Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,286 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.
Absolutely nothing here tells me if you are ANY GOOD AT ALL. You tell us nothing on results, these three points are key. But you do use the word 'care' 6 times, which tells us nothing.
Three measurements will tell me if your stroke hospital is possibly not completely incompetent; DO YOU MEASURE ANYTHING?
Hamad Medical Corporations (HMC)’s stroke service has
undergone an enormous transformation in recent years and is now one of
the leading services of its kind in the region.
The fast and effective treatment of stroke patients has been achieved
despite an increase in the number of stroke patients seen at HMC each
year, said Dr Naveed Akhtar, Head of Stroke Services at HMC.
“We have a standard of care, acute stroke treatment in the country,
which only a few hospitals have in the region. We are seeing increasing
numbers of stroke patients and we have worked hard to ensure we provide
them with the very best care possible,” he told The Peninsula.
“HMC established the Stroke Program few years ago, and it first introduced the Acute Stroke Service,” he added.
Launch of the Stroke Program, recruitment of specialist nurses and
consultants, the opening of dedicated facilities and introduction of
advanced technology - including a dedicated stroke ward with 12 beds, a
Neuroangiograhy Suite – as well as the redesign of care processes, have
delivered improved outcomes for stroke patients.
HMC’s Stroke Program is the first of its kind in the Middle East to
be recertified by the Joint Commission International (JCI), endorsing
the quality and safety of the care it provides to patients. The HMC
Stroke Program operates under Hamad General Hospital (HGH).
About 200 new patients are seen every month at HGH for suspected
stroke. Hence any person who suffers from sudden onset neurologic
symptoms should seek immediate help, as 30-35 percent present with
hyper-acute stroke which require immediate interventional care, said Dr
Akhtar.
Dr Akhtar highlighted the need for prompt treatment of stroke
patients. “The speed at which treatment can be given to stroke patients
is of the highest importance. A stroke leads to the complete or partial
restriction of blood flow in the brain and damages brain cells so they
can no longer work properly. The more time that passes between the onset
and medical therapy and intervention, the greater the damage that can
be done. The term ‘time is brain’ is frequently used to emphasize the
need for fast intervention, as the faster treatment can be given
following a stroke, the better the chances of recovery,” he said. The
treatment methods included giving thrombolysis, a medication injected
within four and a half hours of the onset of an acute stroke. This clot
breaking drug can open the artery and restore the blood flow to the
brain.
Known as ‘door to needle time’, the international benchmark of
treating 50 to 60 percent of patients within 60 minutes from arrival at
hospital relates specifically to the use of thrombolysis, a clot-busting
medication.
In addition to the efficient use of thrombolysis to treat stroke
patients, HMC’s Stroke Service is increasingly utilising interventional
thrombectomy, the retrieval of blocked vessel clots through a catheter.
This intervention has significantly enhanced the outcome of specific
group of patients who need such treatment.
HGH also has a Stroke Prevention Clinic and Rapid Assessment Stroke Unit (RASU).
According to Dr Akhtar, the Stroke Prevention Clinic sees and follows
up on people who are at the high risk of getting recurrent stroke. The
clinic helps in identifying and modifying their risk factors and advices
on life style.
“A major stroke can be prevented if patients with transient symptoms or
minor stroke are treated as early as possible, according to studies. At
RASU any patient who has a minor stroke or reversible symptoms of stroke
will be seen within 12 hours. We do appropriate and urgent follow-ups
and make sure that none of the patients get missed out,” said Dr Akhtar.
“Some of the signs of a minor stroke include mild facial or limb
weakness or numbness on one side, speech difficulty, sensory problems
and visual problems. These symptoms can progress to a major stroke,” he
added.
“The team meets every day including weekends to discuss the management
and plan treatment and disposition of stroke patients. After recovery
from the initial stage about 20 to 25 percent of patients get
transferred to the Qatar Rehabilitation Institute where they get planned
rehabilitation and care,” said Dr Akhtar.
Lots of big words and still the wrong objective. 'Can' and 'may' are two weasel words that should never occur in stroke research. You didn't do enough research then. Your mentors and senior researchers should be relieved of duty for allowing such lazy crapola. Until we get survivors in charge this shit will continue.
Background.
The cortical plastic changes in response to median nerve electrical
stimulation (MNES) in stroke patients have not been entirely
illustrated. Objective. This study aimed to investigate (Should have been produce a protocol on MNES)MNES-related changes in effective connectivity (EC) within a cortical
network after stroke by using functional near-infrared spectroscopy
(fNIRS). Methods. The cerebral oxygenation signals in the
bilateral prefrontal cortex (LPFC/RPFC), motor cortex (LMC/RMC), and
occipital lobe (LOL/ROL) of 20 stroke patients with right hemiplegia
were measured by fNIRS in 2 conditions: (1) resting state and (2) MNES
applied to the right wrist. Coupling function together with dynamical
Bayesian inference was used to assess MNES-related changes in EC among
the cerebral low-frequency fluctuations. Results. Compared with
the resting state, EC from LPFC and RPFC to LOL was significantly
increased during the MNES state in stroke patients. Additionally, MNES
triggered significantly higher coupling strengths from LMC and LOL to
RPFC. The interregional main coupling direction was observed from LPFC
to bilateral motor and occipital areas in responding to MNES, suggesting
that MNES could promote the regulation function of ipsilesional
prefrontal areas in the functional network. MNES can induce muscle
twitch of the stroke-affected hand involving a decreased neural coupling
of the contralesional motor area on the ipsilesional MC. Conclusions.
MNES can trigger sensorimotor stimulations of the affected hand that
sequentially involved functional reorganization of distant cortical
areas after stroke. Investigating MNES-related changes in EC after
stroke may help further our understanding of the neural mechanisms
underlying MNES.
Oh God, excuses, excuses, fucking excuses. There is massive amounts of commonality in stroke disability. Are you that fucking blind and lazy that you can't see that? A different version of: 'All strokes are different, all stroke recoveries are different.' Still a completely lazy way to not solve stroke.
September 30, 2019
SEATTLE
– The effects of a stroke are different for everyone, and that's why
medical professionals say it's crucial to tailor rehabilitation to each
individual.
Seattle resident Courtney Wilkins in 2010 suffered a stroke in her brain
stem at age 30. Afterwards, she couldn't walk, use her right hand or
sense pain or temperature on the left side of her body.
Wilkins stayed in inpatient rehabilitation for a month and then moved
back to Arkansas with her parents for another four months of outpatient
rehabilitation, where she was told she would never live on her own
again.
But Wilkins is proof sticking to therapy is worth it.
"After about 18 months, [I] was able to take my first steps unassisted
and now I walk with one forearm crutch,” she relates. “I had gone from
being in the chair primarily for three years to being on two forearm
crutches to now one forearm crutch."
Wilkins eventually moved back to Seattle, learned how to be left-handed and started a career as a data analyst.
Nearly 800,000 people have their lives changed by stroke every year.
The most rapid recovery typically occurs in the first three to six
months after a stroke, according to health professionals. But Wilkins
notes that doesn't mean people stop getting better after that.
Even now – nine years after her stroke – she continues to make progress.
"It's slower but it is still possible, and some of the progress is not
even so much that you have to have the use back exactly the way you had
it before, but with some creativity, there's very little that you can't
find a way to do one way or another," she states.
It suggests asking your doctor for an assessment of physical and
cognitive challenges and how to address each challenge, managing risk
factors to prevent another stroke, talking with your health care
provider about financial constraints and following up with your doctor
regularly.
Useless, more studies needed. No mention of where these protocols are. This statement shows we still know nothing on rTMS.
Although several studies have been published, a conclusive statement
supporting a systematic use of rTMS in the multifaceted clinical aspects
of stroke rehabilitation is still lacking.
Acute
brain ischemia causes changes in several neural networks and related
cortico-subcortical excitability, both in the affected area and in the
apparently spared contralateral hemisphere. The modulation of these
processes through modern techniques of noninvasive brain stimulation,
namely repetitive transcranial magnetic stimulation (rTMS), has been
proposed as a viable intervention that could promote post-stroke
clinical recovery and functional independence. This review provides a
comprehensive summary of the current evidence from the literature on the
efficacy of rTMS applied to different clinical and rehabilitative
aspects of stroke patients. A total of 32 meta-analyses published until
July 2019 were selected, focusing on the effects on motor function,
manual dexterity, walking and balance, spasticity, dysphagia, aphasia,
unilateral neglect, depression, and cognitive function after a stroke.
Only conventional rTMS protocols were considered in this review, and
meta-analyses focusing on theta burst stimulation only were excluded.
Overall, both HF-rTMS and LF-rTMS have been shown to be safe and
well-tolerated. In addition, the current literature converges on the
positive effect of rTMS in the rehabilitation of all clinical
manifestations of stroke, except for spasticity and cognitive
impairment, where definitive evidence of efficacy cannot be drawn.
However, routine use of a specific paradigm of stimulation cannot be
recommended yet due to a significant level of heterogeneity of the
studies in terms of protocols to be set and outcome measures that have
to be used. Future studies need to preliminarily evaluate the most
promising protocols before going on to multicenter studies with large
cohorts of patients in order to achieve a definitive translation into
daily clinical practice.
The app helping to prevent stroke: FibriCheck
FibriCheck was the first smartphone app designed to detect heart
rhythm disorder, without using any external medical devices, to receive a
Food and Drug Administration (FDA) approval.
Co-founded by Bieke Van Gorp and Lars Grieten in Belgium, FibriCheck
can help prevent stroke by detecting atrial fibrillation and other heart
rhythm disorders using a smartphone or smartwatch.
By placing a finger on the smartphone’s camera, the app measures a
person’s heart rhythm for one minute and gives them a detailed report
and immediate actionable results, reviewed by FibriCheck’s team of
medical experts. Users can then track their heart rhythm history and
look back on how it has changed.
FibriCheck has received Food and Drug Administration (FDA) approval
and designation as a diagnostic device. It can now be used by clinicians
around the world thanks to this as well as its European Conformity (CE)
medical approval. Over 130,000 people have so far been screened using
the app.
Constraint-induced
movement therapy improves outcome after chronic stroke, conforms
experimental observations of neuronal plasticity, and proves the
efficacy of intensive occupational therapy. More acutely instituted
constraint-induced movement therapy has both practical and theoretic
risks and benefits that deserve further careful evaluation.
Constraint-induced
movement therapy (CIMT) provides a vehicle for objectively testing the
efficacy and utility of rehabilitation intervention. It also provides a
platform for designing and testing further advances in rehabilitation
intervention. Finally, by correlating improvements on motor performance
after CIMT with functional neuroimaging, CIMT provides the opportunity
to demonstrate functional imaging as a surrogate outcome measure to
utilize in clinical trials of rehabilitation intervention.
The scientific basis of intensive physical retraining after stroke has recently been validated by the work of Nudo et al,1
among others. Using microelectrode recordings in primate cortex, these
investigators mapped out the motor representation area of the digit,
wrist, and proximal upper extremity in animals at baseline and after a
cortical lesion, both with and without postinfarct rehabilitation
therapy. They were clearly able to demonstrate enlargement of the digit
and wrist areas that were represented on the cortex in those animals
that had postinfarct rehabilitation therapy compared with those that did
not. This work, which has now been replicated in other animal models
and in humans by using functional imaging, has provided a strong
scientific basis for investigations into enhancing rehabilitation
intervention.
CIMT is based on the initial research by Dr Edward Taub,2–5
which was conducted in the late 1970s and 1980s. In primates, he
deprived the upper extremity of somatic sensation by dorsal rhizotomy.
After this procedure, the animal immediately stopped using their
deafferentated extremity. Restoration of use was induced by immobilizing
the intact arm over several days while training the animal to use the
affected arm. This work resulted in the formulation of CIMT for humans.
CIMT
is based on the theory of “learned non-use.” Learned non-use develops
during the early stages following a stroke as the patient begins to
compensate for difficulty using the impaired limb by increased reliance
on the intact limb. This compensation has been shown to hinder recovery
of function in the impaired limb.
There have been a number of studies evaluating the efficacy of CIMT in patients with chronic stroke.6–8 In one of the more recent studies, van der Lee et al9
conducted an observer-blinded, randomized, clinical trial in 66 chronic
stroke patients allocated to CIMT or equally intensive reference
therapy for 2 weeks. One week after the last treatment session, there
was significantly greater improvement in the CIMT group. At 1-year
follow up, there still was a small but lasting improvement in the motor
function of the affected upper extremity.
Recently,
CIMT has been applied to subacute stroke patients with the hypothesis
that earlier intervention may prevent learned non-use from developing in
the first place and may have a greater impact. Dromerick et al,10
conducted a pilot, randomized, controlled, single-blind trial of CIMT
beginning <14 days poststroke in 23 patients. These investigators
found slightly greater improvement in motor function of the affected
upper extremity relative to equal intensity of standard therapy.
Importantly, there were no adverse effects of CIMT in the subacute
phase. This study did not have long-term follow up and no functional
imaging was carried out. A larger study with longer-term follow up is
now underway.
Some
experimental studies in animal models suggest that very early CIMT may
not be helpful and may, in fact, be harmful. This is based on studies of
“forced overuse.”11–13
Schallert and colleagues immobilized the contralateral intact forelimb
in a plaster cast for 14 days, starting immediately after a sensory
motor cortex lesion. They found that such forced overuse of the affected
forelimb within the first 7 days impeded motor recovery of the affected
limb, and enlarged lesion volume. If the casting was delayed until 7 to
14 days after the insult, there was no lesion expansion but there was
still a negative impact on behavioral recovery. Bland et al, forced
overuse of the affected forelimb immediately after a focal cortical
middle cerebral artery stroke, and this increased lesion size and
impaired motor recovery as well. Therefore, it is possible that CIMT, if
started too early, may be harmful. Adverse histological effects of
intensive motor activity started in the first days after stroke may
prevent maximal functional benefit from CIMT. Therefore, the relative
risks and benefits of “acute” CIMT, and its optimal timing, remain to be
determined.
We
have carried out a small pilot study of early CIMT in our center. This
study was intended to test the feasibility and safety of carrying out a
larger efficacy trial in the acute stroke setting, as well as the
feasibility of correlating clinical outcome measures with functional
imaging. Patients at Memorial Hermann Hospital’s Stroke Unit were
randomized within 14 days of stroke onset. To be included, the patients
had to have weakness in one arm and hand, but at least 10° of preserved
movement in the digits of their hand. After baseline testing and
transcranial magnetic stimulation (TMS) brain mapping, patients were
randomized to CIMT or standard of care physical and occupational therapy
for 2 weeks. The CIMT group wore a mitten on the nonaffected upper
extremity for 90% of waking hours and at the same time had therapy that
reinforced the use of the affected upper extremity. Behavioral “shaping”
of the affected upper extremity, using the technique of successive
approximations, was carried out for 3 hours a day, training the impaired
upper limb in various tasks related to activities of daily living. The
control group received treatment aimed at increasing functional use of both
hands, using compensatory techniques as needed, for 3 hours a day for 2
weeks. At the end of 2 weeks of treatment, and again 3 months after
treatment, both clinical and TMS measurements were repeated. Three
different measures of hand and arm function were carried out: Motor
Activity Log (MAL), Grooved Pegboard Test (GPB), and the upper extremity
motor component of the Fugl-Meyer (FM) Test.
One
of the early discoveries in this study was that very few acute stroke
patients qualified on the basis of motor function. Most patients either
had no movement in their hand or excellent recovery during the first 2
weeks. Out of 187 patients screened, 30 had no movement in the hand, 76
had nearly complete recovery of movement in the hand, and 55 had either
no movement or complete recovery of movement coupled with some other
exclusion such as aphasia. Eight patients (5 men) were randomized, 4 to
each group. All had ischemic strokes and were randomized within the
first 2 weeks after stroke onset. While there was no change in the MAL
in those patients randomized to CIMT versus control, in those patients
receiving CIMT there was progressively increased improvement in the GPB
test and in the FM assessment, both at 2 weeks and to an even greater
extent at 3 months of follow-up.
TMS
mapping of the motor cortex hand region was carried out bilaterally in
1-cm increments at baseline, at 2 weeks, and at 3 months. Baseline TMS
studies showed few or no regions on the affected hemisphere that could
be stimulated resulting in contralateral hand movement in either group.
However, in the CIMT group, a greater number of regions could evoke a
response in the contralateral affected hand both at 2 weeks and 3
months. There was a strong correlation between the number of TMS
activation points and GPB and FM test scores (Figure).
In
conclusion, CIMT probably improves upper extremity function in chronic
stroke patients. If instituted in the first 2 weeks after stroke, it is
probably not harmful and it may accelerate recovery. TMS noninvasively
demonstrates the biological effect of CIMT on brain reorganization.
Currently, we are enrolling in a confirmatory study to determine the
efficacy of CIMT in acute stroke patients. Based on the magnitude of
efficacy seen in our pilot study of 8 patients, we anticipate that we
will need 24 patients to detect a difference with 90% confidence.
CIMT
is not without its problems. Most patients in the acute setting do not
qualify, and it imposes substantial demands both on therapists and the
resources of a rehabilitation unit. Furthermore, CIMT probably has
limited effect and may not be cost-effective. In the future, it may be
advantageous to improve the cost benefit of CIMT by employing a less
intense method and combining CIMT with pharmacologic interventions,
particularly neurotropic drugs, or with robotics. Furthermore,
functional imaging such as TMS, magnetoencephalography, or magnetic
resonance imaging, may provide a surrogate outcome measure that will
help in the more efficient and cost-effective assessment of the efficacy
of CIMT and other rehabilitation techniques.
Acknowledgments
This
study was funded by the National Institutes of Health (P50 NS044227 and
R24 HD39629). Dr Noser is funded by NIH training grant T32 NS07412.
Footnotes
Correspondence
to Dr James C. Grotta, Department of Neurology Stroke Program,
University of Texas–Houston Medical School, 6431 Fannin Street, Houston,
TX 77030. E-mail james.c.grotta@uth.tmc.edu
Therapeutics and Clinical Risk Management — Xie W, et al. | September 26, 2019
Researchers performed an updated
meta-analysis of 14 studies to assess the efficacy and safety of aspirin
for the primary prevention of cardiovascular disease. Eligible studies
included randomized, controlled trials comparing aspirin with placebo or
no treatment that were published up to November 1, 2018. The primary
efficacy endpoint was all-cause death, with secondary endpoints
including cardiovascular death, myocardial infarction, and stroke. Major
bleeding, gastrointestinal bleeding, and hemorrhagic stroke comprised
safety endpoints. Compared with placebo or no treatment, aspirin was
linked to a lower risk of myocardial infarction. Compared with control
groups, however, aspirin was no linked to a lower risk of all-cause
mortality or cardiovascular mortality. With respect to safety, aspirin
was associated with a higher risk of major bleeding, gastrointestinal
bleeding, and hemorrhagic stroke. In addition, patients’ clinical
characteristics did not greatly influence the treatment affect.
Your doctor can discuss the pros and cons of each. My carotid arteries were scanned by ultrasound while I did the stress test with angiogram for the coronary. My right carotid was fully blocked but now it seems collaterals have opened around it. I guess two small coronaries at the back of the heart are 30% blocked, doctor doesn't seem concerned.
Journal of Computer Assisted Tomography — Li Ying, Zhu G, Ding V, et al. | September 24, 2019
Researchers compared coronary with
carotid artery imaging, and determined which one demonstrates the
strongest association with atherosclerotic cardiovascular disease
(ASCVD) score. They included two separate series patients (n = 110 in
each group) who completed either coronary computed tomography
angiography (CTA) or carotid CTA, and they recorded the ASCVD scores and
evaluated the CTA imaging. Two-thirds were used to develop predictive
models, and one-third generated predicted ASCVD scores. The
investigators used Bland-Altman analysis to analyze the concordance.
Overall, there were no significant differences between clinical
characteristics. Three imaging variables were included in the carotid
model, and two coronary models (presence of calcium or Agatston score)
were created. The bias between true and predicted ASCVD scores was 0.37 ±
5.72% on the carotid model, and 2.07 ± 7.18% and 2.47 ± 7.82% on
coronary artery models, respectively. According to findings, carotid and
coronary artery imaging features may predict ASCVD score. However, the
carotid artery was more strongly associated with the ASCVD score than
the coronary artery.
Summary:
Researchers have identified a link between traumatic brain injury and
intestinal changes. A new study reports the intestinal changes may
contribute to increased risk of developing infections and could worsen
brain damage in TBI patients. Source: University of Maryland School of Medicine. University
of Maryland School of Medicine (UMSOM) researchers have found a two-way
link between traumatic brain injury (TBI) and intestinal changes. These
interactions may contribute to increased infections in these patients,
and may also worsen chronic brain damage.
This is the
first study to find that TBI in mice can trigger delayed, long-term
changes in the colon and that subsequent bacterial infections in the
gastrointestinal system can increase posttraumatic brain inflammation
and associated tissue loss. The findings were published recently in the
journal Brain, Behavior, and Immunity.
“These results
indicate strong two-way interactions between the brain and the gut that
may help explain the increased incidence of systemic infections after
brain trauma and allow new treatment approaches,” said the lead
researcher, Alan Faden, MD, the David S. Brown Professor in Trauma in
the Departments of Anesthesiology, Anatomy & Neurobiology,
Psychiatry, Neurology, and Neurosurgery at UMSOM, and director of the
UMSOM Shock, Trauma and Anesthesiology Research Center.
Researchers
have known for years that TBI has significant effects on the
gastrointestinal tract, but until now, scientists have not recognized
that brain trauma can make the colon more permeable, potentially
allowing allow harmful microbes to migrate from the intestine to other
areas of the body, causing infection.. People are 12 times more likely
to die from blood poisoning after TBI, which is often caused by
bacteria, and 2.5 times more likely to die of a digestive system
problem, compared with those without such injury.
In this study,
the researchers examined mice that received an experimental TBI. They
found that the intestinal wall of the colon became more permeable after
trauma, changes that were sustained over the following month.
It
is not clear how TBI causes these gut changes. A key factor in the
process may be enteric glial cells (EGCs), a class of cells that exist
in the gut. These cells are similar to brain astroglial cells, and both
types of glial cells are activated after TBI. After TBI, such activation
is associated with brain inflammation that contributes to delayed
tissue damage in the brain. Researchers don’t know whether activation of
ECGs after TBI contributes to intestinal injury or is instead an
attempt to compensate for the injury.
It
is not clear how TBI causes these gut changes. A key factor in the
process may be enteric glial cells (EGCs), a class of cells that exist
in the gut. NeuroscienceNews.com image is in the public domain.
The
researchers also focused on the two-way nature of the process: how gut
dysfunction may worsen brain inflammation and tissue loss after TBI.
They infected the mice with Citrobacter rodentium, a species of bacteria
that is the rodent equivalent of E. coli, which infects humans. In mice
with a TBI who were infected with this the bacteria, brain inflammation
worsened. Furthermore, in the hippocampus, a key region for memory, the
mice who had TBI and were then infected lost more neurons than animals
without infection.
This suggests that TBI may trigger a vicious
cycle, in which brain injury causes gut dysfunction, which then has the
potential to worsen the original brain injury. “These results really
underscore the importance of bi-directional gut-brain communication on
the long-term effects of TBI,” said Dr. Faden.
About this neuroscience research article
Other
authors of this paper include Elise Ma, a doctoral student; Terez
Shea-Donahue PhD, professor of radiation oncology; Bogdan A. Stoica, MD,
associate professor of anesthesiology ; and David Loane, PhD, associate
professor of anesthesiology- all at UMSOM. Source: David Kohn – University of Maryland School of Medicine Publisher: Organized by NeuroscienceNews.com. Image Source: NeuroscienceNews.com image is in the public domain. Original Research:Abstract
for “Bidirectional brain-gut interactions and chronic pathological
changes after traumatic brain injury in mice” by Elise L. Ma, Allen D.
Smith, Neemesh Desai, Lumei Cheung, Marie Hanscom, Bogdan A. Stoica,
David J.,Loane, Terez Shea-Donohue, and Alan I.Fadena in Brain, Behavior and Immunity. Published online November 2017 doi:/10.1016/j.bbi.2017.06.018
I can't successfully dance. The left foot will not get off the floor with any decent amount of speed. I can't jump up and down. The left arm is a dead log that if I get too vigorous will slap other dancers. I didn't feel comfortable even trying to dance last night.
As we grow older we suffer a decline in mental and physical fitness,
which can be made worse by conditions like Alzheimer's disease. A new
study, published in the open-access journal Frontiers in Human Neuroscience,
shows that older people who routinely partake in physical exercise can
reverse the signs of aging in the brain, and dancing has the most
profound effect.
"Exercise has the beneficial effect of slowing down or even counteracting age-related decline
in mental and physical capacity," says Dr Kathrin Rehfeld, lead author
of the study, based at the German center for Neurodegenerative Diseases,
Magdeburg, Germany. "In this study, we show that two different types of
physical exercise
(dancing and endurance training) both increase the area of the brain
that declines with age. In comparison, it was only dancing that lead to
noticeable behavioral changes in terms of improved balance."
Elderly volunteers, with an average age of 68, were recruited to the
study and assigned either an eighteen-month weekly course of learning
dance routines, or endurance and flexibility training. Both groups
showed an increase in the hippocampus region of the brain. This is
important because this area can be prone to age-related decline
and is affected by diseases like Alzheimer's. It also plays a key role
in memory and learning, as well as keeping one's balance.
While previous research has shown that physical exercise
can combat age-related brain decline, it is not known if one type of
exercise can be better than another. To assess this, the exercise
routines given to the volunteers differed. The traditional fitness
training program conducted mainly repetitive exercises, such as cycling
or Nordic walking, but the dance group were challenged with something
new each week.
Dr Rehfeld explains, "We tried to provide our seniors in the dance
group with constantly changing dance routines of different genres (Jazz,
Square, Latin-American and Line Dance). Steps, arm-patterns,
formations, speed and rhythms were changed every second week to keep
them in a constant learning process. The most challenging aspect for
them was to recall the routines under the pressure of time and without
any cues from the instructor."
These extra challenges are thought to account for the noticeable
difference in balance displayed by those participants in dancing group.
Dr Rehfeld and her colleagues are building on this research to trial new
fitness programs that have the potential of maximizing anti-aging
effects on the brain.
"Right now, we are evaluating a new system called "Jymmin" (jamming
and gymnastic). This is a sensor-based system which generates sounds
(melodies, rhythm) based on physical activity.
We know that dementia patients react strongly when listening to music.
We want to combine the promising aspects of physical activity and active
music making in a feasibility study with dementia patients."
Dr Rehfeld concludes with advice that could get us up out of our seats and dancing to our favorite beat.
"I believe that everybody would like to live an independent and
healthy life, for as long as possible. Physical activity is one of the
lifestyle factors that can contribute to this, counteracting several
risk factors and slowing down age-related decline. I think dancing is a powerful tool to set new challenges for body and mind, especially in older age."
This study falls into a broader collection of research investigating the cognitive and neural effects of physical and cognitive activity across the lifespan.
Matteo Paci From the Department of Rehabilitation Medicine, Casa di Cura Villa Fiorita, Prato, Italy The Bobath concept, also known as neurodevelopmental treatment, is a widely used approach in the rehabilitation of hemiparetic subjects in many countries. Despite 50 years of clinical use its effectiveness is questionable. This paper aims to examine whether there is evidence to accept neurodevel-opmental treatment as an effective approach. A systematic literature search was undertaken. Fifteen trials have been selected and classified according to a 5-level hierarchic scale of evidence for clinical interventions. Results show no evidence proving the effectiveness of neurodevelopmental treatment or supporting neurodevelopmental treatment as the optimal type of treatment, but neither do methodological limitations allow for conclusions of non-efficacy. Methodological aspects of selected studies are discussed and requirements for further research are suggested. Key words: Bobath concept, stroke, hemiplegia,rehabilitation.J Rehabil Med 2003; 35: 2–7 Correspondence address: Matteo Paci, Via Vittorio Bottego, 4, IT-50127 Firenze, Italy. E-mail:matteo.paci@applicazione.it Submitted February 14, 2002; accepted June 13, 2002
Maybe they give specifics in the full article but I doubt it. So useless. We don't need improvement, or promise or outlines, we need EXACT STROKE PROTOCOLS with efficacy percentages.
Peter Langhorne, Fiona Coupar, Alex Pollock Loss of functional movement is a common consequence of stroke for which a wide range of interventions has been developed. In this Review, we aimed to provide an overview of the available evidence on interventions for motor recovery after stroke through the evaluation of systematic reviews, supplemented by recent randomised controlled trials. Most trials were small and had some design limitations. Improvements in recovery of arm function were seen for constraint-induced movement therapy, electromyographic biofeedback, mental practice with motor imagery, and robotics. Improvements in transfer ability or balance were seen with repetitive task training, biofeedback, and training with a moving platform. Physical fitness training, high-intensity therapy (usually physiotherapy), and repetitive task training improved walking speed. Although the existing evidence is limited by poor trial designs, some treatments do show promise for improving motor recovery, particularly those that have focused on high-intensity and repetitive task-specific practice.
Introduction
Stroke is a common global health-care problem that is serious and disabling. In high-income countries, stroke is the third most common cause of death and is the main cause of acquired adult disability.
However, as most patients with stroke survive the initial injury, the biggest effect on patients and families is usually through long-term impairment, limitation of activities (disability),and reduced participation (handicap).The most common and widely recognised impairment caused by stroke is motor impairment, which can be regarded as a loss or limitation of function in muscle control or movement or a limitation in mobility.
Motor impairment after stroke typically affects the control of movement of the face, arm, and leg of one side of the body and affects about 80% of patients. Therefore, much of the focus of stroke rehabilitation, and in particular the work of physiotherapists and occupational therapists, is on the recovery of impaired movement and the associated
functions. There seems to be a direct relation between motor impairment and function; for example, independence in walking (function) has been correlated with lower-limb strength (impairment).
Therefore, the ultimate goal of therapy for lower-limb motor impairment is to improve the function of walking and recovery of movement.(Wrong goal! 100% recovery NOT improvement. Get with the program.) In this Review, motor impairment and its associated functional activities are regarded as part of a continuum.Motor impairment can be caused by ischaemic or haemorrhagic injury to the motor cortex, premotor cortex, motor tracts, or associated pathways in the cerebrum or cerebellum.
Such impairments affect an individual’s ability to complete everyday activities(disability) and affect participation in everyday life situations.
A lack of consistency is evident among researchers and clinicians in the use of terminology that describes changes in motor ability after stroke.
Changes in motor ability might occur via several mechanisms: restitution, substitution, or compensation.
Levin and co-workers, however, distinguished motor recovery and motor compensation in accordance with the WHO International Classification of Functioning,Disability and Health framework and proposed that motor recovery relates to: restoration of function in neural tissue that was initially lost; restoration of ability to perform movement in the same way as before injury;and successful task completion as typically done by individuals who are not disabled. Types of motor compensation in these three areas include the acquisition by neural tissue of a function that it did not have before the injury; performance of a movement in a new way; and successful task completion by use of different techniques.
In accordance with these definitions, in this Review we focused on outcomes associated with body functions or structure (impairment) and activity (functional). We favoured activity outcomes when these were used in addition to impairment outcomes as these were believed to be more clinically useful. However, we did not focus on motor recovery or motor compensation separately, as many of the outcomes (particularly those measuring activity) do not distinguish between improvements associated with increasing compensation and movement patterns. Although we recognise the potential limitations of this approach, this Review can only outline the outcomes used in the trials.Motor recovery after stroke is complex and confusing.(So fucking what? Try recovering from a stroke with NO guidance at all)Many interventions have been developed to try to aid motor recovery (recovery of impairment and associated function), and many randomised controlled trials and systematic reviews have been done.
Most of these interventions do not explicitly target a specific pathophysiological process and have been tested using a variety of patient groups and outcome measures. We have, therefore, taken a pragmatic, empirical approach to describing and reviewing these interventions.In this Review, we summarise the available evidence for the treatment of motor impairment and restoration of motor function after stroke. Our aims were to:
(i)summarise the available evidence from systematic reviews of randomised controlled trials;
(ii) identify areas for which interventions show promise of efficacy; and
(iii) relate this information to the current guideline advice on clinical management.
Pang
MY, Harris JE, Eng JJ. A community-based upper-extremity group exercise
program improves motor function and performance of functional
activities in chronic stroke: a randomized controlled trial.
Objective
To
assess the effects of a community-based exercise program on motor
recovery and functional abilities of the paretic upper extremity in
persons with chronic stroke.
Design
Randomized controlled trial.
Setting
Rehabilitation research laboratory and a community hall.
Participants
A sample of 63 people (≥50y) with chronic deficits resulting from stroke (onset ≥1y).
Interventions
The
arm group underwent an exercise program designed to improve
upper-extremity function (1h/session, 3 sessions/wk for 19wk). The leg
group underwent a lower-extremity exercise program.
Multivariate analysis showed a significant group by time interaction (Wilks λ=.726, P=.017),
indicating that overall, the arm group had significantly more
improvement than the leg group. Post hoc analysis demonstrated that
gains in WMFT (functional ability) (P=.001) and FMA (P=.001)
scores were significantly higher in the arm group. The amount of
improvement was comparable to other novel treatment approaches such as constraint-induced movement therapy
or robot-aided exercise training previously reported in chronic stroke.
Participants with moderate arm impairment benefited more from the
program.
Conclusions
The
pilot study showed that a community-based exercise program can improve
upper-extremity function in persons with chronic stroke. This outcome
justifies a larger clinical trial to further assess efficacy and cost
effectiveness.
Has your stroke hospital done ONE DAMN THING to implement group exercises for survivors in the last 7 years? If not, everyone in the stroke hospital, including the board of directors needs to be fired.
The
purpose of this study was to evaluate the physical and psychosocial
effects of an 8-week community-based functional exercise program in a
group of individuals with chronic stroke.
METHODS
Twenty-five
subjects (mean age 63 years) participated in a repeated measures design
which evaluated the subjects with two baseline assessments one month
apart, one post-intervention assessment, and one retention assessment
one month post-intervention. Physical outcome measures assessed were the
Berg Balance Test, 12 minute walk test distance, gait speed and stair
climbing speed. Psychosocial measures assessed were the Reintegration to
Normal Living Index (RNL) and Canadian Occupational Performance Measure
(COPM). The 8-week training consisted of a 60 min, 3 times per week
group program which focused on balance, mobility, functional strength
and functional capacity. The program was designed to be accessible by
reducing the need for costly one-on-one supervision, specialized
settings and expensive equipment.
RESULTS
Improvements
from the exercise program were found for all physical measures and
these effects were retained one-month post-intervention. Subjects with
lower function improved the most relative to their initial physical
status. Significant effects were found for the COPM, but not the RNL
Index, however, subjects with lower RNL improved the most relative to
their initial RNL score.
CONCLUSION
A
short-term community-based exercise program can improve and retain
mobility, functional capacity and balance and result in a demonstrable
impact upon the performance of activities and abilities that were
considered meaningful to the subjects. Implementation of such
community-based programs have potential for improving activity tolerance
and reducing the risk for secondary complications common to stroke
(e.g., falls resulting in fractures and cardiac events).
Keywords: cerebrovascular accident, physical activity, disability, function, walk
Over
fifty thousand Canadians suffer from stroke each year making it the
number one cause of neurological disability in Canada today (23) and a leading cause of disability in the community (19). Ninety percent of stroke survivors have some functional disability with mobility being the major impairment (21).
Although some individuals with stroke will have received some
rehabilitation during the acute and sub-acute phase, rarely does
rehabilitation extend beyond one year post-injury due to the belief that
functional recovery has plateaued by this time (42).
Impairments resulting from stroke, such as muscle weakness, pain,
spasticity and poor balance, in addition to the lack of accessible and
appropriate community-based exercise programs can lead to reduced
tolerance to activity, further sedentary lifestyle, and additional
declines in function and disability status (32).
Activities
which promote mobility and fitness are imperative for the prevention of
further pathological events (e.g., falls resulting in fracture,
recurrent strokes or cardiac events). Stroke is one of the top risk
factors for incurring fractures as a result of a fall in older adults;
Kanis et al. (24)
analyzed 16.3 million hospitalizations due to fractures and reported a
7-fold hip fracture risk for individuals with stroke. In fact, the
incidence of falls has been reported to be as high as 73% of individuals
with stroke falling within six months following hospital discharge to
home with an average of 3.4 falls per person during this six month time
period (18).
In addition, cardiovascular disease is the leading prospective cause of
death in chronic stroke. Inactivity and low cardiovascular fitness, a
major occurrence in persons with stroke, is one of the modifiable risk
factors associated with cardiovascular disease.
In the
past, intensive training in persons with stroke has been controversial
due to the belief that strenuous activity would increase spasticity and
reinforce abnormal movement (5). However, recent evaluation of intensive exercise programs has not found any evidence of an increase in spasticity (39).
Intensive treadmill protocols (30, 34, 37)
are a recent addition to stroke rehabilitation and have resulted in
improvements in gait and aerobic capacity, however, Smith et al. (38)
found no significant improvements in reactive balance using an
endurance treadmill protocol and suggested that functional or
task-specific training may be needed to improve balance. Duncan et al. (14)
also reported no significant improvements for the Berg Balance score
using a randomized controlled home-based individual exercise program
(strengthening and walking program). Functional balance may be difficult
to improve due to the varied tasks and movements under which balance is
required. The one exception was a non-controlled pilot study by Weiss
et al. (43)
which reported a 12% improvement in the Berg Balance Score for 7
individuals with stroke using a one-to-one high intensity strengthening
program. However, Kim et al. (26)
recently undertook a double-blind randomized controlled trial of
strength training in chronic stroke found no carry-over into functional
tasks and these authors emphasized the need for functional task-based
practice.
Intensive rehabilitation programs for
individuals with stroke have traditionally involved a one-to-one
client-therapist ratio due to the close supervision required when
challenging balance in these individuals, in addition to the necessary
monitoring when taxing their cardiovascular function. However, given the
current limited rehabilitation resources, it would be ideal to develop
safe and effective community-based group exercise programs which are
accessible to larger numbers of individuals. There is a clear and
impressive void in the current literature which evaluates
community-based group exercise programs for individuals with stroke and
only three studies have examined such programs. Rimmer et al. (37)
undertook an intensive 12-week community-based group training program
(seven staff to 18 clients) which resulted in improvements in peak VO2,
strength, and back flexibility, but did not measure or train balance. A
recent controlled pilot study which evaluated an 8-week circuit
training program found improvements in walking speed, six minute walk
distance, in addition to weight-bearing ability through the affected
limb for the five experimental subjects (supervised by two physical
therapists) compared to the four control subjects (12). Teixeira-Salmela et al. (39)
found improvements in gait and stair climbing speed, in addition to
muscle strength from a 10-week muscle strengthening and physical
conditioning program for 13 individuals with stroke. No studies to date
have assessed the effect of a community-based group exercise program on
both balance and functional capacity in individuals with stroke, and in
addition, the retention of these effects has never been evaluated.
The
purpose of this study was to evaluate a community-based group exercise
intervention on both balance and functional capacity, two functions
which are severely compromised in persons with stroke and can lead to
devastating secondary complications We evaluated the effects of an
8-week group exercise intervention on balance, walking ability and
functional capacity and the retention of these effects one month
post-intervention. Lastly, the psychosocial effects of exercise are
infrequently evaluated in stroke, despite the well-documented high
incidence of clinical depression in this population (4, 10) and the knowledge that exercise can have substantial benefits to one’s well-being (11, 25). Therefore, we also evaluated the effect of the exercise intervention on measures of health-related quality of life.
With all this good stuff occurring with low sulfated heparins whom will your doctors and stroke hospital contact to get further research done creating a stroke protocol out of this? I bet they will incompetently DO NOTHING because it is easier to wait for SOMEONE ELSE TO SOLVE THE PROBLEM?
S. C. Barnett1, G. Mcanney1, M. Mcgrath1, C. Bavington2, J. Turnbull3
1 University of glasgow, , Institute of Infection, Immunity and Inflammation, glasgow, United Kingdom 2 GlycoMar Ltd, European Centre for Marine Biotechnology, Oban, United Kingdom 3 University of Liverpool, Institute of Integrative Biology, Liverpoll, United Kingdom
Content
The
poor repair that follows CNS injury leads to permanent disabilities for
which effective treatments are limited. After injury, the glial scar
that forms is one factor-preventing repair. Previously, we demonstrated
that heparins modified by selective desulphation (mHeps) reduce features
of astrogliosis. mHeps are a class of glycomolecules with structural
similarities to resident heparan sulfates (HS) that comprise repeating
disaccharide units with variable sulphation patterns. HS are key
modulators of cell signalling by both sequestering ligands (including
chemokine/cytokines) in the ECM and acting as cofactors in the formation
of ligand-receptor complexes. To assess whether mHeps would affect
other neural cell types, we treated mixed neural cultures to determine
their effect on myelination and neurite outgrowth. Using myelinating
co-cultures (MC) we demonstrate that the degree and positions of the
sulphate moieties on mHeps are crucial for their biological effects.
Specifically, monosulphated compounds at C2 and N positions have the
greatest effect on promoting neurite outgrowth and (re)myelination,
whereas, highly sulphated heparin isoforms had detrimental effects. No
effects of mHeps were seen on naturally developing MCs (MC-Dev),
suggesting that the beneficial/detrimental effects of mHeps were due to
interactions with factors secreted during the injury process. Comparison
of the secreted factors from the various MCs illustrated differences in
the profile of chemokines/cytokine released. To identify factors that
interact with the most effective mHep (mHep7) we carried out a TMT-LC-MS
analysis on affinity purified conditioned media. Numerous factors were
identified including amyloid beta A4, further investigation established
the ability of amyloid beta peptide (1-42) to inhibit myelination, this
effect could be overcome with co-treatment of mHep7. We propose that
desulphated mHeps may be novel therapeutics for CNS repair. Acknowledgement
The work was supported by a
project grant ETM/439 from CSO (MM) and a PhD studentship (PhD‐769‐2014)
from Medical Research Scotland (GM), and the Wellcome Trust
(202789/Z/16/Z).