Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 27,814 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.
Coffee has been known to be healthy for many years and your stroke hospital incompetently still doesn't have a 24 hour coffee station? You need to fire your board of directors, they don't know how to run a stroke hospital that doesn't follow and implement research. I'm also doing it to prevent Parkinsons, does your doctor even know about that?
My coffee drinking is based upon research showing lower risks of Parkinsons and dementia.
Drinking Three Cups of Coffee Each Day Could Boost Your Heart Health
Nashia Baker
Brewing and drinking a few cups of coffee
might already be a part of your daily routine, but if it's not, now's
the time to reconsider your morning beverage routine. According to a new
study, there are actually major health benefits associated with
consuming up to three cups of coffee each day. Per CNN,
recent research debuted at the European Society of Cardiology annual
stated that those who drink between half a cup to three cups of coffee
each day lessened their risk of developing heart disease and dying from
from heart disease and stroke than those who didn't drink this beverage
at all.
The team's findings after studying 468,000 people's data
from the United Kingdom Biobank, a system that gathers genetic and
health information from over 500,000 Britains, already adds to existing information
on this coffee topic. Previous research last spring revealed that
consuming at least one cup of plain, caffeinated coffee on a daily basis
could decrease chances of heart failure between five and 12 percent.
For those who drank at least two or more cups, the risks lessened by 30
percent.
"The
association between caffeine and heart failure risk reduction was
surprising," Dr. David Kao, the senior study author and the medical
director of the Colorado Center for Personalized Medicine at the
University of Colorado School of Medicine in Aurora, said back in April.
"Coffee and caffeine are often considered by the general population to
be 'bad' for the heart because people associate them with palpitations,
high blood pressure, etc. The consistent relationship between increasing
caffeine consumption and decreasing heart failure risk turns that assumption on its head."
The American Heart Association did note that the standard cup of coffee
for heart health is eight ounces rather than the "grande" cup, which is
16 ounces. Also, coffee drinkers should avoid altering the beverage
with sugars, dairy, and other flavors, as this could increase calories,
sugar, and fat. "While unable to prove causality, it is intriguing that
these three studies suggest that drinking coffee is associated with a
decreased risk of heart failure and that coffee can be part of a healthy
dietary pattern if consumed plain, without added sugar and high fat
dairy products such as cream," Penny Kris-Etherton, a registered
dietitian and immediate past chairperson of the American Heart
Association's Lifestyle and Cardiometabolic Health Council Leadership
Committee, previously shared in a statement.
Published online by Cambridge University Press: 28 January 2014 M. H. Rahman , M. J. Rahman , O. L. Cristobal , M. Saad , J. P. Kenné and P. S. Archambault Show author details
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To assist physically disabled people with impaired upper limb function, we have developed a new 7-DOF exoskeleton-type robot named Motion Assistive Robotic-Exoskeleton for Superior Extremity (ETS-MARSE) to ease daily upper limb movements and to provide effective rehabilitation therapy to the superior extremity. The ETS-MARSE comprises a shoulder motion support part, an elbow and forearm motion support part, and a wrist motion support part. It is designed to be worn on the lateral side of the upper limb in order to provide naturalistic movements of the shoulder (vertical and horizontal flexion/extension and internal/external rotation), elbow (flexion/extension), forearm (pronation/supination), and wrist joint (radial/ulnar deviation and flexion/extension). This paper focuses on the modeling, design, development, and control of the ETS-MARSE. Experiments were carried out with healthy male human subjects in whom trajectory tracking in the form of passive rehabilitation exercises (i.e., pre-programmed trajectories recommended by a therapist/clinician) were carried out. Experimental results show that the ETS-MARSE can efficiently perform passive rehabilitation therapy. Keywords Robotic exoskeleton Nonlinear control Physical disability Passive rehabilitation Upper limb impairment
1Department of Neuroscience, University of Texas at Dallas, Richardson, TX, United States
2Department of Bioengineering, University of Texas at Dallas, Richardson, TX, United States
Background: Vagus nerve stimulation (VNS) paired
with motor rehabilitation is an emerging therapeutic strategy to enhance
functional recovery after neural injuries such as stroke.
Training-paired VNS drives significant neuroplasticity within the motor
cortex (M1), which is thought to underlie the therapeutic effects of
VNS. Though the mechanisms are not fully understood, VNS-induced
cortical plasticity is known to depend on intact signaling from multiple
neuromodulatory nuclei that innervate M1. Cortical dopamine (DA) plays a
key role in mediating M1 synaptic plasticity and is critical for motor
skill acquisition, but whether cortical DA contributes to VNS efficacy
has not been tested.
Objective: To determine the impact of cortical DA depletion on VNS-induced cortical plasticity.
Methods: Rats were trained on a skilled reaching
lever press task prior to implantation of VNS electrodes and
6-hydroxydopamine (6-OHDA) mediated DA depletion in M1. Rats then
underwent training-paired VNS treatment, followed by cortical motor
mapping and lesion validation.
Results: In both intact and DA-depleted rats, VNS
significantly increased the motor map representation of task-relevant
proximal forelimb musculature and reduced task-irrelevant distal
forelimb representations. VNS also significantly increased tyrosine
hydroxylase (TH+) fiber density in intact M1, but this effect was not
observed in lesioned hemispheres.
Conclusion: Our results reveal that though VNS
likely upregulates catecholaminergic signaling in intact motor cortices,
DA itself is not required for VNS-induced plasticity to occur. As DA is
known to critically support M1 plasticity during skill acquisition, our
findings suggest that VNS may engage a unique set of neuromodulatory
signaling pathways to promote neocortical plasticity.
Several lines of evidence suggest that DA could play a
key role in VNS-driven cortical plasticity. VNS increases the firing
rates of noradrenergic neurons in the locus coeruleus (LC) (Hulsey et al., 2017), which are known to activate dopaminergic neurons in the ventral tegmental area (VTA) (Mejias-Aponte, 2016; Park et al., 2017). VTA then sends dopaminergic projections throughout the forebrain, including to M1 (Lindvall et al., 1974; Hosp et al., 2011).
Vagal signaling has recently been shown to enhance the activation of
midbrain dopaminergic neurons and to increase the expression of
behaviors known to depend on dopaminergic signaling (Han et al., 2018; Fernandes et al., 2020).
Cortical dopaminergic signaling plays a critical role in
motor learning and M1 synaptic plasticity. Behaviorally, early skill
acquisition is associated with increased VTA activation (Leemburg et al., 2018), and disruptions in cortical dopaminergic signaling have been shown to impair motor learning (Molina-Luna et al., 2009; Hosp et al., 2011; Rioult-Pedotti et al., 2015). Synaptically, DA receptor antagonism inhibits long-term potentiation in M1 (Molina-Luna et al., 2009; Rioult-Pedotti et al., 2015), and dendritic spine growth and pruning are differentially controlled by D1 and D2 receptor subtypes, respectively (Guo et al., 2015). Interestingly, after a task becomes well-learned, movement-related VTA activation is reduced (Leemburg et al., 2018), and cortical DA depletion no longer impacts motor performance (Molina-Luna et al., 2009; Hosp et al., 2011).
Combined, these studies suggest that cortical DA is necessary for
promoting the M1 plasticity that underlies new skill acquisition.
We hypothesized that DA may also be a key mediator of
VNS-driven cortical plasticity, as it is during initial motor learning.
To test this hypothesis, we trained rats on a skilled reaching lever
press task prior to implantation of VNS electrodes and 6-OHDA mediated
M1 DA depletion. Our findings indicate that while VNS treatment may
increase cortical catecholaminergic innervation in intact M1, DA itself
is not required for VNS-driven cortical plasticity to occur. These
results raise the possibility that VNS efficacy during stroke
rehabilitation may depend on a set of neuroplasticity-promoting
mechanisms that are distinct from those that underlie initial motor
skill acquisition.
So you've described a problem. What research are you initiating to solve this problem?
Or once again are you sitting on your asses WAITING FORSOMEONE ELSE TO SOLVE THE PROBLEM? If you're doing nothing to actually solve stroke, why are you here?
1Center for Outcomes Research, Houston Methodist Research Institute, Houston Methodist, Houston, TX, United States
2Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, United States
3Department of Nuclear Engineering, Texas A&M University, College Station, TX, United States
4Department of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, United States
5Glenn Biggs Institute for Alzheimer's and
Neurodegenerative Diseases, University of Texas Health Science Center at
San Antonio, San Antonio, TX, United States
6Neurological Institute, Houston Methodist, Houston, TX, United States
Background: Cognitive impairment (CI)
is commonly observed after intracerebral hemorrhage (ICH). While a
growing number of studies have explored this association, several
evidence gaps persist. This review seeks to investigate the relationship
between CI and ICH.
Methods: A two-stage systematic review
of research articles, clinical trials, and case series was performed.
Initial search used the keywords [“Intracerebral hemorrhage” OR “ICH”]
AND [“Cognitive Impairment” OR “Dementia OR “Cognitive Decline”] within
the PubMed (last accessed November 3rd, 2020) and ScienceDirect (last
accessed October 27th, 2020) databases, without publication date limits.
Articles that addressed CI and spontaneous ICH were accepted if CI was
assessed after ICH. Articles were rejected if they did not independently
address an adult human population or spontaneous ICH, didn't link CI to
ICH, were an unrelated document type, or were not written in English. A
secondary snowball literature search was performed using reviews
identified by the initial search. The Agency for Healthcare research and
Quality's assessment tool was used to evaluate bias within studies.
Rates of CI and contributory factors were investigated.
Results: Search yielded 32 articles
that collectively included 22,631 patients. Present evidence indicates a
high rate of post-ICH CI (65–84%) in the acute phase (<4 weeks)
which is relatively lower at 3 (17.3–40.2%) and 6 months (19–63.3%).
Longer term follow-up (≥1 year) demonstrates a gradual increase in CI.
Advanced age, female sex, and prior stroke were associated with higher
rates of CI. Associations between post-ICH CI and cerebral microbleeds,
superficial siderosis, and ICH volume also exist. Pre-ICH cognitive
assessment was missing in 28% of included studies. The Mini Mental State
Evaluation (44%) and Montreal Cognitive Assessment (16%) were the most
common cognitive assessments, albeit with variable thresholds and
definitions. Studies rarely (<10%) addressed racial and ethnic
disparities.
Discussion: Current findings suggest a
dynamic course of post-ICH cognitive impairment that may depend on
genetic, sociodemographic and clinical factors. Methodological
heterogeneity prevented meta-analysis, limiting results. There is a need
for the methodologies and time points of post-ICH cognitive assessments
to be harmonized across diverse clinical and demographic populations.
Introduction
Intracerebral hemorrhage (ICH) is the most common type of hemorrhagic stroke, accounting for 10–20% of all strokes (1), with a global incidence of 24.6 per 100,000 person-years (2). Spontaneous ICH primarily results from either hypertensive microangiopathy or cerebral amyloid angiopathy (CAA) (3),
which are likely to produce varied phenotypes. Hypertensive ICH likely
occurs in deep brain structures while CAA-related ICH generally occurs
in lobar locations (2). Regardless of the cause, ICH is associated with poor outcomes that include early mortality (2, 4) and the loss of functional independence (2).
Cognitive Impairment (CI) commonly coexists with ICH. The
majority of ICH patients exhibit acute phase CI, with impairments
reported in up to 84% of patients (5). While the immediate post-ICH cognitive effects and the potential for long-term CI (6)
are broadly recognized, several evidence gaps persist. The trajectory
of post-ICH CI is poorly characterized and demonstrates considerable
variability. Some ICH patients experience favorable recovery after an
acute cognitive decline while others exhibit persistent or worsening CI (7).
The significant contribution of cognitive function toward quality of
life among ICH survivors has driven an increased research focus on
post-ICH CI and dementia. With the growing body of literature focused on
post-ICH CI, it is important to integrate the available evidence and
characterize cognitive function among ICH patients. This systematic
review aims to collect and summarize current evidence regarding the risk
factors and trajectory of CI after spontaneous ICH, report the strength
and validity of study methodologies, and highlight current knowledge
gaps in the study of post-ICH CI.
Since your doctor and hospital don't know what to do when this occurs they should immediately get research going to solve that problem. YOUR RESPONSIBILITY is to ensure your hospital initiates that research. Or don't you want your children and grandchildren to have better care?
Correspondence to
Adrian R Parry-Jones, Clinical Sciences Building, Salford Royal NHS Foundation Trust, Stott Lane, Salford M6 8HD, UK; adrian.parry-jones@manchester.ac.uk
Abstract
Intracerebral
haemorrhage (ICH) accounts for half of the disability-adjusted life
years lost due to stroke worldwide. Care pathways for acute stroke
result in the rapid identification of ICH, but its acute management can
prove challenging because no individual treatment has been shown
definitively to improve its outcome.(So no protocols for anything here. Good to know you might want to try to have a more treatable stroke to match your doctor's skills.) Nonetheless, acute stroke unit care
improves outcome after ICH, patients benefit from interventions to
prevent complications, acute blood pressure lowering appears safe and
might have a modest benefit, and implementing a bundle of high-quality
acute care is associated with a greater chance of survival. In this
article, we address the important questions that neurologists face in
the diagnosis and acute management of ICH, and focus on the supporting
evidence and practical delivery for the main acute interventions.
This
is an open access article distributed in accordance with the Creative
Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits
others to distribute, remix, adapt, build upon this work
non-commercially, and license their derivative works on different terms,
provided the original work is properly cited, appropriate credit is
given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.
Spontaneous
intracerebral haemorrhage (ICH) refers to non-traumatic bleeding in the
brain parenchyma and is the deadliest form of stroke. The high 1-month
case-fatality rate of ~40% and poor long-term outcome make it a major
contributor to global morbidity and mortality.1 2
Although ICH accounts for a minority of stroke worldwide (10–30%), it
is associated with a greater burden of disability-adjusted life years
than ischaemic stroke, given its high incidence in low- and
middle-income countries.3 Despite dramatic drops in ischaemic stroke mortality rates,3 there has been limited improvement in case fatality from ICH in the last few decades2 4 5 and most survivors are left with severe disability.2 6 7
ICH is not a single entity; 85% of cases are due to
cerebral small vessel disease, predominantly deep perforator
arteriopathy (also termed hypertensive arteriopathy or arteriosclerosis)
and cerebral amyloid angiopathy, while the remainder results from a
macrovascular (eg, arteriovenous malformation, cavernoma, aneurysm and
venous thrombosis) or neoplastic cause. Vascular malformations are the
most common cause of ICH in young adults, accounting for up to one-third
of cases.8
The term ‘primary’ ICH is often applied to cases caused by cerebral
small vessel disease, but it discourages adequate investigation and
accurate classification and is not recommended. Deep haemorrhages
account for about two-thirds of cases, occur in the internal capsule,
basal ganglia or brainstem, and more likely result from deep perforator
arteriopathy. About 5–10% of ICH occurs in the cerebellum. The remainder
is lobar haemorrhage located in cortico-subcortical areas, often near
or reaching the cerebral convexities, of which ~40% are due to
arteriosclerosis alone, ~40% to arteriosclerosis and amyloid angiopathy
and the remaining ~20% to amyloid angiopathy alone.9
There are no medical treatments for acute ICH that have
been definitively proven in primary outcome analyses of randomised
clinical trials. Patients with ICH are frequently referred for surgery,
but the roles of various surgical methods and timing of surgery remain
controversial. In this article, we outline a practical approach to the
diagnosis and management of acute ICH.
There’s growing evidence that inoculation confers significant protective benefits.
WSJ Opinion: What's the Coronavirus Priority? Masks or Vaccination?
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Up Next
WSJ Opinion: What's the Coronavirus Priority? Masks or Vaccination?
Main Street: The CDC should scrap its confusing guidance and
make Covid-19 vaccination the only priority. Images: AFP via Getty
Images Composite: Mark Kelly
By
Covid vaccines enormously reduce the risk of death and
hospitalization in those who have been infected by the novel
coronavirus. But could they also help protect seniors against dementia
and Alzheimer’s disease? There’s reason to hope so.
Growing evidence indicates that seniors who get vaccinated
against illnesses such as tetanus and even the flu are much less likely
to develop Alzheimer’s, the leading cause of dementia, characterized by a
buildup of amyloid plaque and tau tangles in the brain. Scientists
don’t completely understand why, but many hypothesize that vaccines
generate a systemic immune response that can reduce inflammation in the
brain, which results in neuron loss and cognitive decline.
Among the first pieces of evidence was a 2001 study
that tracked roughly 3,600 Canadians over 65. After adjusting for age,
sex and education, the researcher found that past vaccinations for
diphtheria/tetanus, poliomyelitis and influenza were associated with a
59%, 40% and 25% lower risk for Alzheimer’s, respectively.
The study had shortcomings. The differences discovered
between the vaccinated and unvaccinated groups could have been due to
confounding variables. People who get vaccinated, for instance, may also
be more likely to get regular checkups and suffer fewer underlying
conditions like diabetes that increase the risk for Alzheimer’s.
But more-recent studies controlled for these factors and
still found a strongly beneficial association between vaccines and
Alzheimer’s. A research article
published in the Journals of Gerontology in April examined the link
between Alzheimer’s and the Tdap (tetanus, diphtheria and pertussis)
vaccine. By using health records from the Veterans Health Administration
and a large database of private medical claims for seniors over 65,
researchers could adjust for variables such as demographics,
health-services utilization, health conditions and medications. After
these adjustments, they found that seniors who had received the Tdap
vaccine had a 42% lower risk of developing dementia than those who
hadn’t.
Leah
Hardy: ‘The realisation that my ‘normal’ blood pressure is not the same
as an ‘optimal’ reading has shaken me out of my complacency’ -
Heathcliff O'Malley for The Telegraph
When
I was young, carefree and skinny, I was proud that my blood pressure
was at the lower end of the healthy range, no matter how much salt I
poured onto my chips. Now I’m 58, a bit fatter and a lot more stressed,
it’s crept up a bit. But, at around 122/85, my blood pressure is still
regarded as normal. In fact, the average adult in the UK has blood
pressure similar to mine and I’ve certainly never considered taking
medication for it.
Rahimi is the lead researcher of a large study, just published in The Lancet,
which looked at the impact of the drugs across a range of blood
pressure levels on the risk of heart and circulatory diseases. Data from
around 360,000 people aged 21 to 105 from 51 randomised trials was
analysed and blood pressure-lowering was found to be effective at
preventing disease at all ages, even when a patient's blood pressure
levels were as low as 120/60. This is well within the healthy range, and
even lower than mine.
In April, Rahimi published a similar study,
which suggested that more than 20,000 heart attacks, strokes and cases
of heart failure could be prevented every year if drugs to lower blood
pressure were prescribed to people with normal blood pressure.
His
research found that a 5mmHg reduction in blood pressure, a drop that is
usually achievable with medication, led to a 10 per cent fall in risk
for a major cardiovascular disease, a 13 per cent reduction for both
stroke and heart failure, 8 per cent for coronary heart disease and 5
per cent for death from cardiovascular disease.
He says: “The
perception has been that treatments should be reserved for those who
have higher blood pressure. And that is not true.
“It’s true that
the higher your blood pressure, the higher your risk. Our study shows
that reducing blood pressure from let’s say 150mmHg to 140mmHg will have
roughly the same relative effect as reducing it from 130mmHg to
120mmHg, irrespective of age. Clinical guidelines should be changed to
reflect these findings.”
Not
everyone is sure we yet have the evidence we need to recommend offering
medication to people without high blood pressure - EyeEm
My
GP is unlikely to offer me a prescription any time soon, though. In the
UK, the NHS defines ideal blood pressure as anything between 90/60 and
120/80 and only those with a reading of 140 or more are eligible for
blood pressure-lowering drugs.
Also, I would only be offered
medication at this point if I also had other cardiovascular risk factors
such as obesity, diabetes or high cholesterol. Otherwise, my blood
pressure would need to be consistently over 160/90 to merit a
prescription. If I was aged over 80, I wouldn’t be considered for drug
treatment unless I hit 150/90, no matter what my other conditions might
be.
Why? Traditionally it’s been thought that it’s both inevitable
and normal for our blood pressure to rise as we hit midlife and older.
Some specialists have thought that increased pressure might help keep
the brain oxygenated and that lowering it could cause dizziness and
falls. However, Rahimi’s study found that medication cut the risk of a
heart attack among people aged 75 to 84 by almost 10 per cent. Risk of
stroke and death from heart disease also dropped by eight per cent and
heart failure by 18 per cent, all without any major side effects.
The
idea that higher blood pressure is harmless as we age is, he says, both
wrong and potentially dangerous. Not only does it increase the risk of
heart disease and stroke, high blood pressure in midlife also increases
the risk of vascular dementia. But if the argument for offering equal
treatment to older people appears irrefutable, the concept of offering
pills to ‘healthy’ people of any age is more controversial. However,
says Rahimi, many of us, even if we think we are healthy, are walking
around with chronically elevated blood pressure because of our modern
lifestyles. “‘Normal’ is usually defined as the average of the
population,” says Rahimi. “But when the whole population is exposed to
an industrialised lifestyle that increases blood pressure, concluding
that their average is healthy is likely to be misleading.” Factors that
push up blood pressure include salt, alcohol, obesity, lack of exercise
and even traffic noise. In remote populations that are not exposed to
any of these things, he says, “the average blood pressure is typically
around 95/65 across all age groups.”
Rahimi admits that “people
will be puzzled by the finding that blood pressure-lowering is not just
for people with high blood pressure.” But, he says, “treatment should be
viewed as a tool to prevent cardiovascular disease, rather than just
for lowering blood pressure per se.”
That does not necessarily
mean, he says, that everyone should be taking pills. However, for a
small number of people they could form a useful insurance policy against
future ill health. Doctors, he points out, already have standard ways
of assessing cardiovascular risk using a combination of measures
including weight, cholesterol levels, alcohol use, exercise habits and
diabetes. He says that for people with some of these risk factors, but
normal blood pressure, current prescribing guidelines “could lead to
withholding effective treatment from a fraction of high-risk
individuals.”
Not
everyone is sure we yet have the evidence we need to recommend offering
medication to people without high blood pressure. Dr Margaret McCartney
is a GP and author. She says that the trials included in The Lancet
study “were almost all of people who had either what we would already
regard as high blood pressure, or some other condition as well – such as
a heart attack or stroke. These patients are already offered treatment.
As for treating blood pressure in healthy people as low as 120/60,
there are several problems. There were no trials included in the
analysis which routinely did this – and no mention of how frequent side
effects would be. If we are looking at ways to reduce our overall risk,
there may be more effective ways that don't just lower cardiovascular
risk, but our other risks as well – for example, our weight, our diet,
smoking and alcohol. It may be easier for doctors to say ‘take a pill’
but trying to reduce the risks that populations have, like obesity or a
lack of active travel options like safe cycling, is important."
But
while Professor Rahimi admits that the evidence is not yet “perfect”,
the medical issues at stake are urgent. He says, “Every day, doctors are
facing the following scenario: a patient who has a substantially
elevated risk of heart disease and stroke but with a blood pressure that
is deemed normal or nearly normal. It’s not the case that they will
offered blood pressure lowering medications. Even in people with risk
factors or previous cardiovascular disease, NICE - and several other
international guidelines - demand that blood pressure is above a
threshold before treatment is considered. Our study clearly challenges
this and provides evidence against these restriction.”
As for side
effects, he says, “there is no evidence to suggest that if you reduce
blood pressure from 120 to 110 mmHg you will get more side effects than
when it is reduced from 160 to 150 mmHg”. That’s not to say that cycling
or eating better aren’t good for us, or shouldn’t be encouraged. “We
need both public health and medical interventions,” he says. “The two
are not mutually exclusive.”
I ask Professor Rahimi if he thinks
that medication might benefit me, as a middle-aged non-smoker with a
just-about-normal BMI thanks to a post-lockdown diet plus regular yoga
and dog walking, but slightly high cholesterol and a fondness for wine.
He politely declines to diagnose me, but he doesn’t say no. The
realisation that my ‘normal’ blood pressure is not the same as an
‘optimal’ reading has shaken me out of my complacency. I’m planning to
swap my beloved salt for a low sodium replacement – which a new study
has shown can cut the risk of strokes and heart attacks – eat better,
tackle stress and lose a few more pounds.
After all, it appears that when it comes to blood pressure, less is definitely more.
Tae-Sung In,1Jin-Hwa Jung,2Kyoung-Sim Jung,1 and Hwi-Young Cho3
1Department of Physical Therapy, Gimcheon University, Gimcheon, Republic of Korea
2Department of Occupational Therapy, Semyung University, Jecheon, Republic of Korea
3Department of Physical Therapy, Gachon University, Incheon, Republic of Korea
Academic Editor: Ping Zhou
Received08 Mar 2021
Revised30 Jun 2021
Accepted12 Aug 2021
Published25 Aug 2021
Abstract
Background.
Spasticity is a factor that impairs the independent functional ability
of stroke patients, and noninvasive methods such as electrical
stimulation or taping have been reported to have antispastic effects.
The purpose of this study was to investigate the effects of
transcutaneous electrical nerve stimulation (TENS) combined with taping
on spasticity, muscle strength, and gait ability in stroke patients.
Methods.
From July to October 2020, 46 stroke patients with moderate spasticity
in the plantar flexors participated and were randomly assigned to the
TENS group (
) and the TENS+taping group ().
All subjects performed a total of 30 sessions of functional training
for 30 min/session, 5 days/week, for 6 weeks. For therapeutic exercise,
sit-to-standing, indoor walking, and stair walking were performed for
10 min each. In addition, all participants in both groups received TENS
stimulation around the peroneal nerve for 30 min before performing
functional training. In the TENS+taping group, taping was additionally
applied to the feet, ankles, and shin area after TENS, and the taping
was replaced once a day. The composite spasticity score and handheld
dynamometer measurements were used to assess the intensity of spasticity
and muscle strength, respectively. Gait ability was measured using a
10 m walk test.
Results.
The spasticity score and muscle strength
were significantly improved in the TENS+taping group compared to those
in the TENS group (
). A significant improvement in gait speed was observed in the TENS+taping group relative to that in the TENS group ().
Conclusions.
Thus, TENS combined with taping may be useful in improving spasticity,
muscle strength, and gait ability in stroke patients. Based on these
results, an additional application of taping could be used to enhance
the antispastic effect of TENS or other electrical stimulation
treatments in the clinic. A long-term follow-up study is needed to
determine whether the spasticity relieving effect persists after taping
is removed.
1. Background
Stroke is a disease in which brain function is impaired due to a sudden interruption of blood supply to the brain tissue [1].
In stroke patients, the ability of the central nervous system to
control the affected side is compromised, the coordination of agonist
and antagonist muscles deteriorates, and proprioception and balance
control are impaired [2]. In addition, it has been reported that 36%–70% of stroke patients experience spasticity [3, 4], which negatively impacts their functional recovery and results in poor quality of life [5, 6].
In particular, spastic hypertonia of the plantar flexor muscles can
cause abnormal gait related to equinovarus foot deformity [7].
Various
types of physical therapy interventions, antispastic drugs, and
surgical interventions have been used to treat spasticity induced by
stroke [8]. Physical therapy interventions
include positioning training, stretching, thermotherapy, cryotherapy,
facilitatory or inhibitory techniques of voluntary activity,
hydrotherapy, vibratory stimulation, electrical stimulation, and
acupuncture [9, 10].
Functional electrical stimulation (FES) and transcutaneous electrical
nerve stimulation (TENS) are known to have antispastic effects on
patients with certain neurological deficits. These interventions also
have the advantage of being noninvasive, atraumatic, and easily
applicable when compared to acupuncture. In a recent study, relief of
spasticity in patients with spinal cord injury was observed for 4 h
following 30 min of FES and TENS application, and it was reported that
there was no significant difference between the two methods [11].
However, in the case of FES, there is insufficient evidence regarding
its ability to reduce spasticity, especially in patients with stroke [9, 12, 13]. Recently, many studies have reported that TENS [14, 15] and taping [16–18]
are effective interventions for the management of spasticity associated
with neurological disorders. TENS is known to regulate spasticity
through various mechanisms, such as by increasing presynaptic inhibition
or by reducing the excitability of stretch reflexes [19].
According to a meta-analysis study of the effects of TENS on
spasticity, TENS application over nerve or muscle belly in stroke
patients for more than 30 min had a strong therapeutic effect on
improving spasticity [20]. Tinazzi et al.
demonstrated that corticomotor excitability of the area to which TENS
was applied was reduced, suggesting that electrical stimulation applied
to the somatic area may affect and regulate brain plasticity [21].
However, the application time of electrotherapy is approximately only
30 min/day. As the expression of titin and collagen is different in
spastic muscles [22], maintaining the muscle length in a shortened state can change the microstructure over a short period of time [23, 24]. Therefore, additional therapeutic treatments are needed to further enhance and maintain the antispastic effects of TENS.
Recently,
other treatments such as stretching, casting, and taping have been
applied to enhance the effect of botulinum toxin on reducing spasticity,
and taping has been reported to be more effective than electrotherapy
or stretching [17]. In a recent study that
applied taping to increase the efficacy and effect duration of botulinum
toxin injection, it was reported that taping was more effective than
stretching exercises. The authors suggested that taping could strengthen
the internalization of botulinum toxin type A as it continuously
stretches the muscle, thereby exerting a positive effect on the
viscoelastic properties of spastic muscles [25].
To
date, several studies have reported the synergistic effects of taping
and botulinum toxin; however, whether or not taping could enhance the
antispastic effect of TENS has not been studied. Therefore, this study
is aimed at investigating the effects of TENS combined with taping on
spasticity, muscle strength, and gait ability in stroke patients. We
applied TENS and functional training to both the experimental and
control groups to confirm the antispastic effect of TENS, and the
experimental group additionally received taping. We hypothesized that
the TENS application reduces spasticity, while the additional
application of taping around the ankle joint further enhances the
antispastic effect and improves muscle strength and gait ability in
stroke patients.
Well we went from testing in mice in 2020 to rats in 2021. What is your confidence level that your doctors and stroke hospital will get this research initiated in humans in the next 50 years? Mine is zero, there is NO stroke leadership.
Your doctor and hospital are responsible for getting such research initiated in humans.
Exploring
and repurposing a drug have become a lower risk alternative.
Safinamide, approved for Parkinson’s disease, has shown neuroprotection
in various animal models of neurological disorders. The present study
aimed to explore the potential of safinamide in cerebral
ischemia/reperfusion (I/R) in rats. Sprague–Dawley rats were used in
middle cerebral artery occlusion model of stroke. The effective dose of
safinamide was selected based on the results of neurobehavioral
parameters and reduction in infarct size assessed 24 h post-reperfusion.
For sub-acute study, the treatment with effective dose was extended for
3 days and effects on neurobehavioral parameters, infarct size (TTC
staining and MRI), oxidative stress parameters (MDA, GSH, SOD, NOX-2),
inflammatory cytokines (TNF-α, IL-1β, IL-10), apoptosis (Bax, Bcl-2,
cleaved caspase-3 expression, and TUNEL staining), and autophagy (pAMPK,
Beclin-1, LC3-II expression) were studied. The results of dose
selection study showed significant reduction (p < 0.05) in
infarct size and improvement in neurobehavioral parameters with
safinamide (80 mg/kg). In sub-acute study, safinamide showed significant
(p < 0.05) improvement in motor coordination and infarct size
reduction. Additionally, safinamide treatment significantly normalized
altered redox homeostasis and inflammatory cytokine levels. However, no
change was observed in expression of NOX-2 in I/R or safinamide
treatment group when compared with sham. I/R induced deranged expression
of apoptotic markers and increased TUNEL positive cells in cortex were
significantly normalized with safinamide treatment. Further, safinamide
significantly (p < 0.05) induced the expressions of autophagic
proteins (Beclin-1 and LC3-II) in cortex. Overall, the results
demonstrated neuroprotective potential of safinamide via anti-oxidant,
anti-inflammatory, anti-apoptotic, and autophagy inducing properties.
Thus, safinamide can be explored for repurposing in ischemic stroke
after further exploration.
Jackson Brougher
Camilo A. Sanchez
Umaymah S. Aziz1, 
Catherine A. Thorn
Thomas Potter
Vasileios-Arsenios Lioutas
Mauricio Tano
Alan Pan
Daniel Woo
Magdy Selim
Farhaan Vahidy
