Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 32,715 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
Will your competent? doctor put this into a testing protocol, so if problems are found, that EXACT DEMENTIA PREVENTION PROTOCOL WILL BE USED?
Do you
prefer your doctor, hospital and board of director's incompetence NOT
KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand
action!
OH NO! your doctor KNOWS NOTHING AND DOES NOTHING!
We are providing an unedited version of this manuscript to give early access to its findings.
Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.
Abstract
Background
Early detection of Alzheimer’s disease (AD) requires biomarkers sensitive to pre-neurodegenerative dysfunction. Task-evoked ocular responses index arousal‑based gain and the stability of executive timing, but their relationship to brain structure, especially within AD‑signature cortex; regions that thin early in AD, remains poorly characterized. We tested whether ocular metrics map onto cortical thickness and subcortical volumes, and whether brain–ocular coupling differs between cognitively normal (CN) adults and those with mild cognitive impairment (MCI).
Methods
Participants with MCI (n = 212) and CN controls (n = 516) completed an interleaved prosaccade–antisaccade task; binocular pupil diameter and eye movements were time‑locked to cue and target onsets to derive pupil amplitude/variability and saccade metrics. Region‑wise linear mixed‑effects models quantified brain–ocular coupling to cortical thickness and subcortical volumes and tested group (CN vs. MCI) differences in coupling slopes.
Results
Diagnosis‑independent analyses showed that saccade latency variability (Latency SD) and pupil amplitude/variability exhibited robust region‑dependent coupling across cortical and subcortical volumes, whereas mean saccadic latency and pupil timing measures displayed no reliable spatial pattern.
Diagnostic effects were modest and spatially selective but directionally opposite across modalities. For saccades, CN displayed positive thickness–variability slopes in frontal, cingulate, and insular cortices whereas MCI showed negative or near‑zero slopes. In the AD‑signature cortex, this inversionn CN(+)/MCI(−/0) was localized specifically to the supramarginal gyrus (Δβ≈–0.026). Subcortical volumes showed no significant diagnostic differences. For pupils, MCI showed more positive pupil–thickness coupling than CN within global cortex, most prominently in temporal, parietal, and insular regions, and within AD‑signature cortex this selective increase localized to medial temporal cortex (Δβ = 0.042) and to supramarginal gyrus (Δβ = 0.030); subcortical diagnostic differences were not significant after correction.
Conclusions
Task‑evoked ocular signals yield two complementary, region‑specific readouts of early Alzheimer‑relevant dysfunction. Pupil amplitude and variability reflect the strength of phasic, arousal‑linked responses arising from coordinated brainstem control hubs and show selective increases in MCI within medial temporal and temporoparietal regions that are vulnerable early in Alzheimer’s disease. Saccadic latency variability indexes loss of timing stability, revealing a thickness–stability inversion—positive in controls, absent or negative in MCI—that localizes to supramarginal gyrus within attention and executive‑control networks. Effects are modest and spatially circumscribed, positioning ocular measures as scalable, adjunct biomarkers of prodromal disease.
How is your competent? doctor GUARANTEEING that your sleep protocol will do this?
Do you
prefer your doctor, hospital and board of director's incompetence NOT
KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand
action!
OH NO! your doctor KNOWS NOTHING AND DOES NOTHING!
Let's see how long your doctor has been working on this and WHAT HAS BEEN ACCOMPLISHED!
brain clearing(10 posts to August 2012) Do you have one of the incompetent? doctors or a good one? A good one will have an EXACT SLEEP PROTOCOL!
Summary: We’ve long known that sleep “washes” the brain, but we’ve never been able to see it happen in real-time without invasive dyes—until now. Researchers have developed an ultrafast MRI technique that tracks the movement of brain fluids non-invasively.
The study shows that during sleep, the brain’s “operating logic” actually reverses. Instead of neurons controlling blood flow, slow vasomotor waves (vascular pulsations) begin to drive both fluid movement and electrical activity, specifically in the sensory cortex, to flush out metabolic waste.
Key Facts
Contrast-Free Tracking: The new “ultrafast MRI” method tracks water molecules in cerebrospinal fluid directly, requiring only a five-minute scan with no injected chemicals.
The Pulse Shift: During sleep, respiratory and vasomotor pulsations (the “cleaning” waves) speed up, while cardiac pulsations (heartbeat waves) slow down, allowing for more efficient “filtering” of brain tissue.
The Reverse Control: In an awake brain, neurons tell blood where to go. During sleep, the vascular waves take the lead, influencing the neurons and pushing fluid through the posterior brain regions to clear waste.
Wearable Future: Beyond MRI, the team developed wearable sensors that can track these cleansing rhythms in a standard bed, opening the door for routine monitoring of the aging brain.
Source: University of Oulu
Sleep helps the brain to cleanse itself – and now this process can be measured in humans entirely non-invasively.
Researchers at the University of Oulu have developed a method that allows the increased movement of brain fluids during sleep to be tracked quickly and safely, without the need for injected contrast agents.
Slow vasomotor waves below 0.1 hertz become the primary drivers of brain fluid circulation during deep sleep. Credit: Neuroscience News
The brain’s cleansing mechanism is driven by pulsations, natural bodily rhythms that move blood and cerebrospinal fluid through the brain. These pulsations fall into three main categories: cardiovascular pulsations generated by the heartbeat in arteries, respiratory pulsations affecting veins and cerebrospinal fluid spaces, and slow vasomotor waves in the walls of blood vessels. Previous research has shown that both these pulsations and the brain’s waste clearance are enhanced during sleep.
These pulsations drive the flow of fluids through brain tissue, helping to remove metabolic waste. When this fluid circulation weakens, waste products may begin to accumulate in the brain. The phenomenon has been linked to memory disorders, among other conditions, but has been difficult to measure directly in humans.
Fluid flow accelerates during sleep
An ultrafast magnetic resonance imaging method developed by the University of Oulu’s functional neuroimaging research group (OFNI) now makes it possible to measure brain fluid circulation directly by tracking the movement of water molecules in cerebrospinal fluid. The scan takes only about five minutes and does not require contrast agents.
The researchers found that the behaviour of brain pulsations changes markedly during sleep. The propagation of respiratory and vasomotor pulsations—both of which promote brain-cleansing fluid circulation—speeds up, while cardiac pulsations slow down. This shift is thought to reflect more efficient water filtration in brain tissue, alongside a slowing of arterial pulse waves as blood vessels dilate and blood pressure decreases during sleep.
Brain control dynamics partly reverse during sleep
The studies also revealed a shift in the brain’s fundamental operating logic during sleep. When awake, electrical activity in neurons modulates blood flow and fluid movement: neural activation comes first, followed by increased blood flow. During sleep, however, this relationship is no longer strictly one-directional.
“During sleep, vasomotor waves in particular, slow pulsations below 0.1 hertz, begin to locally influence not only fluid movement but also the brain’s electrical activity,” explains Professor Vesa Kiviniemi, who led the research.
This effect is especially pronounced in posterior brain regions, such as the sensory cortex. These same areas also show a marked increase in fluid flow through brain tissue, pointing to enhanced clearance.
New possibilities for monitoring the ageing brain
The findings are based on two recently published studies, one in Advanced Science and the other in The Proceedings of the National Academy of Sciences (PNAS). Both studies involved measurements in healthy volunteers.
According to the researchers, the results provide a more detailed understanding of how and where sleep enhances the brain’s cleaning processes.
It is already known that brain fluid circulation declines with age. “New measurement methods open up possibilities to monitor—and in the future potentially treat—age-related changes in brain fluid dynamics,” says Kiviniemi.
The research group has also developed wearable technology that can track brain electrical activity and blood flow during sleep without the need for MRI. The results correspond well with MRI measurements, suggesting that brain cleansing could in future be monitored more easily in clinical settings.
The team is now working on ways to enhance the fluid circulation and pulsation mechanisms that weaken with age, with the aim of slowing down the effects of ageing on the brain.
Key Questions Answered:
Q: Why can’t the brain just clean itself while I’m awake?
A: When you’re awake, your brain’s “electrical grid” is too busy processing information. The study shows that sleep triggers a specific “pulse shift”: your blood vessels dilate and slow down, which creates the physical space and pressure needed for cerebrospinal fluid to rush in and “scrub” the tissue.
Q: Does this explain why I feel “foggy” after a bad night’s sleep?
A: Exactly. If those slow vasomotor waves don’t get a chance to take over and drive fluid flow, metabolic waste products stay trapped in your brain tissue. This accumulation is linked to long-term memory disorders and that immediate feeling of cognitive “heaviness.”
Q: How is a “wearable” going to measure my brain cleaning?
A: The Oulu team created technology that monitors electrical activity and blood flow simultaneously. Because they now know exactly how these two signals synchronize during the “cleaning” phase, they can use external sensors to confirm if your brain is successfully hitting its “wash cycle” without needing a giant MRI machine.
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: Meri Rova Source: University of Oulu Contact: Meri Rova – University of Oulu Image: The image is credited to Neuroscience News
Original Research: Open access. “Sleep alters neurovascular and hydrodynamic coupling in the human brain” by Tommi Väyrynen, Johanna Tuunanen, Heta Helakari, Ahmed Elabasy, Vesa Korhonen, Niko Huotari, Johanna Piispala, Mika Kallio, Maiken Nedergaard, and Vesa Kiviniemi. PNAS DOI:10.1073/pnas.2510731123
Open access. “Sleep Alters the Velocity of Physiological Brain Pulsations in Humans” by Ahmed Elabasy, Heta Helakari, Tommi Väyrynen, Zalán Rajna, Niko Huotari, Lauri Raitamaa, Ville Isokoski, Matti Järvelä, Mika Kaakinen, Johanna Piispala, Mika Kallio, Vesa Korhonen, Tapio Seppänen, Vesa Kiviniemi. Advances Science DOI:10.1002/advs.202503745
Will your competent? doctor DO ANYTHING AT ALL WITH THIS?
NO? So, doesn't care about your recovery at all! Won't get human testing going either?
Do you
prefer your doctor, hospital and board of director's incompetence NOT
KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand
action!
OH NO! your doctor KNOWS NOTHING AND DOES NOTHING!
Intracerebral hemorrhage (ICH) induces copper overload and cuproptosis in perihematomal brain tissue.
•
The copper chelator TTM mitigates copper accumulation and inhibits cuproptosis in vivo and in vitro.
•
Copper depletion with TTM alleviates ICH-induced brain injury and neuronal death.
•
TTM treatment promotes the expression of neurite regeneration-associated proteins GAP43 and MAP2.
•
Targeting copper-induced cuproptosis is a promising therapeutic strategy for ICH.
Abstract
Background
Intracerebral hemorrhage (ICH) is a severe subtype of stroke. There are currently no specific treatment strategies for secondary brain injury and neurological deficits following ICH. Copper (Cu) is an essential cofactor for all living organisms. Cytotoxicity can occur when copper ion concentration exceeds the homeostatic threshold, leading to cell death. However, the relationship between copper and ICH is unclear.
Methods
In vivo, an ICH model was established in male Sprague-Dawley rats by stereotactically injecting autologous blood into the right basal ganglia. In vitro, we employed hemin and CuCl2 to simulate ICH conditions and induce cuproptosis in BV2 microglial cells. To investigate the role of copper in brain injury and neuronal damage, we administered the copper chelator tetrathiomolybdate (TTM) and knocked down the essential cuproptosis gene ferredoxin 1 (FDX1).
Results
Our findings demonstrate that following ICH, elevated copper levels and FDX1 expression, low expression of lipoylated dihydrolipoamide S-acetyltransferase (DLAT) and lipoic acid synthetase (LIAS), loss of mitochondrial membrane potential and neuronal impairment (increased growth associated protein 43 (GAP43) and decreased microtubule associated protein 2 (MAP2) expression), ultimately lead to neuronal death. Both TTM and si-FDX1 treatment attenuated the copper overload and inhibited cuproptosis, thereby ameliorating the ICH-induced phenotype.
Conclusion
Copper depletion attenuates ICH-induced neuronal damage by inhibiting cuproptosis, highlighting a potential therapeutic strategy for mitigating secondary brain injury and neuronal damage following ICH.
I do coffee all day, takes that long to get in a 12 cup pot of coffee. This won't change my habit, it's mainly to reduce my dementia and Parkinsons risk and no one knows the amounts for that.
I'm still doing a 12 cup pot of coffee daily to prevent Parkinsons
and frailty! Much more important than any problems it can cause.
I'm doing a 12 cup pot
of coffee a day with full fat milk to lessen my chances of dementia and Parkinsons. Tell me
EXACTLY
how much coffee to drink for that and I'll change. Yep, that is a lot
more than the 400mg. suggested limit, I don't care! Preventing dementia
and Parkinsons is vastly more important than whatever problems it can
cause!
Of course, your fuckingly incompetent? doctor did
nothing with this from 2 years ago! And still hasn't created a 24 hour
coffee station
This line is great: The findings indicate that even the Espresso Martini cocktail contains the espresso's beneficial compounds - and can contribute to staving off dementia.
I'm certainly not getting one, my
cognitive health will stay high with all the social connections and
travel I have by not having to worry about a pet when I'm gone. Much easier to be spontaneous! As a friend calls them; 'A furry anchor, keeping you at home'.
Your competent? doctor; if competent at all, already has protocols for all this stuff because they have been keeping up with research! That wasn't really meant as sarcasm, but I'm sure it's not true. Guidelines here; NOT PROTOCOLS! You need protocols, screaming at your doctor will be required, I'm sure!
Although brain and heart conditions share overlapping risk factors and commonly co-occur, current cardiac and neurologic clinical guidelines are typically produced within specialty silos. The objective of this guideline from a Canadian Cardiovascular Harmonized National Guideline Endeavour (C-CHANGE) panel is to expand on current cardiovascular guidelines to include evidence from the neurologic and mental health literature, with specific recommendations for providers managing comorbid brain and heart conditions.
METHODS
The guideline development panel comprised an Executive Steering Committee; 10 expert subgroups to develop research questions and draft recommendations for specific brain-heart conditions; an Evidence Review Team to ensure the rigour and consistent application of the methodology; and an Implementation Committee to facilitate uptake of the recommendations by clinicians and into electronic medical records. The McMaster Evidence Review and Synthesis Team supported the literature searches and critical appraisal. A panel of people with lived experience of specific conditions and caregivers provided input on patient values and perspectives throughout the guideline development process. Our consensus process followed the Appraisal of Guidelines for Research and Evaluation II framework. We used an established evidence appraisal approach to determine the level of evidence and strength of each recommendation, and adhered to the Guidelines International Network's principles for managing competing interests.
RECOMMENDATIONS
We developed 11 recommendations for the management of joint brain and heart diseases. Key recommendations include screening for cognitive decline in atrial fibrillation and depression in coronary artery disease; treatment of depression in coronary artery disease,cognitive impairment in hypertension, and dyslipidemia in stroke; and vaccination to prevent stroke, myocardial infarction, and dementia. We also recommend shared decision-making, including the use of evidence-based decision aids, to support patients with heart-brain diseases.
INTERPRETATION
We sought to produce an implementable and actionable guideline for patients with brain and heart comorbidity. It is primarily targeted to primary care providers, but also relevant to help address and individualize subspeciality care and for interprofessional teams caring for patients with joint brain and heart diseases.
REFERENCES
Management of brain-heart multimorbidity: A clinical practice guideline.
Edwards JD, Li Z, McFarlane P, Rabi DM, Gilbert J, Bajaj HS, MacIntosh BJ, Bittman J.
We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.
Abstract
Using cross-sectional data from 26 general hospitals in China that treated stroke patients in the Department of Rehabilitation Medicine, the aim of this research is to explore the potential association between upper limb motor function and balance function after stroke. We conducted a prospective cross-sectional study involving 1573 stroke patients hospitalized in the rehabilitation medicine departments of 26 hospitals across China. Upper limb motor function and balance were evaluated using the Fugl-Meyer Assessment-Upper Extremity (FMA-UE) and the Berg Balance Scale (BBS), respectively. Linear regression analysis and smoothing curve fitting were performed to examine the relationship between upper limb motor and balance functions. This study included 1573 non-pregnant adults aged 18 years or older, with a mean age of 61.2 ± 12.5 years, of whom 69.0% were male. After adjusting for potential confounders, a significant positive association was observed between upper limb motor function and balance function after stroke (β = 0.48, 95% CI: 0.44–0.51, p < 0.001). Subgroup analyses indicated that this association was more pronounced in the acute phase (≤ 7 days) compared with the subacute and recovery phases. No significant interactions were detected across other subgroups (p > 0.05 for all interactions). Smooth curve fitting revealed distinct saturation effects for FMA-UE and BBS, with inflection points at 25 and 45, respectively. Sensitivity analyses further confirmed these results, supporting the robustness of the findings. This study identified a significant positive association between upper limb motor function and balance function following stroke, highlighting the potential role of upper limb motor recovery in predicting balance outcomes. Further large-scale and multidimensional studies are needed to clarify the underlying mechanisms linking upper limb motor control and post-stroke balance function.
