Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,483 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. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?
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.
From the Stroke Trials Unit, Division of Stroke, University of Nottingham, United Kingdom (S.A., C.R., P.C., N.S., P.M.B.); Department of Stroke, Nottingham University Hospitals NHS Trust, United Kingdom (S.A., N.S., P.M.B.); East Midlands Ambulance Service NHS Trust, Nottingham, United Kingdom (M.F., I.C., A.N.S.); and School of Health and Social Care, University of Lincoln, United Kingdom (A.N.S.).
Correspondence to Philip M. Bath, MD, Division of Stroke, University of Nottingham City Hospital Campus, Hucknall Rd, Nottingham NG5 1PB, United Kingdom. E-mail philip.bath@nottingham.ac.uk
Abstract
Background and Purpose—The practicalities of doing ambulance-based trials where paramedics perform all aspects of a clinical trial involving patients with ultra-acute stroke have not been assessed.
Methods—We performed a randomized controlled trial with screening, consent, randomization, and treatment performed by paramedics prior to hospitalization. Patients with probable ultra-acute stroke (<4 hours) and systolic blood pressure (SBP) >140 mm Hg were randomized to transdermal glyceryl trinitrate (GTN; 5 mg/24 hours) or none (blinding under gauze dressing) for 7 days with the first dose given by paramedics. The primary outcome was SBP at 2 hours.
Results—Of a planned 80 patients, 41 (25 GTN, 16 no GTN) were enrolled >22 months with median age [interquartile range] 79 [16] years; men 22 (54%); SBP 168 [46]; final diagnosis: stroke 33 (80%) and transient ischemic attack 3 (7%). Time to randomization was 55 [75] minutes. After treatment with GTN versus no GTN, SBP at 2 hours was 153 [31] versus 174 [27] mm Hg, respectively, with difference −18 [30] mm Hg (P=0.030). GTN improved functional outcome with a shift in the modified Rankin Scale by 1 [3] point (P=0.040). The rates of death, 4 (16%) versus 6 (38%; P=0.15), and serious adverse events, 14 (56%) versus 10 (63%; P=0.75), did not differ between GTN and no GTN.
Conclusions—Paramedics can successfully enroll patients with ultra-acute stroke into an ambulance-based trial. GTN reduces SBP at 2 hours and seems to be safe in ultra-acute stroke. A larger trial is needed to assess whether GTN improves functional outcome.
From the Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Correspondence to Michael H. Lev, MD, FAHA, FACR, Division of Neuroradiology, Department of Radiology, Massachusetts General
Hospital, Gray B241H, 55 Fruit St, Boston, MA 02114. E-mail mlev@partners.org
Background and Purpose—Previous
univariate analyses have suggested that proximal middle cerebral artery
infarcts with insular involvement have greater
severity and are more likely to progress into
surrounding penumbral tissue at risk. We hypothesized that a practical,
simple
scoring method to assess percent insular
ribbon infarction (PIRI score) would improve prediction of penumbral
loss over other
common imaging biomarkers.
Methods—Of
consecutive acute stroke patients from 2003 to 2008, 45 with proximal
middle cerebral artery–only occlusion met inclusion
criteria, including available penumbral
imaging. Infarct (diffusion-weighted imaging), tissue at risk (magnetic
resonance
mean transit time), and final infarct volume
(magnetic resonance/computed tomography) were manually segmented.
Diffusion-weighted
imaging images were rated according to the
5-point PIRI score (0, normal; 1, <25%; 2, 25%–49%; 3, 50%–74%; 4,
≥75% insula
involvement). Percent mismatch loss was
calculated as an outcome measure of infarct progression. Receiver
operating characteristic
curve and multivariate analyses were
performed.
Results—Mean admission diffusion-weighted imaging infarct volume was 30.9 (±38.8) mL and median (interquartile range) PIRI score was
3 (0.75–4). PIRI score was significantly correlated with percent mismatch loss (P<0.0001). When percent mismatch loss was dichotomized based on its median value (30.0%), receiver operating characteristic
curve area under curve was 0.89 (P=0.0001)
with a 25% insula infarction optimal threshold. After adjusting for
time to imaging and treatment, binary logistic
regression, including dichotomized PIRI (25%
threshold), age, National Institutes of Health Stroke Scale score,
diffusion-weighted
imaging infarct volume, and computed
tomography angiography collateral score as covariates, revealed that
only dichotomized
insula score (P=0.03) and age (P=0.02)
were independent predictors of large (68.2%) versus small (8.1%)
mismatch loss. There was excellent interobserver agreement
for dichotomized PIRI scoring (κ=0.91).
Conclusions—Admission
insular infarction >25% is the strongest predictor of large mismatch
loss in this cohort of proximal middle cerebral
artery occlusive stroke. This outcome marker
may help to identify treatment-eligible patients who are in greatest
need of
rapid reperfusion therapy.
From
the Clinical Audit and Research Unit, London Ambulance Service National
Health Service (NHS) Trust, London, United Kingdom
(R.T.F., M.J.E.); School of Health and
Social Work, University of Hertfordshire, Hatfield, United Kingdom
(J.W.); College
of Medicine, Swansea University, Swansea,
United Kingdom (I.T.R.); and Royal London Hospital, Barts Health NHS
Trust, London,
United Kingdom (P.G.).
Correspondence to Rachael Fothergill, PhD, London Ambulance Service NHS Trust, 8–20 Pocock St, London, SE1 0BW, United Kingdom.
E-mail rachael.fothergill@lond-amb.nhs.uk
Abstract
Background and Purpose—UK
ambulance services assess patients with suspected stroke using the Face
Arm Speech Test (FAST). The Recognition Of Stroke
In the Emergency Room (ROSIER) tool has been
shown superior to the FAST in identifying strokes in emergency
departments but
has not previously been tested in the
ambulance setting. We investigated whether ROSIER use by ambulance
clinicians can improve
stroke recognition.
Methods—Ambulance
clinicians used the ROSIER in place of the FAST to assess patients with
suspected stroke. As the ROSIER includes
all FAST elements, we calculated a FAST score
from the ROSIER to enable comparisons between the two tools. Ambulance
clinicians’
provisional stroke diagnoses using the ROSIER
and calculated FAST were compared with stroke consultants’ diagnosis.
We used
stepwise logistic regression to compare the
contribution of individual ROSIER and FAST items and patient
demographics to the
prediction of consultants’ diagnoses.
Results—Sixty-four
percent of strokes and 78% of nonstrokes identified by ambulance
clinicians using the ROSIER were subsequently
confirmed by a stroke consultant. There was
no difference in the proportion of strokes correctly detected by the
ROSIER or
FAST with both displaying excellent levels of
sensitivity. The ROSIER detected marginally more nonstroke cases than
the FAST,
but both demonstrated poor specificity.
Facial weakness, arm weakness, seizure activity, age, and sex predicted
consultants’
diagnosis of stroke.
Conclusions—The
ROSIER was not better than the FAST for prehospital recognition of
stroke. A revised version of the FAST incorporating
assessment of seizure activity may improve
stroke identification and decision making by ambulance clinicians.
Apathy and hypersomnia
occur after stroke and, by definition, reduce participation in
rehabilitation, but their effect on outcome from acute rehabilitation is
not known. We performed a retrospective review of 213 patients admitted
to a stroke-specialized acute rehabilitation unit in the United States.
All patients had ischemic or hemorrhagic stroke, and no dementia or
dependence on others pre-stroke. We diagnosed apathy and hypersomnia
using standardized documentation by treating therapists. We used
multiple regression analysis to control for overall impairment
(combination of strength, cognitive and sensory measures), age, time
since stroke, and stroke type (ischemic or hemorrhagic). Forty-four
(21 %) of the patients had persistent apathy, and 12 (5.6 %) had
persistent hypersomnia. Both groups were more impaired in cognition,
sustained attention, and more likely to be treated for depression.
Patients with apathy were 2.4 times more likely to go to a nursing home,
and had discharge FIM scores 12 points below the mean. Patients with
hypersomnia were ten times more likely to go to a nursing home, and had
discharge FIM scores 16 points below the mean. These findings indicate
that studies to prospectively define these clinical factors and
potential confounds using standardized tools are indicated, and if
confirmed, justify studies to identify these patients early and develop
targeted interventions.
Purpose:
To develop and evaluate an information and communication technology
(ICT) solution for a post-stroke Personalised Self-Managed
Rehabilitation System (PSMrS). The PSMrS translates current models of
stroke rehabilitation and theories underpinning self-management and
self-efficacy into an ICT-based system for home-based post-stroke
rehabilitation. Methods: The interdisciplinary research team
applied a hybrid of health and social sciences research methods and
user-centred design methods. This included a series of home visits,
focus groups, in-depth interviews, cultural probes and technology
biographies. Results: The iterative development of both the
content of the PSMrS and the interactive interfaces between the system
and the user incorporates current models of post-stroke rehabilitation
and addresses the factors that promote self-managed behaviour and
self-efficacy such as mastery, verbal persuasion and physiological
feedback. Conclusion: The methodological approach has ensured
that the interactive technology has been driven by the needs of the
stroke survivors and their carers in the context of their journey to
both recovery and adaptation. Underpinned by theories of motor
relearning, neuroplasticity, self-management and behaviour change, the
PSMrS developed in this study has resulted in a personalised system for
self-managed rehabilitation, which has the potential to change motor
behaviour and promote the achievement of life goals for stroke
survivors.Implications for Rehabilitation
Radical
innovation and the adoption of a self-management paradigm need to be
considered as a way of delivering home-based post-stroke rehabilitation.
A
hybrid of health and social sciences research and user-centred design
methods are required to ensure that technology for post-stroke
rehabilitation has been driven by the needs of the stroke survivors and
their carers.
Personalised technology
systems for self-managed post-stroke rehabilitation have the potential
to change motor behaviour and promote the achievement of life goals for
stroke survivors.
Is a tendency for people to favor information that confirms their preconceptions or hypotheses. My bias is that the whole stroke world knows nothing, I seek out and find multiple research articles each day that prove that. My assumption is that the stroke world believes in 'All strokes are different, all stroke recoveries are different'. They are constantly reinforced in this belief by looking at their patients and not keeping detailed records to be able to see commonalities. To combat this from the Science Based Medicine blog;
Facts and rational arguments have no effect on a true believer. People
hear only what they want to hear. Most people refuse to listen to
anything that contradicts their beliefs. Their confirmation bias accepts
only confirming evidence to protect their ego from having to admit they
were wrong. And there’s a real danger in arguing with them. They will
come up with rationalizations that allow them to reject everything you
say, and that only serves to reinforce their beliefs. They come out of
an argument believing even more strongly than when they went in.
You could tell them that you are willing to change your mind, and
explain what it would take to make you change your mind. (Essentially the standards for
scientific proof: positive scientific studies that are well-designed and
replicated, leading to a scientific consensus of experts based on a
critical evaluation of all the published evidence).
Department of Medicine, Duke University Medical Center, Durham, NC 27710.
Abstract
To
determine the clinical consequences of reocclusion of an
infarct-related artery after reperfusion therapy, we evaluated 810
patients with acute myocardial infarction. Patients were admitted into
four sequential studies with similar entry criteria in which patency of
the infarct-related artery was assessed by coronary arteriography 90
minutes after onset of thrombolytic therapy. Successful reperfusion was
established acutely in 733 patients. Thrombolytic therapy included
tissue-type plasminogen activator (t-PA) in 517, urokinase in 87, and a
combination of t-PA and urokinase in 129 patients. All patients received
aspirin, intravenous heparin and nitroglycerin, and diltiazem during
the recovery phase. A repeat coronary arteriogram was performed in 88%
of patients at a median of 7 days after the onset of symptoms.
Reocclusion of the infarct-related artery occurred in 91 patients
(12.4%), and 58% of these were symptomatic. Angiographic characteristics
at 90 minutes after thrombolytic therapy that were associated with
reocclusion compared with sustained coronary artery patency were right
coronary infarct-related artery (65% versus 44%, respectively) and
Thrombolysis in Myocardial Infarction (TIMI) flow 0 or 1 (21% versus
10%, respectively) before further intervention. Median (interquartile
value) degree of stenosis in the infarct-related artery at 90 minutes
was similar between groups: 99% for reoccluded (value, 90/100%) compared
with 95% for patent (value, 80/99%). Patients with reocclusion had
similar left ventricular ejection fractions compared with patients with
sustained patency at follow-up. However, patients with reocclusion at
follow-up had worse infarct-zone function at -2.7 (value, -3.2/-1.8)
versus -2.4 (SD/chord) (value, -3.1/-1.3) (p = 0.016). The recovery of
both global and infarct-zone function was impaired by reocclusion of the
infarct-related artery compared with maintained patency; median delta
ejection fraction was -2 compared with 1 (p = 0.006) and median delta
infarct-zone wall motion was -0.10 compared with 0.34 SD/chord (p =
0.011), respectively. In addition, patients with reocclusion had more
complicated hospital courses and higher in-hospital mortality rates
(11.0% versus 4.5%, respectively; p = 0.01). We conclude that
reocclusion of the infarct-related artery after successful reperfusion
is associated with substantial morbidity and mortality rates.
Reocclusion is also detrimental to the functional recovery of both
global and infarct-zone regional left ventricular function. Thus, new
strategies in the postinfarction period need to be developed to prevent
reocclusion of the infarct-related artery.
Men who have at least one hangover per year are at greater risk of having a stroke, a new Finnish study has found. (How much greater?)
In
her doctoral thesis at the University of Eastern Finland, researcher
Sanna Rantakomi found men who drank more than twice a week, were
overweight, or had hypertension were at an even greater risk.
The
research looked at 2,600 men who took part in a long-term study. The men
self-reported their alcohol intake and how often they had a hangover.
She found the likelihood of a man having a stroke increased depending on heavy alcohol consumption leading to a hangover.
Light to moderate drinking isn't an issue in a healthy man, Rantakomi wrote.
"Despite
some evidence showing moderate alcohol drinking to decrease the risk of
stroke, the implications of these findings should be examined
cautiously," she wrote in the study. "Any advice regarding the
consumption of alcohol should be customised to the individual's risks
and potential benefits."
Or another article on this; Excessive alcohol consumption increases the progression of atherosclerosis and the risk of stroke
And how is your doctor reorganizing your brain after your stroke insult? You do expect an answer, Don't you? http://www.frontiersin.org/Journal/10.3389/fnhum.2013.00640/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w43-2013
Training studies, in which the
structural or functional neurophysiology is compared before and after
expertise is acquired, are increasingly being used as models for
understanding the human brain’s potential for reorganization. It is
proving difficult to use these results to answer basic and important
questions like how task training leads to both specific and general
changes in behavior and how these changes correspond with modifications
in the brain. The main culprit is the diversity of paradigms used as
complex task models. An assortment of activities ranging from juggling
to deciphering Morse code has been reported. Even when working in the
same general domain, few researchers use similar training models. New
ways to meaningfully compare complex tasks are needed. We propose a
method for characterizing and deconstructing the task requirements of
complex training paradigms, which is suitable for application to both
structural and functional neuroimaging studies. We believe this approach
will aid brain plasticity research by making it easier to compare
training paradigms, identify “missing puzzle pieces,” and encourage
researchers to design training protocols to bridge these gaps.
Introduction
The idea that the structure and function of the human
brain remains somewhat open to alteration by experience over the
lifespan is now well established (Wan and Schlaug, 2010; Zatorre et al., 2012), although researchers have not yet formed a comprehensive view of how – and under which conditions – this occurs.
Since we tend to have a lot of incorrect muscle synergies, your doctor can use this to tell us how to correct them to get to 100% recovery. http://www.frontiersin.org/Journal/10.3389/fncom.2013.00136/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w43-2013
Muscle redundancy allows the central nervous system (CNS) to choose a
suitable combination of muscles from a number of options. This
flexibility in muscle combinations allows for efficient behaviors to be
generated in daily life. The computational mechanism of choosing muscle
combinations, however, remains a long-standing challenge. One effective
method of choosing muscle combinations is to create a set containing the
muscle combinations of only efficient behaviors, and then to choose
combinations from that set. The notion of muscle synergy, which was
introduced to divide muscle activations into a lower-dimensional synergy
space and time-dependent variables, is a suitable tool relevant to the
discussion of this issue.
The synergy space defines the suitable
combinations of muscles, and time-dependent variables vary in
lower-dimensional space to control behaviors. In this study, we
investigated the mechanism the CNS may use to define the appropriate
region and size of the synergy space when performing skilled behavior.
Two indices were introduced in this study, one is the synergy stability index (SSI) that indicates the region of the synergy space, the other is the synergy coordination index (SCI) that indicates the size of the synergy space.
The results on automatic posture response experiments show that SSI
and SCI are positively correlated with the balance skill of the
participants, and they are tunable by behavior training. These results
suggest that the CNS has the ability to create optimal sets of efficient
behaviors by optimizing the size of the synergy space at the
appropriate region through interacting with the environment.
The neuropeptide, orphanin FQ/nociceptin (OFQ/N or simply, nociceptin),
is expressed in both neuronal and non-neuronal tissue, including the
immune system. In the brain, OFQ/N has been investigated in relation to
stress, anxiety, learning and memory, and addiction. More recently, it
has also been found that OFQ/N influences glial cell functions,
including oligodendrocytes, astrocytes, and microglial cells. However,
this latter research is relatively small, but potentially important,
when observations regarding the relationship of OFQ/N to stress and
emotional functions is taken into consideration and integrated with the
growing evidence for its involvement in cells that mediate inflammatory
events. This review will first provide an overview and understanding of
how OFQ/N has been implicated in the HPA axis response to stress,
followed by an understanding of its influence on natural and learned
anxiety-like behavior.
What emerges from an examination of the
literature is a neuropeptide that appears to counteract anxiogenic
influences, but paradoxically, without attenuating HPA axis responses
generated in response to stress. Studies utilized both central
administration of OFQ/N, which was shown to activate the HPA axis, as
well as antagonism of NOP-R, the OFQ/N receptor. In contrast, antagonist
or transgenic OFQ/N or NOP-R knockout studies, showed augmentation of
HPA axis responses to stress, suggesting that OFQ/N may be needed to
control the magnitude of the HPA axis response to stress. Investigations
of behavior in standard exploratory tests of anxiogenic behavior (eg.,
elevated plus maze) or learned fear responses have suggested that OFQ/N
is needed to attenuate fear or anxiety-like behavior. However, some
discrepant observations, in particular, those that involve appetitive
behaviors, suggest a failure of NOP-R deletion to increase anxiety.
However, it is also suggested that OFQ/N may operate in an anxiolytic
manner when initial anxiogenic triggers (eg., the neuropeptide CRH) are
initiated.
Finally, the regulatory functions of OFQ/N in relation to
emotion-related behaviors may serve to counteract potential
neuroinflammatory events in the brain. This appears to be evident within
the glial cell environment of the brain, since OFQ/N has been shown to
reduce the production of proinflammatory cellular and cytokine events.
Given that both OFQ/N and glial cells are activated in response to
stress, it is possible that there is a possible convergence of these two
systems that has important repercussions for behavior and
neuroplasticity.
You are going to have to be very demanding about this. Don't take non-specific comments for answers. This is your life and health depending on the answers.
12 simple questions for your doctor to respond to. No specific answers, you don't even have a functioning stroke rehab doctor.
1. First question - What exactly are you doing to stop the neuronal cascade of death in the first week? If there is no definite answer or they don't even know what it is, Screamin their faces that they are assisting in killing your neurons. Millions every minute.
2. Which of these 31 possibilities are they doing the first week?
3.Demand to know what the stroke rehab protocols are and their efficacy. Do not back down they should know all this by heart. If they don't they are incompetent. If they haven't been measuring previous patients recovery they are just acting as a doctor, get a new one.
4. How are you planning on getting me to 100% recovery?
5. How are you planning on getting me to 100% recovery?
6. How are you planning on getting me to 100% recovery?
7. How are you planning on getting me to 100% recovery?
8. How are you planning on getting me to 100% recovery?
9. How are you planning on getting me to 100% recovery?
10. How are you planning on getting me to 100% recovery?
ad infinitum until a proper answer is given
11. If you hear 'All strokes are different, all stroke recoveries are different', that is a sure sign of laziness, call them on it, ask for research article proof. This statement is proof your doctor knows nothing about getting you to full recovery.
12. Ask when they are going to tell you all this stuff.
To admin@world-stroke.org, campaigns@world-stroke.org, vkuffer@kenes.com, membership@world-stroke.org Subject; Inteernational Journal of Stroke blog Do you even know it exists and no one responds to comments? You are supporting the quackery of Neuroaid.
So whom is going to add this to the generic crap stroke prevention admonitions? And it seems to be useful immediately post stroke and TBI.
If your doctor is any good at all they should know all this stuff and determine your course of action. But that won't occur unless you tell them about this research. The model of stroke information is totally backwards, patients know more than any of your doctors or therapists.
Then there is this pretreatment model also;
To cite this article: Ryan J. Waters, Gordon
D. Murray, Graham M. Teasdale, Janice Stewart, Ian Day, Robert J. Lee,
and James A.R. Nicoll. Journal of Neurotrauma.
October 15, 2013,
30(20): 1710-1716.
doi:10.1089/neu.2012.2792.
Published in Volume: 30 Issue 20: October 10, 2013
ABSTRACT
Clinical
outcome after traumatic brain injury (TBI) is variable and cannot
easily be predicted. There is increasing evidence to suggest that there
may be genetic influences on outcome. Cytokines play an important role
in mediating the inflammatory response provoked within the central
nervous system after TBI. This study was designed to identify
associations between cytokine gene polymorphisms and clinical outcome 6
months after head injury. A prospectively identified cohort of patients (n=1096,
age range 0–93 years, mean age 37) was used. Clinical outcome at 6
months was assessed using the Glasgow Outcome Scale. In an initial
screen of 11 cytokine gene single nucleotide polymorphisms (SNPs)
previously associated with disease susceptibility or outcome (TNFA −238
and −308, IL6 −174, −572 and −597, IL1A −889, IL1B −31, −511 and +3953,
and TGFB −509 and −800), TNFA −308 was identified as having a likely
association. The TNFA −308 SNP was further evaluated, and a significant
association was identified, with 39% of allele 2 carriers having an
unfavorable outcome compared with 31% of non-carriers (adjusted odds
ratio 1.67, confidence interval 1.19–2.35, p=0.003). These
findings are consistent with experimental and clinical data suggesting
that neuroinflammation has an impact on clinical outcome after TBI and
that tumor necrosis factor alpha plays an important role in this
process.
Its been 3 days since both Amy and I commented on there that they have the quackery blog of Neuroaid listed. This implies they support such quackery and that they don't even read comments. International Journal of Stroke failure
Whether or not your doctor is going. Here are some questions that need answering. Don't passively wait for your doctor to help you. They won't do a damn thing because they don't know a damn thing about 100% recovery. You can easily prove that by asking how to get back to full recovery. You will get the craptastic answer of 'All strokes are different, all stroke recoveries are different' You need to scream in their face that that is a bunch of bullshit.
1. Exactly how does neuroplasticity work? So it can be repeated in clinical research.
2. What percentage of tPA patients fully recover?
3. What percentage of your patients fully recover?
4. When are hyperacute therapies from New Zealand - enzogenol and Japan - edaravone going to make it to the US?
So much praise for my writing, I must be damn good.
Most people know about mild yeast infection but don’t understand that
they are not just a problem which women get. While the most common type
of prevent yeast infections is a vaginal one, they are not the only
kind.
This guy below was trying to have me do the work to try to prove the
stupidity of earthing, I finally had to tell him, write his own damn
blog.
I explained where you could find the links.
And even in your
sceptical review link above you dismiss it with 'anecdotal evidence
mainly' rather than inform your readers the guy's conclusions which are
these - if you will deem to allow this post! :
A large part
of the book contains anecdotal descriptions of people helped by
earthing, which (while intriguing) can’t be counted as objective
support. Thermography images (PDF) of patients’ with a variety of
ailments and injuries show – after a half an hour of grounding (with no
other intervention) – surprising reductions in inflammation where other
medications and therapies have had little impact. Microscopic images
comparing blood samples after less than an hour of grounding in several
subjects suggest a dramatic improvement in viscosity.
One
double-blind, controlled clinical trial demonstrated earthing’s impact
on a number of biomarkers. Subjects who slept grounded showed
statistically significant decreases in serum sodium, potassium,
magnesium, iron, total protein, albumin concentrations, inorganic
phosporus. Free T4 and TSH increased while free T3 decreased. (PDF) In
another study, participants were given exercises that induced muscular
pain. Those who were grounded showed altered immune activity and
reported lesser pain levels than those who were ungrounded. (PDF)
Another
controlled study suggested that sleeping grounded can impact cortisol
levels and sleep quality. Subjects who slept grounded with conductive
mattress pads showed lower night-time cortisol levels as well as an
overall “resynchronization” of cortisol secretion “more in alignment
with the natural 24-hour circadian rhythm profile.” (PDF) Subjects who
were grounded during sleep also reported better sleep and less physical
pain and emotional stress. You can check out links to other earthing
related studies here.
Clearly, something is happening here. The
results are pretty suggestive of some significant phenomenon. As for my
part, I’m hopeful but still cautious about the authors’ general theory
and the compelling (albeit modest) collection of research that supports
earthing’s impact.
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