Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,102 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.
Showing posts with label 33% survivor depression. Show all posts
Showing posts with label 33% survivor depression. Show all posts
It's no secret that negative emotions aren't exactly fun, but according to research published in the journal Nature1, they could have even more of an impact on our health than we previously thought. Here's what the research found, plus some helpful tips for learning how to manage your own emotions.
Studying the connection between emotions and neurodegenerative diseases
For this study, Swiss researchers wanted to take a closer look at the link between negative emotions, anxiety, and depression, and the onset of neurodegenerative diseases and dementia. Namely, they wanted to understand what exactly happens in the brain when people go through emotional distress.
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To do so, they observed brain activity in both young and older participants as they were being confronted with other people's psychological suffering.
Their findings indicated that particularly in older adults, neural connections were "excessively modified" by negative emotions, especially in the regions of the brain associated with emotion management and autobiographical memory.
As the study authors write, "These results indicate that a better management of these emotions—through meditation for example— could help limit neurodegeneration."
What to do about it
Unfortunately, there's no shortage of stressors or suffering in this world—but the good news is, the study authors believe managing negative emotions that subsequently come up could have protective benefits for the brain.
They recommend meditation, for one thing, which has a long-standing reputation for easing stress, improving concentration and mindfulness, and yes, working through emotions.
And even if you don't meditate, mindfulness can still be incorporated throughout your day, helping you to identify and feel your emotions so you can work through them.
Working with a mental health professional who can guide you in emotional management can also be beneficial if you're just getting started.
And if you want any additional help with managing your emotions for the sake of your brain, it wouldn't be a bad idea to incorporate a targeted supplement into your routine.
The takeaway
For the sake our physical and mental health, learning how to manage emotions is proving to become more and more important in this day and age. While we may not be able to stop bad things from happening, we can control how we respond to them, and how we deal with the emotions that arise.
You're so fucking incompetent you haven't known of this earlier research? A review that wasn't needed for competent researchers well versed in stroke research! And the mentors and senior researchers completely failed in their jobs, not knowing about earlier research!
Anxiety or depression after a diagnosis of unruptured intracranial aneurysms (UIAs) was associated with a 33% increased risk for rupture and a 28% higher risk for mortality compared to not having a psychiatric disorder, a new retrospective cohort study showed.
METHODOLOGY:
A retrospective cohort study used data for adults with UIAs from the TriNetX Global Collaborative Network between 2015 and 2025.
A total of 6800 patients diagnosed with anxiety or depression at least 127 days after UIA diagnosis and without aneurysm rupture (mean age, 58 years; 69% female) were propensity score matched with 6800 individuals without a psychiatric diagnosis (control group). Mean follow-up durations were 1550 and 1600 days, respectively.
Primary outcomes were all-cause mortality, aneurysm rupture, endovascular aneurysm treatment, and microsurgical clipping. Secondary outcomes were use of psychiatric medication and healthcare resources.
Patients were followed until the first occurrence of the outcome of interest, death, the end of the 5-year follow-up period, or the end of data availability, whichever came first.
TAKEAWAY:
The anxiety or depression group vs control group had significantly higher rates of all-cause mortality (6% vs 4.5%; adjusted hazard ratio [aHR], 1.28; P < .001) and aneurysm rupture (3% vs 2%; aHR, 1.33; P = .007).
Endovascular treatment rates were higher in the anxiety or depression cohort than in the control cohort, albeit not significantly (3.2% vs 2.7%; aHR, 1.18), and surgical clipping rates were similar between the groups (0.7% for both).
Psychiatric medication use was 60% in the anxiety or depression cohort vs 17% in the control cohort (risk ratio, 3.5; P < .001). Also higher were rates of any kind of hospitalization (25% vs 18.5%; odds ratio [OR], 1.47; P < .001) and emergency department visits (37% vs 29%; OR, 1.45; P < .001).
Medication adherence showed a dose-response relationship with mortality: low adherence (proportion of days covered [PDC] < 50%) had an HR of 1.50 (P = .006), moderate adherence (PDC, 50%-79%) had an HR of 1.29, and high adherence (PDC ≥ 80%) had an HR of 1.16.
IN PRACTICE:
“These results highlight the potential importance of considering mental health during UIA surveillance, including awareness of adherence and follow-up. Future prospective studies are needed to clarify causal relationships and determine whether targeted mental health interventions improve outcomes,” the investigators wrote.
SOURCE:
The study was led by Muhammed Amir Essibayi, MD, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, and Ahmed Y. Azzam, MD, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, West Virginia. It was published online on March 4 in Stroke.
LIMITATIONS:
The 127‑day landmark led to the exclusion of patients with early events. Individuals with severe psychiatric disorders such as schizophrenia were also excluded, potentially limiting generalizability. Residual confounding may explain some of the higher rupture and mortality rates observed in the psychiatric group, and key variables (such as race/ethnicity, medication side effects, psychosocial support, and detailed aneurysm characteristics) were not measured. Additionally, anxiety and depression were identified using diagnostic codes and prescription data, which may have missed milder cases or misclassified transient distress.
DISCLOSURES:
The study did not receive any funding. Four investigators reported having financial or other ties with various sources, which are fully listed in the original article. The other eight reported having no relevant financial relationships. Some of the findings were presented previously at the 2025 Congress of Neurological Surgeons Annual Meeting and the 2025 Society of Vascular and Interventional Neurology Annual Meeting.
Hopefully your competent? doctor solves your anxiety the correct way;100% RECOVERY PROTOCOLS! Using this to address your recovery anxiety is COMPLETE INCOMPETENCE!
You want your doctor to prevent post
stroke depression and anxiety the proper way; 100% RECOVERY PROTOCOLS!
Not any after the fact intervention. If your doctor gives you this: SCREAM BLOODY MURDER about their incompetence!
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?
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.
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.
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.
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.
