091 Zurich, Switzerland; andreas.luft@usz.ch 4 Cereneo, Center for Neurology and Rehabilitation, 6354 Vitznau, Switzerland * Correspondence: bea.essers@kuleuven.be  

 

Abstract: 

 

 We investigated actual daily life upper limb (UL) activity in relation to observed UL motor function and perceived UL activity in chronic stroke in order to better understand and improve UL activity in daily life. In 60 patients, we collected (1) observed UL motor function (Fugl-Meyer Assessment (FMA-UE)), (2) perceived UL activity (hand subscale of the Stroke Impact Scale (SIS- Hand)), and (3) daily life UL activity (bilateral wrist-worn accelerometers for 72 h) data. Data were compared between two groups of interest, namely (1) good observed (FMA-UE >50) function and good perceived (SIS-Hand >75) activity (good match, n = 16) and (2) good observed function but low perceived (SIS-Hand ≤75) activity (mismatch, n = 15) with Mann–Whitney U analysis. The mismatch group only differed from the good match group in perceived UL activity (median (Q1–Q3) = 50 (30–70) versus 93 (85–100); p < 0.001). Despite similar observed UL motor function and other clinical characteristics, the affected UL in the mismatch group was less active in daily life compared to the good match group (p = 0.013), and the contribution of the affected UL compared to the unaffected UL for each second of activity (magnitude ratio) was lower (p = 0.022). We conclude that people with chronic stroke with low perceived UL activity indeed tend to use their affected UL less in daily life despite good observed UL motor function.

METS-IR as an important predictor of neurological impairment severity in patients with severe cerebral infarction: a multicenter study based on the Chinese population

 You do realize that predictions like this ARE ABSOLUTELY FUCKING WORTHLESS FOR GETTING SURVIVORS RECOVERED! 

I'd have you all fired for not doing the research that would prevent this problem!

METS-IR as an important predictor of neurological impairment severity in patients with severe cerebral infarction: a multicenter study based on the Chinese population

Yaqi Hou^1†Xiaohua Wu^2†Yiheng Shi^3†Xiaotian Xu⁴Yu Zhang¹Lei Jiang¹Wei Wang⁴Yan Yang⁴Lanying Hu^5*

• ¹School of Nursing, Yangzhou University, Yangzhou, Jiangsu, China
• ²Department of Endocrinology and Hematology, Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu, China
• ³Department of Gastroenterology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou Jiangsu, China
• ⁴Department of Neurology, Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu, China
• ⁵Department of Nursing, Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu, China

Background: Insulin resistance (IR) is linked to an increased risk of neurological impairment following a stroke and may contribute to poor neurological prognosis in affected patients. The metabolic score for the insulin resistance index, shortened as the METS-IR, generally serves as a surrogate index for IR. However, its association with the severity of neurological impairment in patients with severe cerebral infarction (CI) in neurological intensive care units (ICU) has not been fully established.

Methods: Patients with a diagnosis of CI, admitted to the neurological ICUs of Yangzhou University’s Affiliated Hospital and Xuzhou Medical University’s Affiliated Hospital, were included in the study. A multivariate logistic regression model and restricted cubic splines (RCS) were employed to explore the relationship between the METS-IR index and the severity of neurological impairment in these patients. The predictive capabilities of the METS-IR index and the triglyceride-glucose (TyG) index for outcome measures were compared through the ROC curve. Furthermore, a decision curve analysis was executed, and the integrated discrimination improvement (IDI) index was computed to evaluate the enhancements in predictive performance and clinical utility of various scoring systems with the inclusion of the METS-IR index. Subgroup analysis was conducted regarding age, BMI, and smoking status.

Results: The study ultimately included 504 participants. Adjusted logistic regression and RCS results showed that as the METS-IR index increases, the risk of neurological impairment in patients with severe CI consistently grows (P for overall = 0.0146, P-nonlinear: 0.0689). The METS-IR index’s predictive capability for neurological impairment (AUC = 0.669) was superior to that of the TyG index (AUC = 0.519).

Conclusion: From the study results, the METS-IR index can serve as an important predictor for neurological impairment in ICU patients with severe CI. It can aid in the identification and early intervention of neurological impairment in these patients.

The Foods That Fight Inflammation from the NYTimes

 Just in case your competent? doctor hasn't already given you protocols on this. Ask for specific amounts, not this guideline or suggestion crapola.

The Foods That Fight Inflammation

On the brain-boosting benefits of (healthy, productive) social engagement

The responsibility is your doctors to get you recovered well enough to socialize like you did before stroke. YOUR DOCTOR'S RESPONSIBILITY!

 

 On the brain-boosting benefits of (healthy, productive) social engagement

You have probably read about the many cognitive and brain benefits of social stimulation but, are all types of social engagement equal?

What matters most with social interactions – quantity or quality?

Neuroscientists have found that social engagement can benefit the brain by helping build cognitive and brain reserve and lower stress levels, especially when social interactions are healthy, cognitively complex and productive.

Not surprisingly, the effect of social engagement can be observed directly in the brain. A seminal study focused on the amygdala, a structure in the limbic system that plays a major role in our emotional responses. Researchers reasoned that the amygdala would be a likely candidate to be modified (via neuroplastic changes) by someone’s level of social engagement, measured the size of the amydgala of 60 adults, and assessed the size and complexity of their social networks (i.e., how many people they were in regular contact with and the number of different groups these contacts could be divided into). What they found is that the larger and the more complex a person’s social network actually was, the bigger their amygdala.

You may be wondering: does making more friends trigger growth in the amygdala over time, or do people with bigger amygdalas to begin with tend to make more friends?

Trying to distinguish causality vs. correlation, Oscar Ybarra and his colleagues at the University of Michigan randomly assigned participants to three groups: 1) a social group, in which the participants engaged in a discussion of a social issue for 10 minutes, 2) an intellectual activities group, in which the participants solved stimulating tasks (crossword puzzles and the like) for 10 minutes on their own, and 3) a control group, in which the participants watched a 10-minute clip of the television show Seinfeld. After they participated in the discussion, watched the clip, or solved the puzzles, the cognitive functioning of all the participants was assessed using a speed of processing task and a working memory (WM) task.

Results showed that people in the intellectual activities group did better in the WM task than people who merely watched a video. The same cognitive boost was observed in the social interaction group. And the study suggested, once more, that the average TV watcher would benefit from watching less TV and spending some of that “saved” time on cognitively stimulating activities. As Oscar Ybarra pointed out, “participating in a discussion involves using social cognitive processes, such as inferring what people are thinking, taking someone else’s perspective, memorizing and updating information, and inhibiting inappropriate emotions and behaviors” … which align very well with the need for novelty, variety, and challenge discussed in previous chapters.

From a different perspective, Laura Fratiglioni and colleagues have suggested that the relationship between social stimulation and brain health can also be explained via the stress hypotheses, which states that individuals with more social contacts have more opportunities to engage with other people and thus more opportunities to feel that they are well integrated and socially competent. This may increase their self-esteem and mood and lower their stress levels, which in turn would promote lifelong neuroplasticity and lower risks of cognitive decline. In other words, any positive, stress-reducing social relationship can be beneficial, regardless of whether or not it involves a high level of cognitive complexity.

In essence, then, scientists have found that more social engagement is often better than less, especially via interactions that involve stress-reducing support, novelty, variety, and challenge. Whatever it is we are already doing, there are always new opportunities we could explore.

Through our workplaces and careers–including those difficult transitions: Given extended longevity and rapidly evolving workplaces, our work environment/s play a very important role in our lifelong brain health, providing (or not) brain-boosting benefits through decades of work–and social interactions at work. It is also key to highlight the importance of managing stress and anxiety during career transitions, so we can frame them as opportunities to socialize and grow and not as threats. The longer we live, the more crucial this is going to be: recent studies looking at the United States and 12 other European countries have found that the earlier people retire, the more quickly their memory declines.

Through social groups and volunteering: Another way to connect with people regularly is to join groups, such as a sports or book club, a religious group, or volunteering (at a library, hospital, school, etc.), with a shared purpose. On top of the general brain benefits from social engagement each activity will come with its own specific benefits. A hiking club or a tennis club adds physical health benefits, while a book club adds intellectual stimulation. For example, when Michelle Carlson and her colleagues at the Johns Hopkins Bloomberg School of Public Health conducted a brain imaging study to evaluate the effects of Experience Corps, a program that helps seniors partner with schools to help children improve academically and behaviorally, they found that participants showed improved executive functions compared to controls, as well as increased activity in the part of the brain that supports these functions (the prefrontal cortex).

Remember the Oh, the Places You’ll Go! book and message by Dr. Seuss?

We should add: Oh, the People You’ll Meet!

– This is an adapted excerpt from The SharpBrains Guide to Brain Fitness: How to Optimize Brain Health and Performance at Any Age by Alvaro Fernández Ibáñez and Dr. Elkhonon Goldberg.

To Learn More:

• What are cognitive abilities and how to boost them?
• Lifestyle matters: What we can do in 2024 to optimize cognition and life
• Next Chapter Accelerator For Purpose-Driven Women Leaders: We are proud to collaborate with the WILD Network to offer a new cohort-based six-month program for executives with 20+ year high impact careers ready to chart their path forward.
• Book provides practical guidance to rebalance our lifestyles and build Cognitive Reserve

Movement-dependent stroke recovery: A systematic review and meta-analysis of TMS and fMRI evidence

 In the 16 years since this came out has your COMPETENT? DOCTOR come up with EXACT PROTOCOLS to get you recovered? NO? So you still don't have a functioning stroke doctor after years of stroke research?

Movement-dependent stroke recovery: A systematic review and meta-analysis of TMS and fMRI evidence

2008, Neuropsychologia

Lorie G. Richards 1,2 , Kim C. Stewart 4 , Michelle L. Woodbury 1,2 , Claudia Senesac 1,3 , and James H. Cauraugh 1,4 1 North Florida/South Georgia Veterans Health System 2 Occupational Therapy 3 Physical Therapy 4 Applied Physiology and Kinesiology, University of Florida  

 

Abstract 

 

  Evidence indicates that experience-dependent cortical plasticity underlies post-stroke motor recovery of the impaired upper extremity. Motor skill learning in neurologically intact individuals is thought to involve the primary motor cortex, and the majority of studies in the animal literature have studied changes in the primary sensorimotor cortex with motor rehabilitation. Whether changes in engagement in the sensorimotor cortex occur in humans after stroke currently is an area of much interest. The present study conducted a meta-analysis on stroke studies examining changes in neural representations following therapy specifically targeting the upper extremity to determine if rehabilitation-related motor recovery is associated with neural plasticity in the sensorimotor cortex of the lesioned hemisphere. Twenty-eight studies investigating upper extremity neural representations (e.g., TMS, fMRI, PET, or SPECT) were identified, and 13 met inclusion criteria as upper extremity intervention training studies. Common outcome variables representing changes in the primary motor and sensorimotor cortices were used in calculating standardized effect sizes for each study. The primary fixed effects model meta-analysis revealed a large overall effect size (E.S. = 0.84, S.D. = 0.15, 95% C.I. = 0.76 – 0.93). Moreover, a fail-safe analysis indicated that 42 null effect studies would be necessary to lower the overall effect size to an insignificant level. These results indicate that neural changes in the sensorimotor cortex of the lesioned hemisphere accompany functional paretic upper extremity motor gains achieved with targeted rehabilitation interventions.

Brain Waves Can Be Manipulated While We Dream, And It Could Help Treat Dementia

 Will your competent? doctor follow this up for possible treatment of your likely dementia post stroke?

With your elevated chances of dementia post stroke,  your competent? doctor is responsible for preventing that! Have they taken on that responsibility? Or are they DOING NOTHING?

With your chances of getting dementia post stroke you need solutions. YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING 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 

 

The latest here:

Brain Waves Can Be Manipulated While We Dream, And It Could Help Treat Dementia

Scientists in the UK have manipulated two prominant types of brain wave while volunteers slept, in an effort to develop better tools to study critical neurological activities.

The waves, referred to as alpha and theta oscillations, are strongly associated with resting and relaxing states, including the Rapid Eye Movement (REM) stage of unconsciousness.

Named for the jerking motion of our eyes while in this stage of sleep, REM coincides with the appearance of our most vivid dreams. The stage is also considered to play an important role in memory consolidation and honing cognition, making any brain wave activity an attractive target for scientists.

"Brain oscillations assist in the working of the brain and how it learns and retains information," says neuroscientist Valeria Jaramillo, from the University of Surrey.

"Brain oscillations during REM sleep have been implicated in memory functions – however, their exact role remains largely unclear."

A process called closed-loop auditory stimulation (CLAS) has been successfully used to enhance or disrupt brain waves in non-REM sleep, precisely targeting the ebb and flow of brain waves via sounds delivered through headphones.

The process had rarely been applied to sleepers outside of this state, so researchers from the University of Surrey tested the method on volunteers to determine if it might also apply to waves produced during REM.

Sounds were used to target different types of oscillations. (Jaramillo et al., SLEEP, 2024)

In tests involving 18 participants, the researchers changed both the speed and strength of the brain waves as measured through electrodes on the skull.

Alpha (around 8 to 12 Hertz) and theta (around 4 to 8 Hertz) oscillations typically flow through the brain's frontal region while we're in a relaxed state, such as when we're dozing or deciding whether to get out of bed to start the day.

In fact, these brain waves are pretty similar whether we're awake or in REM sleep. We know that brain waves, pulses of electrical activity triggered by neurons, help in the healthy functioning of the brain. If we can control them to an extent, that's potentially helpful in making sure the brain is working as it should – and in slowing the rate of degeneration associated with dementia.

"Using sound stimulation to change brain oscillations whilst a person sleeps shows therapeutic promise," says University of Surrey neuroscientist Ines Violante.

"There is currently no cure for dementia, only medication that can slow down disease progression or temporarily help a person with their symptoms, so it is important that we think innovatively to develop new treatment options."

A lot more research will be needed to show this can actually have a therapeutic effect on dementia, but scientists have already shown that the symptoms of dementia – trouble with memory and cognitive abilities – often coincide with the slowing of brain wave oscillations, which is something we might now be able to influence.

"This could pave the way for a new approach on how to treat patients with dementia, as the technique is non-invasive and undertaken whilst they are asleep, lessening the disruption to their lives and enabling us to be more targeted in our approach," says Derk-Jan Dijk, a professor of sleep and physiology at the University of Surrey.

The research has been published in SLEEP.

Gut Inflammation Linked to Alzheimer's Disease, Once Again

 What is your competent? doctor doing with this to prevent your likely dementia post stroke?

With your elevated chances of dementia post stroke,  your competent? doctor is responsible for preventing that! Have they taken on that responsibility? Or are they DOING NOTHING?

With your chances of getting dementia post stroke you need solutions. YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING 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 

 

The latest here:

Gut Inflammation Linked to Alzheimer's Disease, Once Again

Researchers connecting pieces of the massive Alzheimer's puzzle are closer to slotting the next one in place, with yet another link between our guts and brain.

Animal studies have demonstrated Alzheimer's can be passed on to young mice through a transfer of gut microbes, confirming a link between the digestive system and the health of the brain.

A 2023 study adds further support to the theory that inflammation could be the mechanism through which this occurs.

"We showed people with Alzheimer's disease have more gut inflammation," University of Wisconsin psychologist Barbara Bendlin said when the research was published, "and among people with Alzheimer's, when we looked at brain imaging, those with higher gut inflammation had higher levels of amyloid plaque accumulation in their brains."

University of Wisconsin pathologist Margo Heston and an international team of researchers tested for fecal calprotectin, a sign of inflammation, in stool samples of 125 individuals recruited from two Alzheimer's prevention cohort studies.

Participants underwent several cognitive tests on enrollment, as well as interviews on family history and tests for a high-risk Alzheimer's gene. A subset of participants took clinical tests for signs of amyloid protein clumps, a common indication that pathology responsible for the neurodegenerative condition was underway.

While levels of calprotectin were generally higher in older patients, it was even more pronounced in those with Alzheimer's characteristic amyloid plaques.

Levels of other Alzheimer's disease biomarkers also increased with levels of inflammation, and memory test scores dropped with higher calprotectin too. Even the participants without a diagnosis of Alzheimer's had poorer memory scores with higher levels of calprotectin.

"We can't infer causality from this study; for that, we need to do animal studies," cautioned Heston.

A laboratory analysis has previously shown gut bacteria chemicals can stimulate inflammatory signals in our brains. What's more, other studies have found increased gut inflammation in patients with Alzheimer's compared to controls.

Heston and colleagues suspect microbiome changes trigger gut changes that lead to system-wide inflammation. This inflammation is mild but chronic, causing subtle, incremental damage that eventually interferes with the sensitivity of our body's barriers.

"Increased gut permeability could result in higher blood levels of inflammatory molecules and toxins derived from gut lumen, leading to systemic inflammation, which in turn may impair the blood-brain barrier and may promote neuroinflammation, and potentially neural injury and neurodegeneration," said University of Wisconsin bacteriologist Federico Rey.

The researchers are now testing mice to see if diet changes associated with increased inflammation can trigger the rodent version of Alzheimer's.

Despite decades of research there's still no effective treatment for the millions of people with Alzheimer's worldwide. But with a greater understanding of the biological processes, scientists are getting closer, piece by piece.

This research has been published in Scientific Reports.

An earlier version of this article was published in January 2024.

SGLT2 Inhibitor Use Associated With Reduced Risk of Dementia, Parkinson Disease

 With your increased risk of Parkinsons and dementia post stroke, what is your doctor's position on this for off-label use? Does your competent? doctor even know and think about these issues?

With your elevated chances of dementia post stroke,  your competent? doctor is responsible for preventing that! Have they taken on that responsibility? Or are they DOING NOTHING?

With your chances of getting dementia post stroke you need solutions. YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING 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 

Parkinson’s Disease May Have Link to Stroke March 2017

 

The latest here:

SGLT2 Inhibitor Use Associated With Reduced Risk of Dementia, Parkinson Disease

Use of sodium-glucose cotransporter-2 (SGLT2) inhibitors among patients with type 2 diabetes significantly reduced the risk of neurodegenerative disorders, independent of various factors including comorbidities and bioclinical parameters, according to a nationwide population-based study published in the journal Neurology.

“We know that these neurodegenerative

click to scroll down to continue reading the article

article continues here

diseases like dementia and Parkinson’s disease are common and the number of cases is growing as the population ages, and people with diabetes are at increased risk of cognitive impairment, so it’s encouraging to see that this class of drugs may provide some protection against dementia and Parkinson’s disease,” said Minyoung Lee, MD, Yonsei University College of Medicine, Seoul, South Korea.

The retrospective study looked at people with type 2 diabetes who started diabetes medication between 2014 and 2019 in South Korea. Patients taking SGLT2 inhibitors were matched with patients taking other oral diabetes drugs. Those taking the SGLT2 inhibitors were followed for an average of 2 years and those taking the other drugs were followed for an average of 4 years.

Among the 358,862 participants with an average age of 58, a total of 6,837 people developed dementia or Parkinson’s disease during the study.

For Alzheimer’s disease, the incidence rate for people taking SGLT2 inhibitors was 39.7 cases per 10,000 person-years, compared with 63.7 cases for those taking other diabetes drugs. For vascular dementia, the incidence rate was 10.6 cases per 10,000 versus 18.7, respectively. For Parkinson’s disease, the incidence rate for those taking the SGLT2 inhibitors was 9.3 cases per 10,000, compared with 13.7 for those taking the other drugs.

After researchers adjusted for other factors that could affect the risk of dementia or Parkinson’s disease, such as complications from diabetes and medications, they found that SGLT2 inhibitor use was associated with a 20% reduced risk of Alzheimer’s disease and a 20% reduced risk of Parkinson’s disease. Those taking SGLT2 inhibitors had a 30% reduced risk of developing vascular dementia.

“The results are generally consistent even after adjusting for factors like blood pressure, glucose, cholesterol, and kidney function,” Dr. Lee said. “More research is needed to validate the long-term validity of these findings.”

He noted that since participants were followed for less than 5 years at the most, it’s possible that some participants would later develop dementia or Parkinson’s disease.

Reference: https://www.neurology.org/doi/10.1212/WNL.0000000000209805

SOURCE: American Academy of Neurology

The Effects of Prayer and Meditative Practices on Neuroplasticity

 Meditation has been known for a long time to be beneficial to stroke recovery. Hasn't your competent? doctor created a protocol on it yet? So an incompetent doctor for over a decade and your stroke hospital still hasn't fired them?

• meditation (60 posts to January 2012)

The Effects of Prayer and Meditative Practices on Neuroplasticity

Sep 2, 2024

—

by

astrastem

in Research Journal

By Masooma Hyder Baig

Throughout our lives, our brains are constantly changing and adapting to our environments. Neuroplasticity is our brain’s ability to reorganize itself by continually forming new neural connections at all life stages: good and bad. This article explores how prayer and meditative practices act as internal stimuli that impact these abilities, where research highlights the changes in brain function.

Understanding Neuroplasticity

Neuroplasticity is defined as the ability of the nervous system to change its activity in response to intrinsic or extrinsic factors by reorganizing its structure, functions, or connections (Mateos-Aparicio and Rodríguez-Moreno, 2019). This often involves the formation of new neural pathways, the strengthening of existing ones, and/or pruning of unused connections. Thus, neuroplasticity is fundamental in determining our ability to learn, memorize, and even recover from brain injuries. It enables the brain to compensate for decreased function and simultaneously maximizes the remaining function if there is damage. 

Meditation and Brain changes

Meditation can refer to several mindful practices involving the individual training themselves to focus on a present moment, object, or situation, allowing them to feel peace and connected to themselves. Studies have shown that long-term meditation practices have been linked to increased cortical thickness in certain brain areas. Primarily, areas related to attention, the perception of the body’s internal conditions, and sensory processing that enable positive habits and practices in individuals. However, one should consider factors like age, sex, genetics, and health status which may also influence cortical thickness alongside the effects meditation may have  (Lazar et al., 2005).

Meditation has also been linked to larger hippocampal volumes in the right hemisphere of the brain (Luders et al., 2009). The hippocampus has numerous functions, that are proven to be vital in learning and memory, emotional behavior, and spatial navigation (Dhikav and Anand, 2012). Thus, it suggests these findings explain why meditators maintain emotional stability and form positive emotions.

Prayer

Prayer encompasses many different practices which can include meditation, deep thought, and/or certain physical movements to demonstrate one’s submission to a superior being or particular way of life. Newburg’s study on the Franciscan nuns performing a contemplative prayer that involved pondering over a Bible phrase demonstrated increased frontal lobe activity and decreased parietal lobe activity (Newberg et al., 2003). The frontal lobe is associated with focused attention, emotional regulation, and decision-making (Kinaan Javed and Forshing Lui, 2019) while the parietal lobe is associated with spatial awareness and sensory perception (Vandenberghe et al., 2001). A case series study on Islamic prayer observed similar results with decreased parietal lobe activity. However, decreased frontal activity was also documented. Newburg suggested that this was due to the centering prayer of the nuns being similar to meditation, where participants were actively focused on a particular religious phrase (Newberg et al., 2015). These different practices correlate with the feeling of submission individuals may experience when in prayer, with anecdotal accounts highlighting how many feel less attached to their current surroundings and more aligned with a presence they assume to be greater than them: providing a sense of comfort during prayer. 

Conclusion

To summarise, prayer and meditation both have profound effects on neuroplasticity. Regular meditation enhances cortical thickness and hippocampal volume contributing to increased attention, emotional stability, and better memory. Prayer produces similar effects to invoking different brain responses where increased frontal lobe activity may be observed. Especially in prayer practices similar to meditation that require deep focus. Other prayer practices that emphasize movement may observe decreased frontal lobe activity as one works to submit to God. Yet, these different practices reiterate the idea of relinquishing control, allowing individuals to find peace. Thus, it is evident that through prayer and meditation, one can reap both spiritual and cognitive benefits: an area of modern neuroscience proving to be abundant in further exploration.

Reference list

Quantifying Nonuse in Chronic Stroke Patients: A Study Into Paretic, Nonparetic, and Bimanual Upper-Limb Use in Daily Life

 Research into nonuse is absolutely fucking useless!

I absolutely hate these pontifications on nonuse. Solve the damn problem of dead brain rehab and this nonuse problem goes away. SOLVE THE CORRECT PROBLEM!

Damn it all, it is NOT learned nonuse. It is the actual inability to use it because of dead neurons. If you had dead brain rehab protocols, this fake learned nonuse idea would cease to exist!

Quantifying Nonuse in Chronic Stroke Patients: A Study Into Paretic, Nonparetic, and Bimanual Upper-Limb Use in Daily Life

2012, Archives of Physical Medicine and Rehabilitation

Marian E. Michielsen, MSc†, Ruud W. Selles, PhD, Henk J. Stam, MD, PhD Gerard M. Ribbers, MD, PhD, Johannes B. Bussmann, PhD ABSTRACT. Michielsen ME, Selles RW, Stam HJ, Ribbers GM, Bussmann JB. Quantifying nonuse in chronic stroke pa- tients: a study into paretic, nonparetic, and bimanual upper- limb use in daily life. Arch Phys Med Rehabil 2012;xx:xxx. Objective: To quantify uni- and bimanual upper-limb use in patients with chronic stroke in daily life compared with healthy controls. Design: Cross-sectional observational study. Setting: Outpatient rehabilitation center. Participants: Patients with chronic stroke (n=38) and healthy controls (n=18). Intervention: Not applicable. Main Outcome Measures: Upper-limb use in daily life was measured with an accelerometry-based upper-limb activity monitor, an accelerometer based measurement device. Uni- manual use of the paretic and the nonparetic side and bimanual upper-limb use were measured for a period of 24 hours. Out- comes were expressed in terms of both duration and intensity. Results: Patients used their unaffected limb much more than their affected limb (5.3h vs 2.4h), while controls used both limbs a more equal amount of time (5.4h vs 5.1h). Patients used their paretic side less than controls used their nondominant side and their nonparetic side more than controls their dominant side. The intensity with which patients used their paretic side was lower than that with which controls used their nondomi- nant side, while that of the nonparetic side was higher than that of the dominant side of controls. Finally, patients used their paretic side almost exclusively in bimanual activities. During bimanual activities, the intensity with which they used their affected side was much lower than that of the nonaffected side. Conclusion: Our data show considerable nonuse of the pa- retic side, both in duration and in intensity, and both during unimanual and bimanual activities in patients with chronic stroke. Patients do compensate for this with increased use of the nonparetic side. Key Words: Ambulatory monitoring; Motor activity; Reha- bilitation; Stroke; Upper extremity. © 2012 by the American Congress of Rehabilitation Medicine F IFTY TO 70% OF PATIENTS with stroke suffer from long-term motor deficits of the upper limb, 1 with a de- creased use of the paretic upper extremity in daily life. 2 Be- cause this latter may have a great impact on the manner in which a patient is able to participate in daily life activities, maximizing purposeful use of the upper extremity in daily life is a key factor in motor rehabilitation following stroke. While it is clear that a decreased motor capacity of the paretic arm influences the use of both extremities, the exact changes in upper-limb use following stroke are not yet fully understood. Regarding the paretic upper extremity, many stud- ies have shown that there is no 1-on-1 relation between motor impairment and functional use. 3,4 This may be related to the phenomenon of learned nonuse, 5 which describes how patients will have “learned” not to use the paretic side to its full capacity. 6 Brain injury causes structural damage to motor path- ways as well as depression of neural excitability near the lesion. Decreasing activity of the upper extremity leads to a further reduction in excitability and as such starts a vicious circle of decreasing excitability and decreasing activity. 7 Even less is known about the consequences of stroke on the nonparetic side. Motor performance of the nonparetic side may be impaired compared with that in healthy subjects, showing, for instance, decreased speed and consistency of performance. 8 In addition, it has been shown that patients with acute stroke have a more reduced use of the nonparetic side in daily life than do healthy subjects. 9 On the other hand, it is generally assumed that poststroke the nonparetic side will be used more to com- pensate for the decreased use of the paretic side. However, to our knowledge, this has not been investigated in patients with chronic stroke. Overall many questions on techniques to optimize the func- tion of the paretic extremity after stroke still need to be an- swered. The optimal rehabilitation technique is still not de- fined, and different approaches in reducing upper-extremity paresis are distinguished. 7 Several therapies have been devel- oped to improve the use of the nonparetic arm in daily life. For example, constraint-induced movement therapy (CIMT), 10,11 or forced use, 12 reported as a beneficial treatment option for motor recovery of the arm, 13 prevents the use of the nonparetic upper limb and aims to counterbalance the learned nonuse. CIMT is an augmentative technique, 7 a high-intensity, uni- manual training aiming to counterbalance the vicious circle of decreasing excitability and decreasing activity. Furthermore, CIMT has aspects of task-specific exercising. Bilateral training programs have also been developed, for example, with rhythmic  auditory cueing. 14 To evaluate and understand the effects of upper-extremity training in daily life conditions, detailed insight is needed in unimanual and bimanual function of the arms in daily life conditions. This is the topic of the current article. Several studies have included the measurement of upper- limb use in daily life. For example, Taub, 11 Mark, 15 and Wolf 5 and colleagues used the Motor Activity Log (MAL) in their studies. However, although validated against an objective mea- sure, 16 the MAL still is a subjective instrument that focuses on how well and how much patients use their most impaired arm in a defined category of activities, and the MAL does not include data on the amount of use of the nonimpaired arm and bilateral use. Another method for assessing upper-limb use in a home setting is provided by accelerometers and other portable devices providing the opportunity to assess how much patients with stroke use their upper limbs in daily life for longer periods. 2 However, so far, studies using these devices assessed only the upper-limb use overall and not in detail. For example, many studies express actual upper-limb use only as a ratio between the use of the affected and the use of the unaffected side, 17 thus omitting information about usage times of the paretic side and the nonparetic side separately. Second, current devices do not differentiate between arm movements resulting from general body movements such as walking and arm move- ments during sitting and standing. Third, most measurement devices cannot differentiate between the duration of use and the intensity of use, and finally, most devices cannot or do not differentiate between unilateral and bilateral usage of the arms. The aim of the present study was to quantify uni- and bimanual upper-limb use in patients with chronic stroke in daily life and compare this with healthy controls. By using an accelerometry- based upper-limb activity monitor, 18 we were able to give an insight into both duration and intensity of upper-limb use and to discriminate between upper-limb movements caused by whole- body movements and movements independent of whole-body movements, thus providing an insight into the amount of func- tional and purposeful upper-limb use in daily life conditions.

 

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Blood–Brain Barrier Disruption and Imaging Assessment in Stroke

 My God, we've known of this problem forever! You're fired for not even trying to solve it, including your mentors and senior researchers! A vast amount of dead wood needs to be removed in stroke, put me in charge and there will be a bloodbath of firing! There are no excuses for such incompetency!

• blood brain barrier (162 posts to March 2011)

Blood–Brain Barrier Disruption and Imaging Assessment in Stroke

• Yuchen Liang,
• Yueluan Jiang,
• Jiaxin Liu,
• Xuewei Li,
• Xinyue Cheng,
• Lei Bao,
• Hongwei Zhou &
• Zhenni Guo 

• 23 Accesses

• Explore all metrics

Abstract

Disruption of the blood–brain barrier (BBB) is an important pathological hallmark of ischemic stroke. Blood–brain barrier disruption (BBBD) is a consequence of ischemia and may also exacerbate damage to brain parenchyma. Therefore, maintaining BBB integrity is critical for the central nervous system (CNS) homeostasis. This review offers a concise overview of BBB structure and function, along with the mechanisms underlying its impairment following a stroke. In addition, we review the recent imaging techniques employed to study blood–brain barrier permeability (BBBP) in the context of ischemic brain injury with the goal of providing imaging guidance for stroke diagnosis and treatment from the perspective of the BBBD. This knowledge is vital for developing strategies to safeguard the BBB during cerebral ischemia.

Signaling roles of sphingolipids in the ischemic brain and their potential utility as therapeutic targets

 But what about this problem with sphingolipids? Hasn't your competent? doctor initiated research to solve this? NO? So you DON'T have a functioning stroke doctor, do you?

Sphingolipids Contribute to Human Atherosclerotic Plaque Inflammation May 2016

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Signaling roles of sphingolipids in the ischemic brain and their potential utility as therapeutic targets

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https://doi.org/10.1016/j.nbd.2024.106682

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Highlights

• •
  Ischemic stroke leads to dysregulation of the sphingolipid metabolism.
• •
  Ceramide accumulation occurring post-stroke deteriorates injury and inhibiting its metabolizing enzymes enhances recovery.
• •
  S1P receptor modulation influences vascular function and immune cell trafficking post-stroke.
• •
  Sphingolipids are important for the formation and release of extracellular vesicles that stimulate brain remodeling.

Abstract

Sphingolipids comprise a class of lipids, which are composed of a sphingoid base backbone and are essential structural components of cell membranes. Beyond their role in maintaining cellular integrity, several sphingolipids are pivotally involved in signaling pathways controlling cell proliferation, differentiation, and death. The brain exhibits a particularly high concentration of sphingolipids and dysregulation of the sphingolipid metabolism due to ischemic injury is implicated in consecutive pathological events. Experimental stroke studies revealed that the stress sphingolipid ceramide accumulates in the ischemic brain post-stroke. Specifically, counteracting ceramide accumulation protects against ischemic damage and promotes brain remodeling, which translates into improved behavioral outcome. Sphingomyelin substantially influences cell membrane fluidity and thereby controls the release of extracellular vesicles, which are important vehicles in cellular communication. By modulating sphingomyelin content, these vesicles were shown to contribute to behavioral recovery in experimental stroke studies. Another important sphingolipid that influences stroke pathology is sphingosine-1-phosphate, which has been attributed a pro-angiogenic function, that is presumably mediated by its effect on endothelial function and/or immune cell trafficking. In experimental and clinical studies, sphingosine-1-phosphate receptor modulators allowed to modify clinically significant stroke recovery. Due to their pivotal roles in cell signaling, pharmacological compounds modulating sphingolipids, their enzymes or receptors hold promise as therapeutics in human stroke patients.

Keywords

Ceramide

Sphingomyelin

Sphingosine-1-phosphate

Ischemic stroke

1. Introduction

1.1. Functional roles of sphingolipids

Sphingolipids are enriched in cellular membranes, but their roles extend far beyond their function as mere structural elements. In comparison to other organs such as heart, spleen and liver, the concentration of the sphingolipids is particularly high in the brain and dysregulation of the sphingolipid metabolism is implicated in neurodegenerative disorders (Muralidharan et al., 2021; Piccinini et al., 2010).

Ceramide is structurally one of the simplest sphingolipid and is considered to be the most studied one. It consists of a sphingoid base, which is linked via an amide bond to a fatty acid (Alonso and Goni, 2018). Ceramide signaling is activated by several stress stimuli such as radiation, UV light or inflammatory cytokines like tumor necrosis factor (TNF) (Chatterjee and Wu, 2001; Martinez et al., 2012; Vit and Rosselli, 2003). Ceramide-rich platforms on cell membranes enable protein oligomerization in order to amplify transmembrane signaling (Stancevic and Kolesnick, 2010). These platforms are critically involved in apoptotic events. CD95 clustering on ceramide-rich platforms for instance precedes death-inducing signaling complex (DISC) formation and caspase activation (Grassme et al., 2003). In view of the importance of ceramide for pro-apoptotic pathways, pharmacological inhibition of ceramide formation was shown to increase cell survival under pathological conditions (Gulbins et al., 2013). More complex ceramide derivates such as galactosylceramide are essential components of myelin sheaths that insulate axons enabling fast transmission of electric impulses (Zoller et al., 2008). Galactosylceramide deficiency causes demyelination which consequently leads to severe impairment of motor coordination (Coetzee et al., 1996; Zoller et al., 2005), which again emphasizes the functional relevance of sphingolipids.

After binding to specific G protein-coupled receptors, bioactive sphingolipids such as sphingosine-1-phosphate (S1P) function as signaling molecules and stimulate the activation of complex cascades, which govern cellular processes such as cell migration and angiogenesis (Blaho and Hla, 2014). Treatment with S1P increases vascular density and further amplifies VEGF-induced angiogenesis (Lee et al., 1999a). S1P also stimulates the assembly of adherens junctions on endothelial cells by activating Rac/ Rho signaling (Lee et al., 1999a). Further, S1P has been attributed an anti-apoptotic effect (Lee et al., 1999a).

Sphingolipids are further implicated in cellular mechanisms that control the endocytic trafficking machinery. Release of exosomes can be reduced by inhibition of neutral sphingomyelinase (NSM)-mediated sphingomyelin hydrolysis using GW4869, spiroepoxide or glutathione (Trajkovic et al., 2008). Disturbed exosome release due to reduced ceramide likely occurs because ceramide-enriched domains facilitate the sorting of cargo destined for exosomal release into multivesicular bodies and inhibition of NSM substantially reduces the amount of specific cargo within the endosomal lumen (Trajkovic et al., 2008). Exosomes that are generated via this endosomal sorting complexes required for transport (ESCRT)-independent pathway typically exhibit a high ceramide content (Trajkovic et al., 2008). Moreover, hydrolysis of sphingomyelin leads to formation of early endocytic intermediates to which sphingosine kinase-1 is recruited, the enzyme that catalyzes phosphorylation of sphingosine to S1P (Shen et al., 2014). The importance of sphingosine kinase-1 for endosomal recycling is depicted by experiments showing that its knockdown causes accumulation of internalized transferrin, which is indicative for endosomal recycling defects (Shen et al., 2014). Further, sphingolipids may alter lysosomal function. Accumulation of unmetabolized sphingolipids results in severe pathological conditions as genetic deficiency of specific enzymes that regulate the sphingolipid metabolism are causative for lysosomal storage disorders that lead to dysfunctional lysosomes and impaired autophagic flux (Carsana et al., 2022; Platt et al., 2012). Niemann-Pick disease type-A, for example, is a severe neurodegenerative disorder associated with early childhood mortality and is caused by inherited acid sphingomyelinase (ASM) deficiency, which leads to accumulation of sphingomyelin in lysosomes (Horinouchi et al., 1995).

Given the importance of sphingolipids for pivotal cellular processes, this review aims to depict the signaling roles of prominent sphingolipids, namely ceramide, sphingomyelin and S1P, for pathological events following ischemic stroke. Another focus of this review is to outline how sphingolipids may serve as targets for potential therapeutic interventions.

 

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