Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 17213 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!Just think of all thetrillions and trillions of neuronsthateach daybecause there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 493 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. My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html
Correlation, but WHAT IS THE REAL CAUSE?
Do some research to find out. I could just as easily speculate that
those who are skipping breakfast are already obese/overweight and are
skipping breakfast to lose weight. The cause is their pre-existing
obesity and not skipping breakfast. Bad research conclusion. What is needed is a cause and effect explanation of why skipping breakfast seems to cause this. This research was useless in providing answers.
Skipping breakfast may increase your risk for cardiovascular disease.
The connection, found in a study of 6,550 adults aged 65 to 75, was particularly strong for stroke.
Almost
60 percent of the participants had breakfast every day, a quarter on
some days, and 16 percent rarely or never. All were free of heart
disease at the start of the study. Over an average 17 years of follow-up
there were 2,318 deaths, including 619 from cardiovascular diseases.
People who never ate breakfast were more likely to be obese and have high cholesterol, but the observational study, in the Journal of the American College of Cardiology, controlled for these and many other health, behavioral and socioeconomic factors.
Compared
with those who had breakfast every day, those who skipped the meal had
an 87 percent increased risk for death from any cardiovascular disease
and a 19 percent increased risk for all-cause death. Breakfast skippers
had a 59 percent increased risk of developing heart disease, and more
than triple the risk of stroke.
“Many
studies have shown that skipping breakfast is related to a higher risk
of diabetes, hypertension” and high cholesterol, said the lead author,
Dr. Wei Bao, an assistant professor of epidemiology at the University of
Iowa. “Our study suggests that eating breakfast could be a simple way
to promote cardiovascular health.
While this is great for what is currently available this is still a complete failure. Survivors don't want 'hope', they want EXACT stroke rehab protocols that deliver results. This is once again the tyranny of low expectations that our stroke medical world is forcing on us because they have no leaders willing to tackle
Objective:
Despite evidence that social support is strongly related to health,
very little is known about the mechanisms underlying this association.
This study investigates whether physical activity, depressive symptoms,
and chronic diseases mediate the associations between social support and
functional capacity. Method: Data from the Longitudinal Aging
Study Amsterdam on 954 participants, aged 75 and older, covering 9
years, are analyzed with latent growth mediation models. Results:
Only the indirect path from the initial level of emotional support to
the initial level of functional capacity through the initial level of
depressive symptoms was significant. All mediators however were
significantly associated with the level of and changes in functional
capacity. Models with reversed pathways were estimated, but model fit
was worse. Discussion: Because only initial levels of social
support relate to functional capacity, and changes in social support do
not, older adults likely receive the support they need.
This is a prime example of the tyranny of low expectations for stroke recovery. 'Reduce' NOT cure. I know she is doing her best but this just points out that no one in stroke has a strategy to cure spasticity which has been known for decades with nothing done. And she obviously does not believe in the stupidity of Dr. William M. Landaus' opinion of not treating spasticity.
So the end result should have been to go back to the original hospital where treated and have them explain what they are doing to prevent these recurrent strokes/readmissions with 100% accuracy. That is what a responsible and excellent hospital would be doing. The board of directors should fire all involved if that isn't occurring. I take no prisoners in trying to identify what needs to be done for solving stroke. You need no medical knowledge to attack this management problem.
Objective:
The goal of this project was to identify the main causes of unplanned
readmission of stroke patients from inpatient rehabilitation to a
surgical or medical unit.
Background:
Stroke patients admitted to inpatient rehabilitation must meet certain
functional and clinical criteria, therefore, the reasons for readmission
maybe different from those reported for all stroke discharges.
Design/Methods:
Using prospectively maintained database of our CARF-accredited stroke
rehabilitation program, patients with diagnosis of stroke (ischemic
stroke, intracerebral hemorrhage, subarachnoid hemorrhage) who were
discharged to acute care hospitals were identified. We excluded patients
who were readmitted for planned surgery/procedure. Patient
characteristics were extracted from the database and retrospective chart
review.
Results:
We identified 101 stroke patients who had an unplanned readmission (age
64±15 years; 38% female; 72% were white). Of these patients, 73
initially suffered from an ischemic stroke, 24 hemorrhagic stroke, and 4
patients had unknown stroke type. The median (IQR) Functional
Independence Measure score was 55 (38–68). The 3 most common causes of
readmission were recurrent/worsening stroke (n=21), cardiac (n=20), and
infection (n=12). There was no difference between ischemic and
hemorrhagic stroke in LOS 8.9±5.7 vs 9.7±9 days (t test p=0.5), however,
the distribution of readmission reasons was different with DVT/PE more
frequent in hemorrhagic stroke while cardiac reasons more frequent in
ischemic stroke (fisher exact test p=0.02 for both). The median length
of stay second admission was 5 (3–8) days after which only 39 returned
to inpatient rehab, 18 went straight to home, 13 transferred to TCU, 9
went to nursing home, and 17 died.
Conclusions:
Several reasons of transfer from inpatient rehabilitation to acute care
are predictable and preventable especially that these patients are
under direct medical supervision.
Stroke
remains the leading cause of long-term disability worldwide.
Rehabilitation training is essential for motor function recovery
following stroke. Specifically, limb linkage rehabilitation training can
stimulate motor function in the upper and lower limbs simultaneously.
This study aimed to investigate limb linkage rehabilitation task-related
changes in cortical activation and effective connectivity (EC) within a
functional brain network after stroke by using functional near-infrared
spectroscopy (fNIRS) imaging. Thirteen stroke patients with either left
hemiparesis (L-H group, n = 6) and or right hemiparesis (R-H group,
n = 7) and 16 healthy individuals (control group) participated in this
study. A multichannel fNIRS system was used to measure changes in
cerebral oxygenated hemoglobin (delta HbO2) and deoxygenated
hemoglobin (delta HHb) in the bilateral prefrontal cortices (PFCs),
motor cortices (MCs), and occipital lobes (OLs) during (1) the resting
state and (2) a motor rehabilitation task with upper and lower limb
linkage (first 10 min [task_S1], last 10 min [task_S2]). The
frequency-specific EC among the brain regions was calculated based on
coupling functions and dynamic Bayesian inference in frequency
intervals: high-frequency I (0.6–2 Hz) and II (0.145–0.6 Hz),
low-frequency III (0.052–0.145 Hz), and very-low-frequency IV
(0.021–0.052 Hz). The results showed that the stroke patients exhibited
an asymmetric (greater activation in the contralesional versus
ipsilesional motor region) cortical activation pattern versus healthy
controls. Compared with the healthy controls, the stroke patients showed
significantly lower EC (p < 0.025) in intervals I and II in
the resting and task states. The EC from the MC and OL to the right PFC
in interval IV was significantly higher in the R-H group than in the
control group during the resting and task states (p < 0.025).
Furthermore, the L-H group showed significantly higher EC from the MC
and OL to the left PFC in intervals III and IV during the task states
compared with the control group (p < 0.025). The significantly
increased influence of the MC and OL on the contralesional PFC in low-
and very-low-frequency bands suggested that plastic reorganization of
cognitive resources severed to compensate for impairment in stroke
patients during the motor rehabilitation task. This study can serve as a
basis for understanding task-related reorganization of functional brain
networks and developing novel assessment techniques for stroke
rehabilitation.
You will need this in conjunction with the shooting in the dark interventions/guidelines your
doctor/therapist is doing. You will need lots of muscle mass to accomplish the
millions of repetitions needed for your recovery. Even though no one in the world knows how many repetitions are exactly needed to accomplish recovery. Your doctor should know exactly how much muscle atrophy is occurring and the protocols to correct it.
Your doctors' responsibility is to get you 100% recovered. Ask for the protocols that will accomplish that. If your doctor states; 'All strokes are different, all stroke recoveries are different.' you have a doctor that understands nothing about stroke, fire him/her.
All these problems in stroke to solve. And then the minor problem of 100% recovery for all.
1. Well obviously it is not our fucking failures of stroke associations. They can't even do the minimum of a stroke research and protocol database. They have no strategy at all.
2. Obviously not our stroke doctors? They never do anything more than the status quo. Even though 90% of their patients don't make it to 100% recovery. No contact with researchers to solve the reasons why their patients are not recovering. They should all be fired for incompetence.
3. Not our stroke therapists. They know their therapy interventions barely work but don't send those failures up the chain of command to get resolved and fixed.
4. Emergency room doctors? Of course not, even though they knew immediately that tPA only worked to completely reverse the stroke 12% of the time,
they seemed to have raised no hue and cry about that failure. For 20
years the stroke medical profession has been pushing to expand the
timeframe for a failed intervention.
5. Researchers? Of course not, they are following their own muse rather than any sort of strategy that will help survivors recover.
8. Patients? Yep, it is you. You are responsible for the failures of all these Drs., Ph.Ds and the complete stroke medical world.
9. Dean? Yes, you are responsible Dean. Get cracking on those solutions. You are that someone else. You are the only one who seems to understand that stroke currently is not treatable but can see a path forward.
Robotic arm therapy devices that incorporate actuated assistance can enhance arm recovery,
motivate patients to practice, and allow therapists to deliver semi-autonomous training.
However, because such devices are often complex and actively apply forces, they have
not achieved widespread use in rehabilitation clinics or at home. This paper describes
the design and pilot testing of a simple, mechanically passive device that provides
robot-like assistance for active arm training using the principle of mechanical resonance.
Methods
The Resonating Arm Exerciser (RAE) consists of a lever that attaches to the push rim
of a wheelchair, a forearm support, and an elastic band that stores energy. Patients
push and pull on the lever to roll the wheelchair back and forth by about 20 cm around
a neutral position. We performed two separate pilot studies of the device. In the
first, we tested whether the predicted resonant properties of RAE amplified a user's
arm mobility by comparing his or her active range of motion (AROM) in the device achieved
during a single, sustained push and pull to the AROM achieved during rocking. In a
second pilot study designed to test the therapeutic potential of the device, eight
participants with chronic stroke (35 +/- 24 months since injury) and a mean, stable,
initial upper extremity Fugl-Meyer (FM) score of 17 +/- 8 / 66 exercised with RAE
for eight 45 minute sessions over three weeks. The primary outcome measure was the
average AROM measured with a tilt sensor during a one minute test, and the secondary
outcome measures were the FM score and the visual analog scale for arm pain.
Results
In the first pilot study, we found people with a severe motor impairment after stroke
intuitively found the resonant frequency of the chair, and the mechanical resonance
of RAE amplified their arm AROM by a factor of about 2. In the second pilot study,
AROM increased by 66% +/- 20% (p = 0.003). The mean FM score increase was 8.5 +/-
4 pts (p = 0.009). Subjects did not report discomfort or an increase in arm pain with
rocking. Improvements were sustained at three months.
Conclusions
These results demonstrate that a simple mechanical device that snaps onto a manual
wheelchair can use resonance to assist arm training, and that such training shows
potential for safely increasing arm movement ability for people with severe chronic
hemiparetic stroke.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
I wouldn't trust the click bait headline since it is vastly more likely
that smoking is the problem, not the marijuana. Or just an increase in marijuana use among the young. 'Could' is the key word here, they can't prove what the headline says. Go back to the drawing
board and figure out the real reason for increased strokes. I'm doing
marijuana
after my next stroke, it is only 90 miles to Canada and Michigan has
legalized it. I see nothing here that would explain how marijuana causes strokes. This is just fear mongering.
(Ozge Yagmur/EyeEm) The
vast majority of strokes occur in people over 65, but the number of
younger adults having strokes is rising. New research suggests growth in
illegal drug use could be playing a role.
Past research has shown higher cardiovascular death rates for young adults who used cocaine or marijuana. But the new study,
presented this week at the American Stroke Association's International
Stroke Conference in Honolulu, investigates trends in illegal drug use
among 18- to 54-year-olds who had a stroke.
Researchers looked at
20 years of drug tests and self-reported data involving more than 2,200
young adults who had a stroke in greater Cincinnati and northern
Kentucky. While alcohol and cigarette use in the stroke victims remained
stable over the two-decade study period, drug use rose dramatically,
from 4.4 percent in 1993-1994 to 30.3 percent in 2015.
"It's
concerning. We need to be doing more to curb this growing problem, and
young people especially need to be aware that illicit substances are
associated with an increased risk to your health – specifically, the
risk of stroke," said the study's lead author, Dr. Felipe De Los Rios La
Rosa, a neurologist and medical director of the stroke program at
Baptist Health South Florida in Miami.
The statistics could be
impacted by several factors, De Los Rios La Rosa said, including the
opioid epidemic, increases in hospital drug testing and the decrease in
stigma about marijuana prompting more people to self-report that they
use it.
Dr. Deepak L. Bhatt, a Brigham and Women's Hospital
cardiologist and Harvard Medical School professor who was not involved
in the study, said that even though marijuana isn't as harmful or
addictive as cocaine, it still carries health risks.
"Marijuana
has been linked to heart attacks and strokes, which is something that
shocks a lot of people," Bhatt said. "Marijuana use will surely grow as
it becomes increasingly legalized, but people should realize there's
likely going to be health consequences down the road."
Bhatt called for more research on how rising opioid use is impacting strokes in young people.
De
Los Rios La Rosa said he'd like to see future studies that explore the
health effects of newer drugs marketed as "bath salts," "K2" and
"synthetic marijuana."
"We need better tests for these designer
drugs," he said. "They all have different chemicals that are often
modified, so you can't test for them in the emergency room."
Bhatt
said the new study shows doctors need to step up their efforts to get
young adults to understand the health consequences of using drugs.
"It's
an uncomfortable question for some doctors to ask, but this tells us
it's important for us to be asking young people about illicit drug use
before a stroke or heart attack occurs," Bhatt said.
"It might
seem inconceivable to an 18-year-old that they could have a heart attack
or stroke from drug abuse," he said. "We have to get out the word that
it could happen. A stroke could be fatal, or it could leave you with a
significant disability."
The trickier task, Bhatt said, is helping young patients who are already addicted recover before it's too late.
"We
have to encourage them to enter a drug rehabilitation program and get
assistance," he said. "Instead of just saying, 'Don't do drugs,' we have
to offer something that can actually help them get off these highly
addictive drugs." If you have questions or comments about this story, please email editor@heart.org.
I had massive fatigue immediately post stroke and continuing for years.
My doctor stupidly said I needed to get more cardiovascularly fit. He
never tested my cardio fitness. Three years after my stroke I had a
physical where my resting heart rate
was 54 at the age of 53. That means my cardiovascular fitness was that
of an athlete, even after doing nothing on it for 3 years. Yet I was still completely fatigued everyday.
The original study had this as a result so I don't see why the second study is needed. But I'm not medically trained and there is no stroke database of research to consult and see why stroke research is being done.
Results—One
thousand one hundred twenty-one patients with stroke were screened and
41 patients included, 21 received modafinil. The
primary end point, the Multidimensional
Fatigue Inventory-20 general fatigue score, did not differ between
groups.
Are you experiencing debilitating fatigue after your stroke? Researchers are trialling a wakefulness drug that could help.
The MIDAS2 study (Modafinil in Debilitating Fatigue After Stroke 2)
is looking for people who have severe persisting fatigue after stroke to
test the wakefulness medication called modafinil.
A previous study tested modafinil in stroke survivors with
debilitating fatigue. They found that 6 weeks of treatment reduced
fatigue and improved the quality of life for many trial participants.
This MIDAS 2 study will test whether 200mg of modafinil taken for 56
days is safe and can alleviate stroke-related fatigue in a much larger
group of stroke survivors. There are currently hospitals in Newcastle,
Melbourne and Adelaide participating in the study. Participants can
choose to continue in the study for up to 12 months to test the
long-term effectiveness of the drug. Watch: David, Mark & Tracey & Michelle on their experience with modafinil in the previous MIDAS study
Who can participate in the research?
People who have had a stroke at least 3 months ago, and
People who have severe, persistent and debilitating fatigue
Modafinil may not be suitable for people with high levels of
anxiety. People with stroke who are pregnant, or planning to become
pregnant are not able to participate in this trial. A neurologist will
perform a detailed medical assessment to see if you are eligible and
whether it is safe for you to participate in the trial.
Mark
and Tracey Laverick - Mark needed to nap 2-4 hours every day. After the
previous modafinil trial, he rarely needed to nap and was able to get
back into activities with his family.
Why is the research being done?
Fatigue affects up to 70% of stroke survivors. Fatigue has been
defined as ‘a feeling of early exhaustion with weariness, lack of energy
and aversion to effort that develops during physical or mental activity
and is usually not improved by rest'. There are currently no approved
medical therapies available for stroke survivors to help manage their
fatigue.
What would you be asked to do?
If you’re happy to participate and you meet all of the eligibility criteria , you will be asked to do the following
1) Come to HMRI for 3 visits over the initial 8-week
period. You will be reimbursed for parking costs for these visits.
During these appointments, you will be asked to complete surveys, have health assessments (approx. 1-3 hours).
You will be asked for information on your health and function,
fatigue levels, quality of life. You will also undergo testing of your
current thinking and cognitive skills, fatigue, depression and anxiety.
2) Take tablets every day containing either 200mg modafinil or a placebo
(an identical tablet with no active ingredients). There is a ½ or 50%
chance of being in the modafinil group and neither you nor the doctors
and scientists seeing you as part of the trial will know whether you’re
receiving modafinil or placebo. In emergency situations, your study
doctor can find out if needed. You can also choose to take part in any or all of 3 sub-studies:
1) Extra 10 month trial of modafinil
After the first 8 weeks, participants can choose if they want to
enrol for a further 10 months. The long-term safety and reliability of
modafinil will be studied. There is no placebo arm to this sub-study so
all patients who take part will be supplied with modafinil for the
10-month duration.
2) Physical activity monitoring
This will involve wearing a FitBit activity monitor for a period of 1 week during the course of the study.
3) Extra cognitive testing
This involves a more thorough set of cognitive tests at each visit to HMRI and adds approximately 40-60 minutes to each visit. Click here to download a detailed Participant Information Statement
Researchers: Dr Andrew Bivard, Prof Chris Levi, Prof Neil Spratt, Dr Carlos Garcia-Esperon, Dr Tom Wellings, Dr Shyam Gangadharan, Linda Belevski, Thomas Lillicrap, Prof Michael Nilsson To find out more or to register your interest please contact Linda Belevski on (02) 4922 3187 or Linda.belevski@hnehealth.nsw.gov.au
The study is being supported by The Greater Charitable Foundation.
This study is also inviting people from the Hunter Stroke Research Volunteer Register to participate. To be invited to participate in other studies in stroke rehabilitation and recovery, register here: https://hmri.org.au/stroke-register
I must be missing something, why not stop aspirin use once it is objectively determined that it is causing bleeding? And this research was tested on healthy patients and youngsters at that, so not really transferable to stroke patients. So, a higher cost drug is the result.
The novel antiplatelet
agent ACT017 confers reduced risk for bleeding and may be a safe and
effective alternative for patients with stroke, according to early
findings published in Arteriosclerosis, Thrombosis and Vascular Biology. Christine Voors-Pette, MD,
a principal investigator and manager of medical operations at QPS
Holdings LLC in the Netherlands, and colleagues evaluated the safety,
tolerability, pharmacokinetics and pharmacodynamics of ACT017 (QPS
Holdings LLC), a glycoprotein VI antibody, in healthy subjects.
“There is a clear need for a novel antiplatelet agent that resolves platelet aggregation and clot formation without raising the risk for bleeding,” Martine Jandrot-Perrus, MD, PhD,
a scientist at France’s National Institute of Health and Medical
Research, said in a press release. “Such a therapy would considerably
improve and expand our current therapeutic arsenal for the treatment of
acute stroke.”
The researchers analyzed data of six cohorts of
eight healthy male and female subjects (aged 18 to 65 years) receiving
ascending single doses of ACT017 (six in each cohort) or placebo (two in
each cohort). The doses were administered as a 6-hour IV infusion, with
one-fourth of the total dose administered within 15 minutes and the
remainder administered within 5 hours and 45 minutes.
The investigated doses ranged from 62.5 mg to 2,000 mg, Voors-Pette and colleagues wrote.
No serious adverse events occurred during the study and all doses of ACT017 were tolerated, the researchers wrote.
Template
bleeding time was not affected in a clinically significant manner by
any of the ACT017 doses, Voors-Pette and colleagues.
There was no change in platelet count, platelet
glycoprotein VI (GPVI) expression assessed by flow cytometry or plasma
levels of soluble GPVI assessed by enzyme-linked immunosorbent assay
(ELISA), the researchers wrote.
Administration of ACT017
inhibited collagen-induced platelet aggregation measured by light
transmission aggregometry on platelet-rich plasma, and the extent and
duration of the effect were dose-dependent, Voors-Pette and colleagues
wrote.
“Our results are quite encouraging because they show
the candidate compound is well-tolerated at does even twice as high as
the ones targeted for a future treatment and without any signs of
bleeding,” Jandrot-Perrus said in the release. “Another encouraging
finding is the fact that the drug’s action on platelets is rapid,
specific and largely reversable within 24 hours.” Disclosures:
The study was funded by QPC Holdings LLC. Voors-Pette reports being
employed by QPC Holdings LLC. Jandrot-Perrus reports she holds equity
and received consulting fees in Acticor-Biotech. Please see the study
for all other authors’ relevant financial disclosures.
European Journal of Clinical Investigation — Steensig K, et al. | April 15, 2019
In patients without atrial fibrillation, researchers ascertained if the CHA2DS2-VASc
score can predict the risk of atrial fibrillation and thromboembolic
events. For this investigation, coronary angiography patients were
grouped according to CHA2DS2-VASc score between 2004 and 2012. A total of 78,233 patients with group sizes ranging between 8,299 (CHA2DS2-VASc >4) and 19,882 (CHA2DS2-VASc 2) were included. The CHA2DS2-VASc
score predicted a future diagnosis of atrial fibrillation and the
composite risk of ischemic stroke, transient ischemic attack, or
systemic embolism in patients without atrial fibrillation undergoing
coronary angiography. In a patient with atrial fibrillation, a CHA2DS2-VASc score of 3 was related to a risk that would justify prophylactic oral anticoagulation treatment.
In this meta-analysis of 19
prospective observational cohort studies, researchers ascertained if
physical inactivity is a risk factor for dementia, focusing on the role
of cardiometabolic disease in this association, and reverse causation
bias resulting from changes in physical activity during the preclinical
(prodromal) phase of dementia. According to results, physical inactivity
was non-significantly linked to dementia among people in whom
cardiometabolic disease preceded dementia. Physical inactivity was not
related to all-cause dementia or Alzheimer’s disease in analyses that
addressed bias due to reverse causation, although an indication of
excess dementia risk was noted in a subgroup of physically inactive
people who developed the cardiometabolic disease.
Ask your doctor, and not politely, if their failure to get you 100% recovered leaves you with enough physical activity to get these benefits. This is non-negotiable.
Potential benefits on brain aging may accrue at lower activity levels
by Judy George, Senior Staff Writer, MedPage Today
Incremental physical activity, even
at a light intensity, was tied to larger brain volume, an analysis of
middle-age adults in the Framingham Heart Study showed.
Each additional hour of light-intensity physical activity per day was
associated with higher cerebral total brain volume, even among people
not meeting national physical activity guidelines, reported Nicole
Spartano, PhD, of the Boston University School of Medicine, and
colleagues in JAMA Network Open.
"The
research emphasizes the relationship we are seeing between people doing
more light-intensity physical activity and also having maintained brain
structures," Spartano said.
Past research has focused on moderate to vigorous physical activity, as have the U.S. Health and Human Services guidelines,
she noted, but many adults are unable to meet the national exercise
guidelines of 150 minutes of moderate to vigorous physical activity a
week.
"Our study results don't discount moderate or vigorous physical activity as being important for healthy aging," Spartano told MedPage Today.
"We are just adding to the science, suggesting that light-intensity
physical activity might be important, too, especially for the brain."
The analysis compared the number of steps walked per day and dose of
exercise (intensity x duration) with MRI total cerebral brain volume in
2,354 third-generation Framingham Heart Study
participants who were a mean age of 53. The sample was predominantly
white; 54.2% were women and 46.7% met the nationally recommended
physical activity guidelines, averaging at least 21.4 minutes of
moderate to vigorous physical activity per day. People with stroke,
dementia, or other disorders that might affect brain MRI measures were
excluded.
Each participant wore a hip-belt accelerometer for 8 days. The
researchers classified activity measures of 200-1,486 counts/min as
light activity and >1,486 counts/min as moderate to vigorous
activity.
Their analysis showed:
Each
additional hour of light-intensity physical activity per day was
associated with approximately 1.1 years of less brain aging (β estimate
0.22, SD 0.07; P=0.003).
For people who didn't meet the physical activity guidelines, each hour of light-intensity activity (β estimate 0.28, SD 0.11; P=0.01) and achieving 7,500 steps or more per day (β estimate 0.44, SD 0.18; P=0.02) were associated with higher total brain volume, equal to about 1.4 to 2.2 years of less brain aging.
Achieving 10,000 or more steps a day was associated with higher brain volume compared with fewer than 5,000 steps per day.
After adjusting for light-intensity activity, increasing moderate to
vigorous activity levels was not significantly associated with total
cerebral brain volume.
The overall results suggest the threshold of the favorable
association for physical activity with brain aging may be at a lower,
more achievable level of intensity and duration, the researchers noted.
"The main finding that physical activity, even fairly light, seems
beneficial to brain volume maintenance is of considerable interest from a
public heath viewpoint," said James Mortimer, PhD, of the University of
South Florida School of Public Health, who was not involved with the
study.
"Brain atrophy is a major correlate of dementing illnesses," Mortimer told MedPage Today. "Starting with more brain volume, therefore, may delay onset of these illnesses, including Alzheimer's."
But
other variables may have affected the findings in this study, he
observed. "We know from several published studies that greater education
is associated with greater brain volume, especially gray matter," he
said. "The effect reported here on physical activity and brain volume
could in part be due to the association between more education and
larger brain volumes."
The study had other limitations, the researchers noted. It was
cross-sectional and time relationships between physical activity and
brain volume were unknown. Brain atrophy also may have led to changes in
physical activity.
Longitudinal studies with longer follow-up times are needed, they
added. "It will be important to test whether light-intensity physical
activity interventions in older adults can actually play a role in
healthy brain aging," Spartano said. "We don't have effective
preventions or treatment solutions to address the growing public health
crisis of climbing dementia rates. So focusing on lifestyle
interventions, which have shown some potential benefit, are vital at
this point."
Because certain minority populations may have higher risks of
developing dementia, effective prevention measures also need to be
studied in different race, ethnic, and socio-economic groups, she added.
This study was
funded by grants from the National Heart, Lung, and Blood Institute,
the National Institutes of Health, the National Institute on Aging, the
National Institute of Neurological Disorders and Strokes, and the
American Heart Association. Researchers reported no conflicts of
interest.
Good to know that your doctor has absolutely nothing to do with your
recovery. So if you don't get 100% recovered you can only blame
yourself. See how this works in your doctors and hospital favor. They do
nothing but still get paid. I bet they didn't include spasticity patients in their research subjects. Spasticity is obviously too fucking hard to solve for all these smart people.
A Call to Arm Rehabilitation to End Neuro-Nihilism
Stroke
is among the top three causes of disability in our species. Motor
deficits are the most common problem after stroke and a major
contributor to this disability. Activity-based training (e.g., physical
therapy or occupational therapy) can improve behavioural outcomes, with
meta-analysis suggesting that higher doses of activity-based therapy
targeting the motor system improve behavioural outcomes after stroke.1
However, many patients do not receive high doses of rehabilitation
therapy after stroke, for reasons that include economic factors, access,
and a paucity of data to guide decision-making regarding therapy
intensity.
In this context, Ward et al2
examined whether providing patients with a very large dose of
rehabilitation therapy produces enduring gains in motor function, with
critically important results. These authors …
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Well I got the worse physical health out of the way at age 50 so I get to be disabled for half my life. All because our stroke medical world has completely failed at even attempting to get survivors to 100% recovery. Even chronic survivors like me should recover, you just need to solve neuroplasticity and neurogenesis and make them repeatable on demand. Fuck them, I'm going for 100 regardless.
The idea of living past 100 years of age may
be a difficult sell for some, but to others it’s alluring. Granted, an
elderly person who is relatively healthy may have a much stronger desire
to live past 100 than a younger person who is cushioned from the
inevitability of aging.
Positive mindset plays an important role in exceptional longevity.
Throughout the world, the global population
is aging at a historic rate. The number of nonagenarians (people in
their 90s) rose from 7.8 million to 16.5 million between 2000 and 2015.
The number of centenarians (people age 100 and older) is expected to
jump from 180,000 in 2000 to 3.2 million by 2050. In nonagenarians and centenarians, exceptional longevity is
characterized by positive psychological traits and mindset, hard work,
and strong bonds with family, faith, and land, according to the results
of a mixed-methods quantitative-qualitative study recently published in International Psychogeriatrics. “Studying the strategies of exceptionally long-lived and lived-well
individuals, who not just survive but also thrive and flourish, enhances
our understanding of health and functional capacities in all age
groups,” wrote the authors, led by Anna Scelzo, PsyD, MSc, Department of
Mental Health and Substance Abuse, Azienda Sanitaria Locale 4,
Chiavarese, Italy. The investigators examined positive psychological traits among 29
nonagenarians and centenarians and 51 “young-old” family members (aged
51-75 years) by using standardized rating scales of mental and physical
well-being, resilience, optimism, anxiety, depression, and perceived
stress.
The researchers also conducted qualitative interviews to detail
personal narratives, such as migrations, beliefs, and traumatic events.
Next, they interviewed the young-old family members regarding the
personality traits of their nonagenarian and centenarian relatives. The researchers found that nonagenarians and centenarians experienced
worse physical health but maintained better mental well-being vs their
younger relatives. This superior mental well-being was negatively
associated with levels of depression and anxiety. This “paradox” of
better well-being in the elderly despite worsened physical state jibes
with previous research on the topic. In qualitative interviews, themes that emerged included positivity
(resilience and optimism), working hard, and strong ties to both family
and religion(neither for me). Nonagenarian and centenarian subjects exhibited a strong need for
control (ie, domineering). These older individuals also wanted to be in
charge of their own social lives and were described as “stubborn” by
their younger relatives. Among all subjects, engagement in social
activities was cited as a necessity to feel responsible, important, and
connected. Resilience was also identified an integral part of nonagenarian and
centenarian identity. The authors highlighted that centenarians are role
models for resilience because they have survived decades of risk and
threats. They have had to adapt to countless daily stressors through a
long life. Furthermore, exceptional longevity could represent
sustainability, which involves a complex mix of identity, tradition, and
change—thus indicating the importance of resilience, optimism, and
purpose in life.
This study was conducted in Cilento, a city in southern Italy, which
is the “Birthplace of the Mediterranean diet.” The investigators
suggested that, based on previous research in this population, there
could be partially linked heritability of longevity and positive traits. One major limitation of this study is that it relied on retrospective
accounts of life experiences, which could be biased. The investigators
also used semi-structured vs in-depth interviews, which could make it
more difficult to elicit themes. “Exceptional longevity was characterized by a balance between
acceptance of and grit to overcome adversities along with a positive
attitude and close ties to family, religion, and land, providing purpose
in life,” the researchers concluded.
Postgraduate Research Opportunity - University of Essex
This would already seem to be covered in this research already but what the hell do I know? I'm stroke-addled and shouldn't dare to challenge University professors. It would seem that there is already enough research out there for these professors to write a protocol on it already. But that is just my business look at it, they would be fired for incompetence already. I love being the devils advocate.
