Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 27,840 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.
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.
Monday, April 29, 2024
A Peek Inside the Brains of ‘Super-Agers’
Is your competent? doctor testing you for these traits? Why not?
A Peek Inside the Brains of ‘Super-Agers’
This paragraph is instructive:
Experts don’t know how someone becomes a super-ager, though there were a
few differences in health and lifestyle behaviors between the two
groups in the Spanish study. Most notably, the super-agers had slightly
better physical health, both in terms of blood pressure and glucose
metabolism, and they performed better on a test of mobility.(I managed to do 14 and I'm 68 so I guess I passed. Getting an ejection seat recliner would mean you'll never pass the power test!)
The super-agers didn’t report doing more exercise at their current age
than the typical older adults, but they were more active in middle age.
They also reported better mental health.(I haven't been depressed a day in my life and I never will!)
Let’s Talk: Web-Based Chats Boost Brain Function in Older Adults
What EXACT PROTOCOL does your competent? doctor have to boost your brain function post stroke? NONE? So you don't have a functioning stroke doctor? Why are you seeing them? Find someone better!
There is no way I could get my 95 year old Mom to work a smartphone without someone sitting next to her and guiding every key stroke.
Let’s Talk: Web-Based Chats Boost Brain Function in Older Adults
Summary: Internet-based conversations can significantly improve cognitive functions in socially isolated older adults. The trial, known as I-CONECT, involved 186 participants aged 75 and older who engaged in structured video chats four times weekly, which helped enhance memory and executive function, particularly among those with mild cognitive impairment.
Over the course of a year, these interactions not only increased cognitive scores but also improved emotional well-being and increased connectivity in brain regions associated with attention. The findings suggest that digital conversations can be a viable strategy to combat social isolation and its cognitive repercussions.
Key Facts:
- Enhanced Cognitive Function: Participants in the I-CONECT trial who engaged in frequent digital conversations showed improvements in global cognitive test scores and language-based executive functions.
- Improved Emotional Well-Being: Both the control and intervention groups experienced boosts in emotional health, indicating that regular social contact, even brief, can have positive effects.
- Neurological Benefits: Brain imaging revealed increased connectivity within the dorsal attention network of the intervention group, highlighting the potential of conversational interactions to enhance brain function.
Source: Harvard
Just talking to other people can stimulate different brain functions among socially isolated older adults, even when the interactions are internet-based, according to a new clinical trial out of Massachusetts General Hospital.
The results are published in The Gerontologist.
“We initiated the first proof of concept behavioral intervention study in 2010, nearly a decade prior to the COVID-19 pandemic drawing attention to the detrimental effects of social isolation on our overall health,” explained lead author Hiroko H. Dodge, the principal investigator of the National Institutes of Health–funded trials.
The 186-participant phase 2 randomized trial, called I-CONECT, used the internet and webcams to allow for conversational interactions between trained interviewers and socially isolated individuals aged 75 years and older who had normal cognition or mild cognitive impairment.
Investigators rotated conversation partners assigned to each participant to enhance the novelty of the experience, provided user-friendly devices allowing participants without any internet/webcam experience to easily engage in video-based conversations, and encouraged conversations with standardized daily themes and picture prompts.
Thirty-minute conversations were conducted four times per week for six months and then twice per week for an additional six months. A control group of similar individuals did not participate in such conversations, but both the intervention and control groups received weekly 10-minute telephone check-ins.
After the initial six-month period, the intervention group had a higher global cognitive test score compared with the control group with a large effect size among those with mild cognitive impairment. Also, intervention group participants with normal cognition had scores indicating higher language-based executive function.
At the end of final six-month period, intervention group participants with mild cognitive impairment had test scores indicating better memory-related brain function than those in the control group.
Measures of emotional well-being improved in both control and intervention groups, suggesting that emotion can be boosted by brief weekly telephone calls while improving cognitive function requires frequent conversational engagement.
Also, brain imaging tests showed that the intervention group had increased connectivity within the dorsal attention network—a region important for the maintenance of visuospatial attention—relative to the control group, although this finding must be interpreted carefully because of the limited number of participants assessed due to COVID-19–related research restrictions.
Upon requests from former trial participants asking to continuously have conversations, Dodge and her colleagues have established a nonprofit organization, the I-CONNECT Foundation. The foundation has been providing social interactions to isolated older individuals in the community free of charge, using the same materials used in the trial.
“Our next goal is to extend these activities to reach more isolated individuals in need, as well as to delve into the biological mechanisms underlying the impact of social interactions on our brain functions,” said Dodge.
“Providing frequent stimulating conversational interactions via the internet could be an effective home-based dementia risk-reduction strategy against social isolation and cognitive decline.
“We plan to extend this therapy to geriatric outpatient populations, for which we are currently fundraising, and also examine its effectiveness for mild to moderate depressive symptoms.”
The team is also exploring the possibility of providing conversational interactions via chatbot — an artificial intelligence – trained robot that provides stimulating conversations as a cost-effective intervention.
“We are aware that human contacts are critically important for our emotional well-being, but for cognitive stimulations, chatbots might work as effectively as humans, which we are currently investigating,” said Dodge, who serves as the director of Research Analytics at the recently inaugurated Interdisciplinary Brain Center at MGH and is a faculty member of the Harvard Medical School.
Funding: Funding was provided by the National Institute on Aging.
About this cognition and aging research news
Author: Tracy Hampton
Source: Harvard
Contact: Tracy Hampton – Harvard
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Internet-Based
Conversational Engagement Randomized Controlled Clinical Trial
(I-CONECT) Among Socially Isolated Adults 75+ Years Old With Normal
Cognition or Mild Cognitive Impairment: Topline Results” by Hiroko H. Dodge et al. The Gerontologist
Normal Sleep
Has your competent? doctor ever figured out a sleep protocol for you?
Back in 2006 , when I had my stroke, nurses were handing out sleeping pills like candy at 10pm. Is that part of your protocol?
Usually at 7am the vampires came into my quad to drain blood from one of the patients, waking everyone up. Is preventing that part of your protocol?
Normal Sleep
Introduction
Sleep comprises one third of our adult life. It is essential for normal functioning; without it, we experience memory lapses, have difficulty with concentration, experience mood alterations, become more prone to accidents, perform poorly at work, experience breaches in interpersonal relationships and develop more medical and psychiatric problems. Animals deprived of sleep will experience metabolic abnormalities and eventually die. Despite all of this information, however, we do not fully understand the whys of sleep.
Scientists have yet to determine how physical and psychological restorative processes are coordinated during sleep and why such a behaviorally disconnected state is necessary to accomplish these tasks. The clearance of beta-amyloid, a neurotoxic waste product that accumulates in the brain during wakefulness, is enhanced during sleep. This and similar information suggests that the restorative function of sleep is a result of its importance in maintaining metabolic homeostasis through the removal of toxins that accumulate during wakefulness.
From a behavioral standpoint, sleep is characterized by diminished responsiveness to, and perceptual disengagement from, the environment. In these ways, it is similar to coma, with the exception that it is readily reversible. However, from a neurophysiologic standpoint, it bears no resemblance to comatose state at all. During sleep, the brain is highly active and undergoes characteristic changes that translate into parallel changes, not just in the central nervous system (CNS), but throughout the body. The apparent quiescence of the sleeper is a product of active processes that diminish responsiveness to environmental stimuli. Sleep seems to be an important aspect of the 4 Rs: rest, restore, rejuvenate and repair.
At the same time, there is a perceptual disengagement from the environment. However, this disengagement is not complete when important environmental sensory information is monitored, again emphasizing the active nature of the brain during sleep. An example is the mother who responds to the infant’s whimper yet sleeps through other loud noises of lesser significance.
Decades of sleep research have confirmed Aserinsky and Kleitman’s original discovery of rapid eye movement (REM) sleep in 1953 and have conclusively demonstrated that sleep is comprised of two fundamentally distinct states, REM and non-REM (NREM) sleep, which repeat in cyclical (ultradian) fashion throughout the night, forming a pattern widely known as sleep architecture (Figure 2-1). Proper characterization of sleep stages necessitates the simultaneous monitoring of the numerous physiologic parameters, a process known as polysomnography. Minimally required are the electroencephalogram (EEG), electro-oculogram (EOG) and electromyogram (EMG) of skeletal muscle, usually the submentalis.
The Rechtschaffen and Kales (R & K) sleep scoring manual was published in 1968, 15 years after REM sleep was discovered. For several decades, the manual has provided the methodology for human sleep research, dictating the scoring of sleep stages. Advances in the field have warranted a re-appraisal of these evaluation systems for sleep. In 2007, the American Academy of Sleep Medicine (AASM) standards manual provided revised criteria for scoring sleep stages, including standardizing epoch length, redefining sleep terminology and criteria, and simplifying certain scoring rules. Table 2-1 shows a comparison of the R&K and AASM sleep stage scoring systems.
In the American Academy of Sleep Medicine (AASM) Visual Scoring system, sleep is classified into four stages: stages N1-N3 (NREM), and stage R (REM). Patterns for each of these parameters during the sleep of a young adult are depicted in Figures 2-2 through 2-4. In addition to sleep scoring, the AASM criteria also include scoring of arousals, respiratory events, sleep-related movement disorders and cardiac abnormalities.
The relative distribution of sleep stages changes with age (Figure 2-5). N3 sleep is maximal in children and diminishes markedly with age, especially during adolescence. Seniors may have little or no N3 sleep. The loss of N3 sleep with age may be a consequence of the diminution in cortical synaptic activity. In contrast, N1 sleep increases with age. With aging, there is a general tendency toward sleep fragmentation, characterized by an increase in the frequency of awakenings and brief arousals. Older adults with specific EEG sleep characteristics (sleep latency >30 minutes, sleep efficiency <80%, REM sleep percentage in the lowest or highest 15% of the total sample distribution) have an excess risk of dying beyond that associated with age, gender, or medical burden.
Cognitive mental processes seem to be at a low level during N1 sleep since sleepers who are awakened from it usually report experiencing thought fragments or vague images. Most individuals awakened from delta (N3) sleep report no mental activity at all. In contrast, most sleepers report dreams when awakened from REM sleep.
Sleep needs are quite variable from individual to individual. Although the average nightly sleep duration is approximately 8 hours, children obtain about 10 hours, and the elderly <7 hours. Sleep lengths vary even within similar age groups, with some individuals reportedly requiring as little as 3 hours of nightly sleep. The most prudent answer to the question of “How much sleep do I need?” is that amount of sleep that results in optimal daytime alertness, no need to “catch up” on sleep on non-work days, and no tendency to fall asleep unintentionally during the course of normal daytime hours. Achieving sleep needs should lead to a sense of mental efficiency and well-being.
Polysomnography
Polysomnography is typically performed in specialized facilities called sleep disorders centers and laboratories. In preparation for polysomnography, patients are introduced to their sleeping quarters during their initial office-based evaluation and provisions are made for special needs. On the night of the test, they arrive at the laboratory well in advance of the study time to acclimate to the new environment. Studies are conducted in noise-free and private rooms and comfort is maximized by making rooms aesthetically pleasing.
As noted earlier, characterization of sleep stages requires, at the minimum, an EEG, EOG and EMG of the submentalis. However, a typical clinical polysomnogram also includes monitors for airflow at the nose and mouth, respiratory-effort strain gauges placed around the chest and abdomen, and noninvasive oxygen-saturation monitors that function by introducing a beam of light through the skin. Other parameters include the electrocardiogram and EMG of the anterior tibialis muscles, which are intended to detect periodic leg movements (PLMs). Finally, a patient’s gross body movements are continuously monitored by audiovisual means (Figure 2-6).
Mechanisms Underlying Sleep and Wakefulness
Sleep and wakefulness are believed to be the net effect of the interaction of two opposing, mutually inhibitory, interdependent processes (Figure 2-7).
Arousal Neurophysiology
The wake-promoting system is consists of noradrenergic, cholinergic (ACh), serotoninergic (5-HT), dopaminergic and histaminergic (His) neurons, which produce cortical arousal via two pathways: a dorsal route through the thalamus and a ventral route through the hypothalamus and basal forebrain (Table 2-2). The dorsal branch of ascending neurons receives input from cholinergic cell groups in the upper pons, the pedunculopontine and laterodorsal tegmental nuclei, which facilitate transmission of signals from the thalamus to the cerebral cortex.
The second branch of ascending neurons receives input from the monoaminergic neurons in the upper brainstem and caudal hypothalamus. This pathway also receives contributions from peptidergic neurons in the lateral hypothalamus (LH) containing orexin and from basal forebrain neurons containing acetylcholine and γ-aminobutyric acid (GABA). All of these ascending arousal pathways traverse the region at the midbrain-diencephalic junction, where it was observed that lesions caused hypersomnolence.
The neuropeptide hypocretin/orexin plays an important role as a stabilizer and maintainer of wakefulness, minimizing unplanned transitions to the sleep state through the reinforcement of wake-promoting signaling in the brain (Figure 2-8). Orexin deficiency results in narcolepsy in many species, suggesting that this system is particularly important for maintenance of wakefulness, although not necessarily its initiation. Orexin neurons receive abundant input from the limbic system and activate waking active monoaminergic and cholinergic neurons in the hypothalamus and brainstem regions to maintain a long, consolidated waking period. These neurons also interact with systems that regulate emotion, reward and energy homeostasis to maintain appropriate vigilance states.
Sleep Neurophysiology
After the identification of arousal centers more than 3 decades ago, it remained unclear how the arousal system was turned “off” so that sleep could be initiated and maintained. It was not until the mid-1990s that the identity of this sleep-promoting circuitry was revealed. It was demonstrated that wake-promoting neurons are inhibited during sleep by a system of ventrolateral preoptic nucleus (VLPO) neurons, which contain sleep-active cells that contain the inhibitory neurotransmitters GABA and galanin.
Primarily active during sleep, VLPO neurons project to all of the main cellular components in the hypothalamus and brainstem that participate in arousal. Inhibition of the arousal system by the VLPO during sleep is critical for the maintenance and consolidation of sleep. Work by Batini and colleagues has provided support for the concept that an active sleep-promoting area is located near the nucleus of the solitary tract in the medulla, but this remains largely unconfirmed. Because the VLPO neurons do not have orexin receptors, actions of the orexin neurons are primarily to reinforce the wake-promoting systems rather than to directly inhibit the VLPO (Figure 2-8).
Transitioning Between Wakefulness and Sleep
Transitions between the discrete states of wakefulness and sleep are rapid and complete and can be described as a “flip-flop” switch. As signaling from one side increases, so does its inhibitory influence on the signaling of the opposing process (Figure 2-9). As long as signaling from one side exceeds the other, that state is maintained. While the flip-flop switch avoids prolonged intermediate states between sleep and wakefulness, transitions can also occur with little warning and may have negative consequences. To minimize unplanned transitions from wake to sleep, wake signaling consists of redundant pathways that are stabilized via orexin neuropeptides, collectively making wake asymmetrically favored.
Factors Modulating Arousal and Sleep
There are many influences that affect the activity of the wake-sleep circuit, which can be categorized within three major factors — circadian rhythms, homeostatic drive and allostatic signaling.
The homeostatic influence is believed to be based on the accumulation of the drive for sleep during prolonged wakefulness and relief of this need during sleep. The mechanism for this homeostatic regulation may be linked to the accumulation of a sleep-promoting substance (believed to be adenosine) that enhances the activity of sleep-promoting cells and reduces the activity of wake-promoting neurons.
Circadian rhythms are governed mainly by the suprachiasmatic nucleus (SCN) area in the brain, which serves as a biological clock of roughly 24 hours. Signals from various areas in the body connect to the dorsal and ventral subparaventricular zones, as well as the dorsomedial nucleus of the hypothalamus (DMH). Neurons in these regions relay information necessary for organizing daily cycles of wake–sleep and rhythms of body temperature (Table 2-3). DMH neurons drive circadian cycles of sleep, activity, feeding and corticosteroid secretion. These integrative connections allow circadian rhythms to mold the daily cycles of sleep-wakefulness in accordance with internal and external cues.
Rather than maintaining a rigid sleep/wake schedule, the physiologic systems within the body are able to fluctuate to meet demands from external forces via allostatic signaling. Allostatic signaling adapts sleep and wakefulness to external behavioral events, such as environmental, sensory, cognitive and emotional inputs. These are thought to be mediated in part by cues from visceral sensory systems and feeding regulatory systems to the arousal systems, involving inputs to the SCN, VLPO and orexin neurons from corticolimbic sites.
The process of sleep is important for physical and mental restoration and normal functioning, although the mechanism by which sleep produces these effects is a matter of ongoing research. Nevertheless, the complex array of changes that is seen both in the brain and the peripheral organs during sleep is proof that sleep represents an active state that is highly regulated. The states of sleep and wakefulness are governed by different, but interconnected neural circuits in the brain, which are mutually interdependent and inhibitory. The transition between the distinct sleep/wake states is fast and complete, governed by many factors, such as circadian rhythms, homeostatic drive and allostatic signaling.
Virtual Reality-Based Interventions to Improve Balance in Patients with Traumatic Brain Injury: A Scoping Review
Do we have ANYONE in the stroke medical world that looks at this and says; 'We need to do the same research for stroke survivors, and we'll assign these people to get it done!' That will never occur, there is NO STROKE LEADERSHIP ANYWHERE!
Virtual Reality-Based Interventions to Improve Balance in Patients with Traumatic Brain Injury: A Scoping Review
Abstract
1. Introduction
Promoting Action Observation in Stroke Rehabilitation by Facilitating Knowledge Translation Facilitating Knowledge Translation
Hopefully your competent? doctor, hospital and therapists have already found these 400 action observation videos on YouTube so you can benefit from them. But I bet you'll have to tell them how to be competent!
Promoting Action Observation in Stroke Rehabilitation by Facilitating Knowledge Translation Facilitating Knowledge Translation
Abstract
Exploring the Structural Plasticity Mechanism of Corticospinal Tract during Stroke Rehabilitation Based Automated Fiber Quantification Tractography
No clue! Absolutely useless for survivors to bring to their medical staff for recovery. But great word salad though!
Exploring the Structural Plasticity Mechanism of Corticospinal Tract during Stroke Rehabilitation Based Automated Fiber Quantification Tractography
Abstract
Background
Methods
Results
Conclusions
Get full access to this article
VIDEO: ‘Increasing evidence’ shows link between cannabis use and heart attack
I'm doing it after my next stroke.
My 13 reasons for marijuana use post-stroke.
Don't follow me, I'm not medically trained and I don't have a Dr. in front of my name.
They never say if this is smoked marijuana or gummies, so for me this research is incomplete.
But this:
Pot Smoking Baby Boomers Are On The Rise, Why Are Scientists So Happy For Them? Hint: Benefits For The Aging Brain
And this:
The Experiments Revealing How Marijuana Could Treat Dementia
The latest here:
VIDEO: ‘Increasing evidence’ shows link between cannabis use and heart attack
BOSTON — In this video, an expert reviews current topics in addiction medicine, like ties between cannabis use and cardiovascular health, buprenorphine access and pre-operative alcohol assessments.
According to Charlie Reznikoff, MD, FACP, FASAM, an associate professor of medicine at the University of Minnesota, there is “increasing evidence that cannabis use causes cardiovascular events,” such as “heart attacks, atrial fibrillation and worsened angina.”
“I don’t think we’ve ever recognized that fully,” he said. “But what we’re seeing now is that Baby Boomers are aging up ... gaining more medical illness and returning to cannabis use.”
While Baby Boomers may have used cannabis when they were younger, the difference now is “they have more medical problems,” Reznikoff, who presented at the ACP Internal Medicine Meeting, said.
Reznikoff also discussed the prevalence of “significant” racial disparities in addiction medicine, which “are resulting in disparities in death rates.”
“It’s really important for us to treat everyone, and to recognize that there are racial disparities,” he said.
Reference:
- Reznikoff C. Addiction medicine: What's new in the clinic? Presented at: ACP Internal Medicine Meeting; April 18-20, 2024; Boston.
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Healio Interviews
Climbing stairs reduces risk for all-cause, cardiovascular death
But this goes against standard age-proofing your home:
One of the best ways to age-proof a house is by having a master bedroom and bathroom on the first floor, says Mark Hager, founder of AgeInPlace.com. “You want to have everything you need on one level so that you don't have to climb stairs as you get older,”
I'll be climbing stairs until the day I die. Or as we hear from our medical staff; 'Use it or lose it'.
Climbing stairs reduces risk for all-cause, cardiovascular death
Key takeaways:
- Climbing stairs was associated with a 39% reduced risk for death from heart disease.
- It was also associated with a 24% reduced risk for death from any cause.
In a meta-analysis of studies covering more than 400,000 people, climbing stairs was associated with reduced risk for all-cause mortality and death from heart disease.
“If you have the choice of taking the stairs or the lift, go for the stairs, as it will help your heart,” Sophie Paddock, MBBS, interventional cardiologist at the University of East Anglia and Norfolk and Norwich University Hospital Foundation Trust, Norwich, U.K., who presented the findings at ESC Preventive Cardiology 2024, said in a press release. “Even brief bursts of physical activity have beneficial health impacts, and short bouts of stair climbing should be an achievable target to integrate into daily routines.”
Paddock and colleagues reviewed nine studies with data from 480,520 participants and conducted a pooled analysis of five studies with 455,649 participants to determine the relationship between stair climbing and all-cause and CV mortality. The pooled cohort included healthy individuals as well as those with prior MI or peripheral artery disease. The age range was 35 to 84 years and 53% were women.
Stair climbing was associated with a 39% reduced risk for CV mortality (RR = 0.61; 95% CI, 0.48-0.79; I2 = 84%; z-test = 3.76; P = .0002) and a 24% reduced risk for all-cause mortality (RR = 0.76; 95% CI, 0.62-0.94; I2 = 85%; z-test = 2.5; P = .01), according to the researchers.
In a qualitative synthesis, the researchers concluded that there was a positive association between stair climbing and CVD including MI, ischemic stroke and HF.
“Based on these results, we would encourage people to incorporate stair climbing into their day-to-day lives,” Paddock said in the release. “Our study suggested that the more stairs climbed, the greater the benefits — but this needs to be confirmed. So, whether at work, home, or elsewhere, take the stairs.”
Reference:
Climb stairs to live longer. https://www.escardio.org/The-ESC/Press-Office/Press-releases/Climb-stairs-to-live-longer. Published April 26, 2024. Accessed April 26, 2024.
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Paddock S, et al. Optimal exercise modalities for primary and secondary prevention. Presented at: ESC Preventive Cardiology; April 25-27, 2024; Athens, Greece.
Sunday, April 28, 2024
Article Commentary: “CTP-Defined Large Core Is a Better Predictor of Poor Outcome for Endovascular Treatment Than ASPECTS-Defined Large Core”
Oh fuck, when will management stop with the research that predicts failure to recover and do useful research like maybe: GETTING SURVIVORS RECOVERED!
I'd have all of management here fired!
Article Commentary: “CTP-Defined Large Core Is a Better Predictor of Poor Outcome for Endovascular Treatment Than ASPECTS-Defined Large Core”
- Mitch Wilson, MD, MSc
The authors of the present study address an important and topical question: What is the best imaging modality to define large core infarcts?
Over the last 2 years, multiple RCTs (RESCUE-Japan Limit, ANGEL-ASPECT, SELECT-2) have demonstrated the efficacy of endovascular thrombectomy (EVT) for large core infarcts. These studies used a combination of modalities to define large core, including non-contrast head CT (NCCT) using the Alberta Stroke Program Early Computed Tomography Score (ASPECTS), as well as advanced imaging, such as CT perfusion (CTP) and MRI. More recently, in the TENSION trial, EVT improved outcomes when NCCT/ASPECTS was used as the sole imaging modality to measure core infarct size.
Here, the authors performed a retrospective cohort study to determine whether functional outcomes differed when large core was defined by NCCT versus CTP. Patients were selected from the International Stroke Perfusion Imaging Registry (INSPIRE), a large cohort of patients with acute ischemic stroke, all of whom underwent NCCT and CTP. Patients included in this study represented a subset of the INSPIRE registry who had large vessel occlusion treated with EVT. Large core was defined as ASPECTS ≤5 by NCCT or core volume ≥70mL by CTP. The primary outcome was a poor functional outcome as determined by a modified Rankin Scale (mRS) score of 5-6 at 3 months.
In total, there were 1115 patients with LVO who underwent EVT, of which 90 (8.1%) had ASPECTS ≤5 and 97 (8.7%) had CTP core ≥70 mL. Patients were categorized into 1 of 4 groups: 1) ASPECTS >5 and CTP<70mL (N=962); 2) ASPECTS ≤5 and CTP <70mL (N=56); 3) ASPECTS >5 and CTP ≥70mL (N=63); and 4) ASPECTS ≤5 and CTP ≥70mL (N=34). Compared to group 1 (no large core by NCCT or CTP), patients in group 2 (ASPECTS-defined large core) were equally likely to have a poor functional outcome at 3 months (29% vs 23%, adjusted OR 1.84 [0.91–3.73]; P=0.089). Conversely, compared to group 1, patients in group 3 (CTP-defined large core) were more likely to have a poor functional outcome (60% vs 23%, adjusted OR 3.91 [2.01–7.60]; P<0.001). In a subgroup analysis, it was demonstrated that when EVT was performed after 6 hours, patients with ASPECTS ≤5 were more likely to have a poor outcome than those with ASPECTS >5 (50% versus 27%, P=0.004), whereas when EVT was performed within 6 hours, there was no difference in the proportion with a poor outcome between ASPECTS ≤5 vs >5. CTP-defined large core showed increased likelihood of poor outcome in both time strata.
The results of this study suggest that CTP-defined large core may provide better prognostic information than ASPECTS-defined large core, particularly during the early time window — when CTP is not recommended in the current American Heart Association guidelines. These findings provide some evidence that foregoing CTP for patients with large core infarcts may lead to more patients undergoing EVT that are unlikely to benefit.
8-Hour Time-Restricted Eating Linked to Higher Cardiovascular Mortality Risk
But these! Ask your competent? doctor for guidance.
,Ketogenic, intermittent fasting diets may be heart-healthy September 2020
This Is How Intermittent Fasting Improves Your Brain by Debbie Hampton January 2021
Intermittent fasting increases adult hippocampal neurogenesis April 2020
Hungry stomach hormone promotes growth of new brain cells April 2017
The latest here:
8-Hour Time-Restricted Eating Linked to Higher Cardiovascular Mortality Risk
A daily 8-hour time-restricted eating (TRE) plan is associated with a significantly increased risk of cardiovascular mortality in the general population and in patients with cardiovascular disease (CVD) or cancer, compared with eating for a duration of 12 to 16 hours, according to research presented at the American Heart Association’s Epidemiology and Prevention/Lifestyle and Cardiometabolic Health Scientific Sessions 2024.
Researchers analyzed data on dietary patterns in participants from the 2003 to 2018 National Health and Nutrition Examination Survey and mortality data through December 31, 2019, from the National Death Index database.
A total of 20,078 adults aged 20 years or older and not pregnant were included. Their mean age was 48.5 years, 50% were men, 73.3% were White, 17.9% were current smokers, and their mean body mass index was 28.7. In addition, 8.2% had CVD, and 11.0% had cancer.
Of the cohort, 414 individuals had a daily eating duration of less than 8 hours, 1492 had a daily eating duration of 8 to less than 10 hours, 4832 had a daily eating duration of 10 to less than 12 hours, 11,831 had a daily eating duration of 12 to 16 hours, and 1509 had a daily eating duration of more than 16 hours.
For all-cause mortality, participants with a daily eating duration of less than 8 hours had an overall hazard ratio (HR) of 1.26 (95% CI, 0.91-1.74), compared with those who had a duration of 12 to 16 hours. The HR was 1.14 (95% CI, 0.93-1.39) in individuals with a daily eating duration of 8 to less than 10 hours, 1.05 (95% CI, 0.92-1.20) in those with a duration of 10 to less than 12 hours, and 0.99 (95% CI, 0.78-1.25) in those with a duration of longer than 16 hours.
For cardiovascular mortality, the HR was 1.91 (95% CI, 1.20-3.03) in individuals with a daily eating duration of less than 8 hours vs those with a duration of 12 to 16 hours. The HR was 1.25 (95% CI, 0.92-1.71) in those with a duration of 8 to less than 10 hours. Among patients with CVD, those with a daily eating duration of less than 8 hours had an HR for cardiovascular mortality of 2.07 (95% CI, 1.14-3.78). In patients with cancer, the HR for cardiovascular mortality was 3.04 (95% CI, 1.44-6.41) for those with a daily eating duration of less than 8 hours.
Regarding cancer mortality, the overall HR for individuals with a daily eating duration of less than 8 hours was 1.20 (95% CI, 0.62-2.32) vs a reference group of those with an eating duration of 12 to 16 hours. In patients with CVD, the HR for cancer mortality was 0.69 (95% CI, 0.25-1.90) for those with an eating duration of less than 8 hours and 1.33 (95% CI, 0.64-2.78) in those with a duration of greater than 16 hours. For patients with cancer, the HR for cancer mortality was 0.44 (95% CI, 0.13-1.49) in those with a daily eating duration of less than 8 hours.
“These findings require replication but do not support long-term use of 8-hour TRE for prevention of cardiovascular death nor for improving longevity,” the study authors concluded.
This article originally appeared on The Cardiology Advisor
References:
Chen M, Xu L, Van Horn L, et al. Association of 8-hour time-restricted eating with all-cause and cause-specific mortality. American Heart Association’s Epidemiology and Prevention/Lifestyle and Cardiometabolic Health Scientific Sessions 2024. March 18-21, 2024, Chicago, Illinois. Abstract P192.