Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,134 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 cognitive ability. Show all posts
Showing posts with label cognitive ability. Show all posts
Aging and cognitive resilience depend on genetic and epigenetic factors.
•
Dendritic spines and microglia are at the forefront of aging and cognitive resilience.
•
Dendritic spines and microglia improve cognitive resilience.
•
Outcomes may be boosted if these approaches are combined.
As
the global population ages, the need to prolong lifespan and healthspan
becomes increasingly imperative. Understanding the molecular
determinants underlying cognitive resilience, together with changes
during aging and the (epi)genetic factors that predispose an individual
to decreased cognitive resilience, open avenues for researching novel
therapies. This review provides a critical and timely appraisal of the
molecular mechanisms underlying cognitive resilience, framed within a
critical analysis of emerging therapeutic strategies to mitigate
age-related cognitive decline. Significant insights from both animals
and human subjects are discussed herein, directed either toward active
pharmaceutical ingredients (drug repositioning or macromolecules), or,
alternatively, advanced cellular therapies.
In recent years, aging rates have been increasing due to greater longevity combined with falling birth rates around the world.(p1)
The increase in human life expectancy over the last two centuries
represents a remarkable achievement of modern civilization. However, it
has also become a worldwide concern; in particular, there is a need to
discover the mechanisms underlying cognitive aging given the increase in
dementia cases in Portugal and worldwide.(p2)
Aging,
a complex, natural, and gradual process experienced by all living
beings, is characterized by physical, psychological, and social changes
that can affect the quality of life of individuals. It can represent
both an opportunity for society (people gain increased experience) and a
threat (due to the high costs to families associated with dementia, as
well as limited medical resources).(p1) The aging process is associated with decreased function of organs and systems, leading to various diseases and health problems.(p3),(p4),(p5)
Brain
aging is characterized by physiological, structural, and functional
modifications, culminating in cognitive decline and a heightened
susceptibility to develop neurodegenerative disorders such as
Alzheimer's disease (AD) and Parkinson's disease (PD).(p4)
However, there are multiple factors during fetal development and
childhood, and throughout the living adult lifespan, which promote,
intensify, or even protect against the pathophysiologic processes that
lead to neurodegeneration and its consequent clinical expression.(p3),(p4),(p5) These factors, some of which are negative, may operate together, hampering their investigation on an individual basis.(p4),(p5),(p6),(p7)
The
research on cognitive decline demonstrates how important cognition is.
Cognition includes functions like memory, attention, perception, and
language, among others,(p1)
and encompasses the acquisition, storage, manipulation, and use of
information. With aging, cognition is commonly compromised. For
instance, processing speed decreases, as well as working memory and the
ability to multitask.(p1)
With the increasing number of elderly persons, it has become important
to investigate the effects of the aging process on cognition to develop
cognitive-behavioral interventions and public health policies, including
preventive psychological therapeutic strategies.(p6),(p8)
These strategies are expected to promote healthy aging, improve the
quality of life of elderly people, and reduce the risk of dementia
development.(p8)
However, for this emergent field to achieve maximum development and
benefit, it is essential to address major unanswered questions.(p9)
In
this context, the current monography aimed to provide a comprehensive
overview of existing conceptual models of cognitive reserve and
resilience, along with their associated mechanisms. Additionally, it
endeavors to investigate the pivotal determinants impacting cognitive
resilience and clarify the mechanisms. In parallel, the molecular
attributes responsible for preserving cognitive function are critically
discussed herein to highlight their potential as therapeutic targets for
both neurodegenerative disorders and healthy aging.
NeNose with lower cognitive ability. The study found higher cognitive ability associated with more controlled emotional response.w research suggests people with high cognitive ability exhibit slower, less intense emotional reactions compared to those with lower cognitive ability. The study found higher cognitive ability associated with more controlled emotional response.New research suggests people with high cognitive ability exhibit slower, less intense emotional reactions compared to those with lower cognitive ability. The study found higher cognitive ability associated with more controlled emotional response.New research suggests people with high cognitive ability exhibit slower, less intense emotional reactions compared to those with lower cognitive ability. The study found higher cognitive ability associated with more controlled emotional response.New research suggests people with high cognitive ability exhibit slower, less intense emotional reactions compared to those with lower cognitive ability. The study found higher cognitive ability associated with more controlled emotional response.New research suggests people with high cognitive ability exhibit slower, less intense emotional reactions compared to those with lower cognitive ability. The study found higher cognitive ability associated with more controlled emotional response.New research suggests people with high cognitive ability exhibit slower, less intense emotional reactions compared to those with lower cognitive ability. The study found higher cognitive ability associated with more controlled emotional response.
New research suggests people with high cognitive ability exhibit slower, less intense emotional reactions compared to those with lower cognitive ability. The study found higher cognitive ability associated with more controlled emotional response.
My
doctor told me I had a bunch of white matter hyperintensities but never
showed me them on any scan, so I don't know the size, location or any
intervention needed, because my doctor knew nothing and did nothing. I have zero cognitive impairment and I'm 16 years out.
A combination of decline in cognition and independence is associated
with the presence and progression of white matter hyperintensities (WMH)
in the year after a stroke, according to a study in Neurology.
Previous research has found worse WMH at stroke presentation are
associated with worse cognition concurrently and long term. However,
it’s not clear whether longitudinal WMH change predicts co-existent
post-stroke cognitive or functional impairment. The objective of the
current study was to assess longitudinal interrelationships between
changing white matter hyperintensities, cognition, and function after
stroke.
A total of 264 patients who presented for stroke
services in Edinburgh, UK, for an acute minor ischemic stroke were
enrolled. The participants were evaluated 1 to 3 months post-stroke,
which included magnetic resonance imaging (MRI), cognitive, and modified
Rankin Score (mRS) assessments. The patients had a follow-up MRI at 1
year and additional cognitive and mRS assessments at 1 and 3 years. All
patients underwent the Addenbrooke’s Cognitive Examination–Revised
version (ACE-R) at all 3 visits.
Today’s top picks on the Haymarket Medical Network
The researchers recorded mRS, imaging, and cognitive data at baseline
(mRS n = 264; imaging: n = 264; cognitive n = 157), 1 year (mRS n =
264; imaging: n = 196; cognitive n = 151), and 3 years post-stroke (mRS n
= 222; no imaging; cognitive n = 152).
Participants’ mean age at baseline was 66.9 (SD 11.8) years, 41.7%
were female, and their median mRS was 1 (interquartile range, 1-2).
ACE-R scores were very weakly associated with WMH volumes (cube root
as % of intracranial volume [ICV]) (β = 0.105; 95% CI, -0.265 to 0.054
more WMH per 1-point ACE-R decrease; P =.195) at baseline. At 1
year, the associations between ACE-R scores and WMH volumes became more
evident (β = -0.259; 95% CI, -0.407 to -0.111 more WMH per 1-point
ACE-R decrease; P = .001). A strong ACE-R/mRS association was found at 3 years (β = -0.272; 95% CI -0.429 to -0.115; P =.001).
The changes in ACE-R scores were associated most strongly with age (β = -0.30; 95% CI, -0.44 to -0.16; P <.001) and National Adult Reading Test scores (β = 0.53; 95% CI, 0.40- 0.66; P <.001), followed by normalized WMH volume changes from baseline to 1 year (β = -0.113; 95% CI, -0.233-0.007; P =.065).
According to multivariate change-change analysis, patients who had a
change in ACE-R and mRS from baseline to 1 year were more likely to have
had a change from baseline to 1 year in their WMH volumes and NIH
Stroke Scale scores compared with patients without any change in ACE-R
and mRS.
The researchers noted that they did not invite participants to
undergo MRI at 3 years and that longer-term WMH volumes would have
strengthened their analysis and better reflected changes in WMH,
cognition, and mRS at all 3 time points. Also, not all participants
completed cognitive assessments, and depression was not included as a covariate.
The findings suggest “that dynamic WMH in the weeks after a stroke do
not reflect permanent brain damage but by 1 year, perhaps when any
modifiable component of WMH such as interstitial edema has cleared, WMH
volumes may more closely represent the underlying ‘permanent’ damage and
hence better correlate with cognition,” according to the researchers.
My
doctor told me I had a bunch of white matter hyperintensities but never
showed me them on any scan, so I don't know the size, location or any
intervention needed, because my doctor knew nothing and did nothing. I have zero cognitive impairment.
White matter hyperintensity volumes at 1 year strongly correlated
with contemporaneous cognitive scores after stroke, according to study
results published in Neurology.
“Although numerous
studies have assessed baseline [white matter hyperintensities (WMH)] and
[modified Rankin Score (mRS)] change after stroke, we are not aware of
any studies that have assessed WMH progression and mRS change after
stroke, or if WMH progression or severity at specific time-points
affects variation between both mRS and cognition post-stroke, despite
these measures being collected increasingly by ongoing studies,” Una Clancy, MB, BAO, BCh, of
Edinburgh Imaging and the U.K. Dementia Research Institute at the
University of Edinburgh, and colleagues wrote. “The present in-depth
analysis builds on previous work from the Mild Stroke Study-2 on 1- and
3-year outcomes after stroke, which included predictors of cognition and
cognition-mRS relationships but did not assess longitudinal change
incorporating all three elements of cognition, mRS and WMH.”
Source: Adobe Stock
Clancy and colleagues recruited 264 patients (mean age, 66.9 years; 41.7% women; median mRS = 1) within 3 months of a minor ischemic stroke, defined as NIHSS score less than eight and not expected to lead to an mRS greater than two. Repeat MRI occurred
at 1 year and cognitive and mRS assessments at 1 and 3 years.
Researchers used longitudinal mixed-effects models to examine change in
Addenbrooke’s Cognitive Examination-Revised (ACE-R) and mRS.
At 1
year after stroke, results showed a stronger association between
normalized WMH volumes and 1-year ACE-R (beta = –0.259; 95% CI, –0.407
to –0.111 more WMH per 1-point ACE-R decrease) compared with subacute
WMH volumes and ACE-R (beta = 0.105; 95% CI, –0.265 to 0.054).
Researchers noted an association between 3-year mRS and 3-year ACE-R
(beta = –0.272; 95% CI, –0.429 to –0.115), as well as between combined
change in baseline-1-year jointly assessed ACE-R/mRS and fluctuating WMH
volumes.
“We need to closely track the natural history of dementia
post-stroke and determine whether clinically and radiologically distinct
dementia subtypes emerge over time,” Clancy and colleagues wrote.
“Identifying subgroups will allow future triage of clinical
presentations to appropriate services, the development of
disease-specific management strategies and targeted entry into future
research trials.”
How is your doctor treating your arterial stiffness? This stiffness is precisely why you should never get your neck cracked by a chiropractor, with no testing you have no clue how flexible your vertebral arteries are.
You and your chiropractor are making the assumption with no knowledge that your cervical
arteries running thru your spine are flexible enough and contain no
plaque that they will withstand the twisting motion. How do you know
that is the case?
This
study was conducted to evaluate whether and how arterial stiffness is
associated with cognitive performance, and the role of microvascular
dysfunction. Researchers selected cross-sectional data of 2,544
individuals (age, 59.7 years; 51.0% men; 26.0% type 2 diabetes
mellitus). Carotid-femoral pulse wave velocity and carotid
distensibility coefficient were applied as measures of aortic and
carotid stiffness, respectively. A composite score of microvascular
dysfunction based on magnetic resonance imaging features of cerebral
small vessel disease, flicker light-induced retinal arteriolar and
venular dilation response, albuminuria, and plasma biomarkers of
microvascular dysfunction (soluble intercellular adhesion molecule-1,
soluble vascular adhesion molecule-1, sE-selectin [soluble E-selectin],
and von Willebrand factor) were estimated. The data exhibited that
aortic stiffness, but not carotid stiffness, is independently correlated
with worse cognitive performance, and that this correlation is in part
explained by microvascular dysfunction.
Well then it is obvious that your first task is to get the survivor back to their original cognitive ability. This is your doctor's responsibility. Don't let them abdicate responsibility by using the statement: 'All strokes are different, all stroke recoveries are different.'. Screaming may be required, no excuses are allowed from your stroke medical 'professionals.'
Introduction:
Patient engagement during inpatient stroke rehabilitation (ISR) is
critical to long-term outcomes. Cognitive deficits have demonstrated
impact on engagement in rehabilitation. Here, we prospectively
investigated the relationship between specific cognitive domains and
patient engagement during ISR. Methods: Of 423 patients completing ISR, 127 (30%) had complete data with mean age=67.63+15.46 years, NIHSS=6.78+5.68, and onset from stroke to ISR admission=8.55+7.72
days. The sample comprised 55% males and 56.7% had a college education
or more. The National Institute of Neurologic Disorders - Canadian
Stroke Network (NINDS-CSN) 30-minute cognitive screening battery was
administered within 72 hours of ISR admission to assess verbal fluency,
executive functioning, and memory. The Hopkins Rehabilitation Engagement
Ratings Scale (HRERS; total score 0-30, higher=greater engagement) was
completed by treating therapists at ISR discharge. Spearman rank-order
correlations (rs) examined the relationships between the
HRERS total score and the NINDS-CSN total (the mean z-score across
subtests) as well as its 8 subtests. Items with correlations p<.10
were entered into a logistic regression (controlling for age,
comorbidity, and stroke severity) to predict low (HRERS ≤ 25) versus
high engagers (HRERS > 26). Results: NINDS-CSN
total and 6 subtests assessing verbal fluency and executive function
were weakly to moderately correlated with HRERS scores (rs=0.23-.38,
all p’s <.01). Memory subtests were not associated with HRERS.
Higher NINDS-CSN total score and subtests reflecting executive functions
modestly increased the odds of being a high engager (Odds Ratios ranged
from 1.03-1.08, 95% CIs ranged from 1.013-1.134, all p’s < .01). Conclusion:
Poor executive functioning may pose a barrier to patient engagement in
ISR. Executive functions may impact patients’ ability to shift among
activities, maintain attention, and rapidly process information during
therapy. Rehabilitation therapists should consider making environmental
modifications, providing more frequent guidance and positive
reinforcement, and presenting simplified material to increase engagement
in stroke patients with executive dysfunction.
. Useless and repetitive. No protocol provided. Not repeatable since there seems to be no objective starting point for any survivor. Music has been proven many many times to be helpful in stroke rehab.
Maybe your doctor has heard about it? You'd have to be brain dead not to have heard of music helping stroke recovery.
Reviewed byDr. Victor Marchione, MD. Written byBel Marra Health Published onMay 13, 2019
New research shows that mindfulness music may help those who have
suffered a stroke to recover impaired cognitive ability. The study
published in the International Journal of Stroke
reported the outcomes of a study that aimed to investigate the effect
of combining music listening and mindfulness techniques on recovery of
cognitive ability after a stroke.
The study titled The Measuring the Effects of Listening for Leisure
on Outcome After Stroke, or MELLO, involved 72 participants from acute
stroke units within the NHS Greater Glasgow and Clyde area in the UK.
Each patient had suffered an ischemic stroke, the most common type of
stroke, which is caused when blood flow supply to the brain is blocked,
for example, due to a blood clot in the brain.
The study involved placing participants into three groups. One of the
groups was asked to listen to music, another to music combined with
mindfulness practice, and the last group to audiobooks. They all used an
iPod and had to listen for an hour a day for eight weeks during their
recovery immediately after being discharged from the hospital.
They were all free to choose their own books and music and were
required to keep a daily written record of their listening patterns. The
researchers followed up with each participant on a weekly basis and
recorded progress. The participants in the mindfulness and music group
were also taught two five-minute exercises that were designed to help
with attention if their mind wandered while listening.
The researchers conducted tests of attention, mood, and memory at the
beginning of the study. They followed up with the same tests at the
three and six-month markers after the stroke to determine how each
participant’s cognitive functions and mood changed as a result of the
listening.
Increased Cognitive Ability
At the end of the eight-week listening period, they found that
participants in the mindful music listening group felt relaxed and had
increased cognitive ability as they were able to concentrate, focus, and
manage emotions after listening. The patients in the music listening
group also often reported that the music increased their activity
levels. Both music listening groups reported that music stimulated
recall of memories from the past. Both music groups also showed better
recovery of memory functions compared to the audiobook group. Between
all three groups, there was no difference in mood.
Lead author of the study, Dr. Satu Baylan, from the University of
Glasgow’s Institute of Health and Wellbeing, said “People who have
suffered a stroke are often left with cognitive difficulties that affect
the ability to concentrate and remember information yet there is
limited rehabilitation input for these problems. Many people also
experience low mood and anxiety, which can have a negative impact on
recovery and their level of engagement in everyday activities.
“Previous research has suggested that daily music listening might
improve memory and attention after stroke. Mindfulness on the other hand
is known to improve mood in the general population and in those with
depression but there is very little examination of mindfulness in people
after stroke. We were keen to investigate whether combining music
listening with mindfulness might help address some of the difficulties
that people commonly face after a stroke using an approach that can
potentially be both enjoyable and accessible.
Professor Jonathan Evans, the paper’s principal investigator and
corresponding author said, “Although more research is needed, the MELLO
study’s encouraging results suggest that this low-cost intervention,
which can be done at home, may have positive benefits for people
recovering from a stroke. What is particularly positive is that our
results are consistent with another study done in Finland that also
found that daily music listening improved memory and concentration,
compared to audiobook listening or usual care.”
What a waste, 'more' and 'higher levels' mean absolutely nothing. Don't you fucking understand that protocols are needed? Exact amounts and types. How do you measure cognitive reserve? How much do I need to be like Bernadette the nun? I need to know since I have to rebuild mine after using it all up in surviving and recovering from my stroke.
More physical activity, better motor skills correlate with reduced risk of dementia
register today
Earn Free CME Credits by reading the latest medical news in your specialty. sign up
by Vicki Brower, CME Writer, MedPage Today
Action Points
Higher levels of
physical activity and better motor ability were independently associated
with better cognition in older adults living in a community setting,
even in the presence of brain lesions or dementia-associated biomarkers.
Understand
that physical activity may provide cognitive reserve to maintain
function, independent of accumulating brain pathologies.
CME Author: Vicki Brower Study Authors: Aron S. Buchman, Lei Yu, et al.; James A. Mortimer, Yaakov Stern Target Audience and Goal Statement:
Neurologists, neuropsychologists, neuropsychiatrists, psychiatrists,
gerontologists, primary care physicians, family medicine specialists,
and internists
The goal was to study the associations of physical activity,
Alzheimer's disease (AD) and other brain pathologies, and cognition in
older adults living in the community. Questions Addressed:
What is the
relationship, if any, between physical activity, motor abilities, and
common brain pathologies in community-dwelling older adults?
What
are possible explanations for the association, found in this study and
elsewhere, between physical activity and cognitive function in this
group of elderly individuals?
Study Synopsis and Perspective:
In
an ongoing longitudinal cohort study of 450 older adults, average age
of 91 at death, researchers found that higher levels of physical
activity and better motor ability were independently associated with
better cognition, even in the presence of brain lesions or
dementia-linked biomarkers.
Aron S. Buchman, MD, of Rush University Medical Center in Chicago,
and colleagues monitored individuals' daily activity, tested motor
performance, and conducted postmortem brain autopsies to detect 10 brain
pathologies, based on data from the Rush Memory and Aging Project.
The project is a community-based cohort of older adults who agreed to
annual detailed clinical examinations, and brain donation at the time of
death.
The analysis included 454 participants, 73% of whom were women. A
total of 191 participants had been diagnosed with dementia, and 263 with
no dementia.
As described in the study online in Neurology, the
team conducted 10 supervised motor performance tests to determine
global motor ability scores and used continuous multi-day accelerometer
recordings to monitor physical activity.
Activity results were collected about 2 years before death, and
measured in counts/day. The overall average was 156,000 counts/day, with
participants without dementia averaging 180,000 counts/day, and people
with dementia averaging 130,000 counts/day.
Buchman
and co-authors tested study participants for five cognitive abilities:
semantic memory, episodic memory, working memory, perceptual speed, and
visuospatial abilities.
At autopsy, the researchers assessed brain tissue for the following:
Alzheimer's disease pathology (neuritic plaques, diffuse plaques, and neurofibrillary tangles)
Nigral neuronal loss
Lewy body disease pathology
TAR DNA-binding protein 43
Hippocampal sclerosis
Macroscopic cerebral infarcts
Cerebral atherosclerosis
Microscopic cerebral infarcts
Cerebral arteriolosclerosis
Cerebral amyloid angiopathy
A total of 85% of study participants had two or more different brain pathologies.
The team performed regression analyses to examine whether motor
abilities or the amount of daily physical activity attenuated the
association of indices of AD pathology with the level of cognitive
function proximate to death.
Higher levels of total daily activity (estimate 0.148 ± 0.049, 95% CI 0.053-0.0.244, P=0.003) and better motor abilities (estimate 0.283 ± 0.055, 95% CI 0.175-0.390, P<0.001)
were both independently associated with better global cognition
proximate to death. These independent associations remained significant
when interaction terms for AD and other pathologies were added, the
researchers reported.
Each
standard deviation increase of total daily activity or motor capacity
was associated with a reduction of dementia risk (total daily activity
31%; motor abilities 55%). Moreover, these associations were additive,
as the association of total daily physical activity with cognition did
not vary with motor abilities.
"Physical activity may provide cognitive reserve to maintain function
independent of accumulating brain pathologies," Buchman told MedPage Today.
Still, the investigators said, it is possible that "the association
between total daily activity and cognition may have been observed
because higher total daily activity may lead to better cognition or
because poorer cognition, ie., dementia, might lead to reduced daily
activity."
In their analysis, the researchers concluded that motor abilities
remained independently associated with better cognition and that poorer
cognition did not account for the association of total daily activity
and motor abilities with cognition proximate to death.
"These data provide support for the idea that strategies or behaviors
that lead to a more active lifestyle and better motor abilities may
provide cognitive reserve, which may maintain cognitive function in
older adults despite the accumulation of Alzheimer's disease and other
common brain pathologies," the researchers wrote. "Further work is
needed to clarify to what extent the risk factors and the types and
duration of interventions to increase total daily physical activity and
motor abilities are distinct and can be disentangled." Source References: Neurology, online Jan. 16, 2019; DOI: 10.1212/WNL.0000000000006954f
Editorial: Neurology, online Jan. 16, 2019; DOI: 10.1212/WNL.0000000000006935 Study Highlights: Explanation of Findings
Buchman and co-researchers found that in this group of elderly
adults, "a more active lifestyle and better motor abilities proximate to
death were independently associated with better cognitive function and
reduced odds of dementia with controlling for AD and nine other common
age-related brain pathologies." The associations between both physical
activity and motor abilities with better cognition and lower risk of
dementia are "independent and additive," the team noted.
"Moreover, there was also no evidence that a more active lifestyle or
better motor abilities modified the associations of these brain
pathologies with cognitive function proximate to death," the researchers
wrote, concluding that "together, these data suggest that the cognitive
reserve associated with physical activities and motor abilities is
unrelated to the presence of common brain pathologies and that the
molecular mechanisms that underlie this reserve remain to be
identified."
The researchers explained that previous studies, including one from
the same patient cohort, have suggested that higher levels of physical
activity may slow the rate of cognitive decline and reduce the risk of
AD dementia, but the mechanisms whereby this may occur remain unclear.
Studies in animals indicate that more physical activity may prevent the
accumulation and progression of AD pathology, and brain imaging research
in older adults suggests that higher levels of physical activity are
associated with lower levels of infarcts and better white matter brain
integrity.
In addition, studies with PET imaging show that higher levels of
β-amyloid deposits are associated with poorer motor function. But
Buchman et al. noted that in the few studies that have focused on
physical activity, there has not been a consistent relationship with
physical activity level and brain imaging levels of β-amyloid or
cerebral spinal fluid (CSF) markers of AD.
The lack of human data "makes it difficult to explicate the
pathologic mechanisms" that underlie the association of a more active
lifestyle with better cognition in older adults, the researchers wrote.
In an accompanying editorial,
James Mortimer, PhD, of the University of South Florida in Tampa, and
Yaakov Stern, PhD, of Columbia University in New York City, echoed
Buchman and co-authors, noting that numerous observational studies have supported an association between physical exercise and reduced cognitive decline.
"The results of randomized trials of physical exercise suggest that
exercise leads to increases in brain tissue, including in the
hippocampus, where atrophy is an early and important finding in
Alzheimer's disease," the editorialists wrote. For example, one trial
showed that aerobic exercise led to increased levels of brain-derived neurotrophic factor (BDNF) and increased hippocampal volume; other studies suggested that higher BDNF gene expression may help slow cognitive decline. "Alternatively, physical exercise itself might reduce brain pathology," and mouse models have shown that higher physical activity levels reduce the accumulation of AD pathology, Mortimer and Stern added.
Buchman and co-authors noted that while their cross-sectional results
should be interpreted with caution, the findings do provide support for
the idea that even in the absence of treatment for AD and related
disorders, a more active lifestyle, including physical and cognitive
activities, may help maintain cognition in older adults.
Study limitations, the team said, include that because the data were
cross-sectional, causal inferences cannot be drawn. It is also possible
that some of the association resulted from reverse causality (i.e., that
lower cognitive function led to less activity).
In addition, the accelerometers used in the study did not
differentiate between various physical activities (such as steps vs arm
movements), and activity was assessed only at one point later in life,
so it remains unknown whether physical activity in early life may have
played a role.
Mortimer and Stern also stated that in order to prove causation,
longitudinal studies of physical activity and cognition with brain
imaging would be needed to document the influence of pathology on the
demonstrated association.
I bet testing was done coming in with no practice. A sure way to fail all stroke patients. I barely passed my road test, now I drive anywhere, anyplace, anytime.
This
study investigated the relationship between cognitive ability and
driving after stroke. Thirty-nine pre-stroke drivers were assessed using
a battery of cognitive tests followed by a road test over a set route.
Subjects were graded into Pass, Borderline or Fail categories on the
basis of the road test. Cognitive test results were compared across
grades of driving performance and significant differences were found on
nine of the 23 measures. A discriminant function analysis identified 10
tests which together predicted the grading of 94% of subjects into Pass
or Fail categories.
