In-hospital strokes get worse care than those presenting to ER, study finds

Be careful out there, don't get sick while in the hospital.
Diane, for your attorney.
http://www.theheart.org/article/1543035.do?utm_medium=email&utm_source=20130527_heartwire&utm_campaign=newsletter

Patients who have a stroke receive better care if they have their stroke outside the hospital than while admitted, a new study based on data from the American Heart Association's Get With the Guidelines-Stroke program has found.

"Maybe the emergencies we are least prepared for are the emergencies that happen right in our very backyard," Dr Ethan Cumbler (National Stroke Association, Centennial, CO) said here at Hospital Medicine 2013.

Approximately 35 000 to 75 000 in-hospital strokes are reported annually in the US, but even this high number may underestimate cases, often underreported, noted Cumbler.

In an interview, Cumbler said these data point to the need for improvements in rapid recognition of stroke symptoms by hospital providers as well as systematic changes to allow inpatients to receive appropriate thrombolysis in a timely manner.

"Patients who suffer their stroke while under our care deserve the same consideration for treatment, which could reduce their deficits and improve their outcome, as any patient who has a stroke at home," he emphasized.

Session moderator Dr Eduard Vasilevskis (Vanderbilt University Medical Center, Nashville, TN) said, "I definitely agree that the data clearly show an opportunity for improvement with regard to inpatient stroke."

He added, "Hospitalized patients who are already sick and then have a stroke are going to do worse. The question is, if we improve quality, can we at least diminish how much worse they're going to do?"

Worse outcomes

Data for the study came from 1280 hospitals reporting at least one in-hospital stroke to the Get With the Guidelines program. Investigators compared patient characteristics, comorbid illnesses, medications, quality-of-care measures, and outcomes between the 21 349 in-hospital ischemic strokes and 928 885 community-onset ischemic strokes.

The in-hospital stroke patients had more thromboembolic risk factors, including atrial fibrillation, prosthetic heart valves, carotid stenosis, and heart failure (p<0.001). However, they were less likely to have had a prior stroke, hypertension, or use tobacco (p<0.0001).

In-hospital strokes were more severe, with a median National Institutes of Health Stroke Scale score of 9.0 compared with 4.0 for the community strokes (p<0.001).

Achievement of the Get With the Guidelines quality metrics for the in-hospital stroke patients was significantly worse for all seven achievement measures and for all but three of the eight quality measures.

Stroke education didn't differ between the two groups, and both rehabilitation assessment and intensive statin treatment were better for the in-hospital stroke patients.

The gap in defect-free care was larger than I expected.

Defect-free care, defined as the proportion of patients who received all of the achievement measure interventions for which they were eligible, was significantly worse for the in-hospital stroke group, just 60.8% vs 82.0% for community-onset stroke (p<0.0001).

"The gap in defect-free care was larger than I expected," Cumbler said.

However, of the 11% of in-hospital stroke patients who did receive appropriate thrombolysis, multivariate analysis showed a lower rate of intracranial hemorrhage compared with community strokes (odds ratio [OR] 0.80, p=0.049).

"Many patients with in-hospital stroke are candidates for aggressive intervention with thrombolysis and do not appear to have higher rates of hemorrhage when treated," Cumbler pointed out.

Deaths during hospitalization occurred in 14% of in-hospital stroke patients, compared with 5% for community strokes (OR 2.72, p<0.0001). Patients with in-hospital strokes were less likely to be discharged home (OR 0.37) and less able to ambulate independently at discharge (OR 0.42).

"It makes sense that two problems are worse than one problem. If you come in with a heart attack, you will do worse than if you only had a stroke. However, there's also the disquieting hypothesis that some of these discrepancies in outcomes are related to the discrepancies in performance of quality metrics," Cumbler said.

Vasilevskis noted that most patients who have a stroke in the community arrive at the hospital in the emergency department, which is prepared to provide rapid stroke care. "In the ER, there's a stroke alert, there's a stroke team, everyone comes, there's an order set. It's all been worked out for the ER," he said. "We just haven't worked it out for the inpatient setting because it's much less common."

And he added that family members may be better than hospital personnel at detecting sudden differences in a person's usual behavior that might signal a stroke.

The specialist advantage

Cumbler said that beyond basic differences in workflow between the ER and the wards that affect the ability to respond to time-critical emergencies, strokes from the community are often cared for by dedicated neurology or stroke services. Patients who are already hospitalized may be on cardiology, cardiothoracic surgery, or medicine services staffed by personnel who are "less attuned to the elements of quality processes for stroke care."

The solution, he said, is for both individual providers to learn to better recognize new neurologic deficits and systems to be improved to allow evaluation and treatment decisions to occur within 60 minutes of symptom recognition.

"As individuals, we need to get the stroke program involved at the onset of stroke symptoms so that the quality metrics can be met and reported appropriately. As systems, we need to create bundles of these interventions, which can be an overlay onto existing orders for patients who experience stroke during hospitalization," he said.

And because there is evidence that in-hospital strokes are underreported, "We should be reporting in-hospital strokes just as we do community-onset strokes to quality databases so that we can accurately understand the quality of care we are providing, identify gaps, and perform process improvement to close any discrepancies."

The divided brain Iain McGilchrist vs. Jill Bolte-Taylor

You can believe in the split brain statements of Jill Bolte-Taylor as referenced in her book, Stroke of Insight and her TED talk here;
http://www.ted.com/talks/jill_bolte_taylor_s_powerful_stroke_of_insight.html

Or you can listen/watch  Iain McGilchrist here:
http://www.youtube.com/watch?feature=player_embedded&v=dFs9WO2B8uI
I think this is much better. See what your doctor has to say about the subject and exactly how the stroke affected the sides working with each other.

You do expect your doctor to know the details of getting your two halves working together again, Don't you?

People with higher IQ have the ability to get rid of distractions

So these people should be able to recover from stroke better because they should be able to stop the synergy of all your muscles moving. Well I consider myself in that category and it hasn't helped my recovery one bit.
The analysis article here:
http://saypeople.com/2013/05/24/people-with-higher-iq-have-the-ability-to-get-rid-of-distractions/#axzz2USgJvFRo
The abstract here:
A Strong Interactive Link between Sensory Discriminations and Intelligence

• Highlights
• IQ scores are predicted by individual differences in sensory discriminations
• High IQ is associated with motion perception impairments as stimulus size increases
• The results link intelligence and low-level suppression of sensory information
• Suppressive processes are a key constraint of both intelligence and perception

Summary

Early psychologists, including Galton, Cattell, and Spearman, proposed that intelligence and simple sensory discriminations are constrained by common neural processes, predicting a close link between them [1,2]. However, strong supporting evidence for this hypothesis remains elusive. Although people with higher intelligence quotients (IQs) are quicker at processing sensory stimuli [1,2,3,4,5], these broadly replicated findings explain a relatively modest proportion of variance in IQ. Processing speed alone is, arguably, a poor match for the information processing demands on the neural system. Our brains operate on overwhelming amounts of information [6,7], and thus their efficiency is fundamentally constrained by an ability to suppress irrelevant information [8,9,10,11,12,13,14,15,16,17,18,19,20,21]. Here, we show that individual variability in a simple visual discrimination task that reflects both processing speed and perceptual suppression [22] strongly correlates with IQ. High-IQ individuals, although quick at perceiving small moving objects, exhibit disproportionately large impairments in perceiving motion as stimulus size increases. These findings link intelligence with low-level sensory suppression of large moving patterns—background-like stimuli that are ecologically less relevant [22,23,24,25]. We conjecture that the ability to suppress irrelevant and rapidly process relevant information fundamentally constrains both sensory discriminations and intelligence, providing an information-processing basis for the observed link.

Three Ways to Fight Back Against Daytime Sleepiness - Shawn Radcliffe blogging

For all you stroke fatiguers, I'm sure your doctor has already given you useless ideas. So ask them what research points to about fixing stroke fatigue, don't accept bland statements, specifics only from documented research. If non-existant, ask when their study will start up. And don't be polite about it.
http://branain.com/three-ways-fight-daytime-sleepiness/?utm_source=rss&utm_medium=rss&utm_campaign=three-ways-fight-daytime-sleepiness

Shoe wear from stroke walking

About three months ago I bought a new pair of velcro shoes from Payless.

Only 29.99, compared to my first pair that were extra wide, extra deep for $140 this was a bargain. However the soles are a fairly soft manmade material and my good foot(right) heel strike wore down the heel until the air compartment in the heel showed thru. Filled it with Shoe Goo to keep it useable. I have no left foot heel strike. I'm sure a PT could tell me exactly what I'm doing wrong but that's not going to occur.

Experts raise doubts over pop-up heart and stroke screening clinics

I know the experts are right about  this being almost worthless unless you have indications. This would have prevented my stroke if the question had been asked, 'Do either of your parents have atherosclerosis?' I had no other indications.

Experts raise doubts over pop-up heart and  stroke  screening clinics

Medical experts say they have doubts over pop-up clinics that screen for heart attacks and strokes in a procedure that they say is not appropriate for people without any symptoms.
Consumer authorities in two Australian states are looking into the clinics offered by Screen for Life.
The Screen for Life website says it offers fast, painless and affordable preventive health screening.
Medical director Professor Scott Kitchener says the clinics are run by registered nurses, with screenings performed by highly trained sonographers.
The results are reviewed by a cardiologist and are delivered to the patient within 21 days.
He says they have identified serious health problems in some patients.
"If there is a finding on the screening of concern then we discuss it with their GP. And occasionally I've even called vascular surgeons and cardiologists to further discuss the signals we've found on screening," he said.
Screen for Life offers a range of medical tests, including ultrasound of the carotid arteries.
However, medical experts such as Professor Paul Glasziou, director of the Centre for Research in evidence-based practice at Bond University, says the procedure is not appropriate for people without any symptoms.
"The ultrasound screens of the carotid artery, which is one of the screens that is being done, is generally not recommended," he said.
"The College of General Practitioners here doesn't recommend it, the US preventative task force doesn't recommend it for the general population."
The US preventative services task force is an independent US government panel that evaluates screening.
It estimates that doctors would need to screen more than 4,300 people with ultrasound and a follow-up magnetic resonance imaging testing to prevent a single stroke.
Professor Glasziou says there are some specific groups, such as people who have had a mini stroke, where it is really important to do ultrasound screening of carotid arteries.
"But as a general screening, it is not a particularly good idea. I personally don't have it and I wouldn't do it for my patients," he said.
"It is much more important that they just get the routine checks.
"'Do you smoke? What's your cholesterol? What's your blood pressure? Do you have diabetes?', And do those first.
"If there are any indications from those things then I may consider [those] in very high-risk groups getting that sort of ultrasound screening."

More at link.

Can acupuncture help stroke survivors?

Considering who is sponsoring the study, this is biased from the start. First you have to somehow believe there are energy meridians.
http://www.alberniportal.ca/2013/05/can-acupuncture-help-stroke-survivors/
A study is looking at whether acupuncture could help improve gait and limb movements after a stroke.
Weakness and paralysis are one of the most significant, and disabling, after effects of stroke. There is no obvious way of reversing the problem, although time and rehabilitation measures may produce some improvement. Researchers at the New England School of Acupuncture, together with colleagues at Masssachusetts General Hospital and others, are looking at whether acupuncture can improve functioning following a stroke.
Stroke patients will be given either real or ‘sham’ acupuncture. Advanced computer technology will be used to analyse gait and limb movements and brain imaging will examine any changes in blood flow patterns. The study should shed light on the value of acupuncture in stroke – previous research has proved inconclusive.

Statins decrease stroke after heart attack

But what about all these other stroke risk reduction possibilities?
Here: http://oc1dean.blogspot.com/2013/03/stroke-risk-reduction-ideas.html
I like the 50% reduction using marijuana buds.

They don't point to the study so I can't tell anything useful or who sponsored the study.
http://www.newsfix.ca/2013/05/26/statins-decrease-stroke-after-heart-attack/

Hutch Regional is given stroke-care designation - Hutchinson, KS

The KISS initiative is way too important to leave to medical professionals. Get involved and demand action. At least make it public.
http://hutchnews.com/Bizmore/SUN--BIZ-briefs-5-26
Hutchinson Regional Medical Center has been classified an Emergent Stroke Ready hospital by the American Heart Association and the Kansas State Stroke Task Force, indicating the facility is able to adequately care for stroke patients.
The hospital, a member of the Hutchinson Regional Healthcare System, provided the necessary documentation to receive the designation as part of the Kansas Initiative for Stroke Survival (KISS).
KISS is led by a team of 50 medical professionals who make up the Kansas State Stroke Task Force, which was created in 2004 to study and address the issue of stroke care in Kansas and develop a comprehensive system of care.

Inflammation Triggered by Traumatic Brain Injury May Continue to Harm the Brain for a Lifetime

But does it harm the brain for a lifetime in stroke? What researcher is going to answer that question?
http://journals.lww.com/neurosurgery/Citation/2013/06000/Inflammation_Triggered_by_Traumatic_Brain_Injury.7.aspx
No abstract available so if interested have your doctor buy it.

Physiology and Plasticity of Interhemispheric Connections

A total of 10 articles in 112 pages. I'm not going to read this, your doctor needs to tell you how to recover your  Interhemispheric Connections.
Article titles here:
Physiology and Plasticity of Interhemispheric Connections, Matteo Caleo, Giorgio M. Innocenti,
and Maurice Ptito
Volume 2013, Article ID 176183, 2 pages
The Visual Callosal Connection: A Connection Like Any Other?, Kerstin E. Schmidt
Volume 2013, Article ID 397176, 11 pages
Splenium of Corpus Callosum: Patterns of Interhemispheric Interaction in Children and Adults,
Maria G. Knyazeva
Volume 2013, Article ID 639430, 12 pages
Axon GuidanceMechanisms for Establishment of Callosal Connections, Mitsuaki Nishikimi, Koji Oishi,
and Kazunori Nakajima
Volume 2013, Article ID 149060, 7 pages
Functional Topography of Human Corpus Callosum: An fMRIMapping Study,
Mara Fabri and Gabriele Polonara
Volume 2013, Article ID 251308, 15 pages
Maturation of Corpus Callosum AnteriorMidbody Is Associated with NeonatalMotor Function in Eight
Preterm-Born Infants, Preethi Mathew, Kerstin Pannek, Pamela Snow, M. Giulia D’Acunto, Andrea
Guzzetta, Stephen E. Rose, Paul B. Colditz, and Simon Finnigan
Volume 2013, Article ID 359532, 7 pages
Motor Control and Neural Plasticity through Interhemispheric Interactions, Naoyuki Takeuchi,
Yutaka Oouchida, and Shin-Ichi Izumi
Volume 2012, Article ID 823285, 13 pages
Interhemispheric Control of UnilateralMovement, Vincent Beaul´e, Sara Tremblay, and Hugo Th´eoret
Volume 2012, Article ID 627816, 11 pages
Activity-Dependent Callosal Axon Projections in NeonatalMouse Cerebral Cortex,
Yoshiaki Tagawa and Tomoo Hirano
Volume 2012, Article ID 797295, 10 pages
Deafferentation-Induced Plasticity of Visual Callosal Connections: Predicting Critical Periods and
Analyzing Cortical Abnormalities Using Diffusion Tensor Imaging, Jaime F. Olavarria, Andrew S. Bock,
Lindsey A. Leigland, and Christopher D. Kroenke
Volume 2012, Article ID 250196, 18 pages
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http://scholar.google.com/scholar_url?hl=en&q=http://downloads.hindawi.com/journals/specialissues/373719.pdf&sa=X&scisig=AAGBfm0qOkKxJZz2w5K7sQ_6zUt0iD35Zw&oi=scholaralrt

LIMITS OF LITHIUM

This one paragraph from here needs more studying by our researchers.
http://cen.acs.org/content/dam/cen/91/12/09112-cover.pdf

Ebselen, an anti-inflammatory antioxidant, was originally developed by Daiichi Sankyo, in Japan, to treat patients who had suffered a stroke. But the compound was never marketed and has since come off patent. It’s also part of the National Institutes of Health Clinical Collection—several hundred small molecules that have, to some extent, gone through the gamut of human clinical trials and have been found to be safe, but never reached final FDA approval

Search for link between strokes and dementia

Once again proving that researchers don't keep current with their field.
Do strokies have to do everything?
From Sept. 2012 in Canada and written up in an Australian website.
Stroke key to dementia
Written up in Sept. 2012 in Sage journals - Therapeutic Advances in Neurological Disorders; 
White matter dementia
This study from May 2012 has this fascinating line;

"The study demonstrates that damage to the brain's vascular system may play a key role in Alzheimer's disease, and highlights growing recognition of potential links between stroke and Alzheimer's-type dementia," said Roderick Corriveau, Ph.D., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the research.

NIH-Funded Research Provides New Clues on How Apoe4 Affects Alzheimer's Risk

The latest in the news;
http://www.canberratimes.com.au/national/health/search-for-link-between-strokes-and-dementia-20130525-2n3rj.html
World-first: Australian researchers are investigating why some stroke victims slide into dementia.
In a world-first study, Australian researchers are investigating why one out of three stroke victims - even when they appear to make a good recovery - slide into dementia.
It takes two or three years for dementia symptoms to develop and the reasons have never been explained. Really?
Lead researcher Amy Brodtmann from the Florey Institute of Neuroscience and Mental Health said people had problems with thinking, speech and memory immediately after a stroke but ''usually recover''.
''What's happening down the track is some people, not everyone, are developing cognitive decline and some people are developing dementia,'' Dr Brodtmann said.

Advertisement

The project involves studying the brains of 135 Melbourne people, who are being recruited within a day or two of suffering a stroke.
Over three years, they will undergo four MRI scans - taken upon recruitment, at three months, one year and three years - to measure any changes in the brain, including shrinkage. The results are correlated with evidence of memory and cognitive impairment.
Dr Brodtmann says that understanding these changes may give some clues as to how to predict which patients will suffer cognitive impairment and may be assisted by early intervention.
One aspect of brain degeneration being looked for are lesions in the white matter of the brain that have been strongly linked to a reduction in cognitive capacity.
Fifty people have already been recruited, including a pilot group that began their scans two years ago. Dr Brodtmann says these people seem to have undergone changes in the brain that are typical of patients with Alzheimer's disease without the dementia.

Read more: http://www.canberratimes.com.au/national/health/search-for-link-between-strokes-and-dementia-20130525-2n3rj.html#ixzz2ULwNBkM2

Long-term prediction of functional outcome after stroke using single items of the Barthel Index at discharge from rehabilitation centre

This is stupid, using a secondary measure to predict outcomes. You should be using something objective like how large and where is the dead area.
http://informahealthcare.com/doi/abs/10.3109/09638288.2013.793411

Abstract

Purpose: To determine the prognostic value of single items of the Barthel Index (BI) at discharge from rehabilitation, in predicting independence in personal activities of daily living (ADL) (BI score ≥95/100) at five years after stroke. Method: People with stroke were recruited consecutively from four European rehabilitation centres. BI was assessed on discharge and at five years after stroke. Stepwise multivariate logistic regression analysis was used to determine independent predictors of BI score ≥95/100 at five years after stroke. Thereupon, percentage chance of reaching BI ≥ 95/100 at five years after stroke was calculated. Results: Data were available for 153 patients. Independence in dressing (odds ratio (OR) = 5.22, 95% confidence interval (CI) = 1.85–14.76, p = 0.002) and bathing (OR = 8.10, 95% CI = 3.40–19.32, p  < 0.0001) were independent predictors. Independence in both items resulted in 74.1% (57.6–85.8) chance of reaching BI ≥ 95/100 at five years after stroke. Dependence in both items resulted in 6.3% (5.1–7.9) chance. Independence in bathing, but dependence in dressing resulted in 35.4% (30.7–40.4) chance whereas the opposite resulted in 26.1% (20.7–32.3) chance. Conclusion: Simple assessment of dressing and bathing on discharge from rehabilitation enables therapeutic staff to predict prognosis for long-term independence in personal ADL. This method can be used for early identification of persons with stroke who need intensive follow-up.Implications for Rehabilitation

• (In)dependence for dressing and bathing at discharge from a rehabilitation centre are significant factors in the prediction of (in)dependence in personal ADL at five years after stroke.
• This predictive tool can be used for targeting inpatient stroke rehabilitation and early identification of those patients who need intensive follow-up.

Read More: http://informahealthcare.com/doi/abs/10.3109/09638288.2013.793411

Interaction and Antagonistic Roles of NF-kappaB and Hes6 in the Regulation of Cortical Neurogenesis

I have no clue what this means and no understanding of what cortical progenitor cells are. Doctor question it is.
 http://mcb.asm.org/content/early/2013/05/15/MCB.01610-12.abstract

ABSTRACT

The involvement of nuclear factor-kappaB (NF-κB) in several processes in the postnatal and adult brain, ranging from neuronal survival to synaptogenesis and plasticity, has been documented. In contrast, little is known about the functions of NF-κB during embryonic brain development. It is shown here that NF-κB is selectively activated in neocortical neural progenitor cells in the developing mouse telencephalon. Blockade of NF-κB activity leads to premature cortical neuronal differentiation and depletion of the progenitor cell pool. Conversely, NF-κB activation causes decreased cortical neurogenesis and expansion of the progenitor cell compartment. This effect is antagonized by the pro-neuronal transcription factor Hes6, which physically and functionally interacts with RelA-containing NF-κB complexes in cortical progenitor cells. In turn, NF-κB exerts an inhibitory effect on the ability of Hes6 to promote cortical neuronal differentiation. These results reveal previously uncharacterized functions, and modes of regulation, for NF-κB and Hes6 during cortical neurogenesis.

Role of HIF-1α-activated Epac1 on HSC-mediated neuroplasticity in stroke model

I have no clue what this means and no understanding of what an ischemic muscle is. Doctor question it is.
http://www.sciencedirect.com/science/article/pii/S0969996113001484

Abstract

Exchange protein activated by cAMP-1 (Epac1) plays an important role in cell proliferation, cell survival and neuronal signaling, and activation of Epac1 in endothelial progenitor cells increases their homing to ischemic muscles and promotes neovascularization in a model of hind limb ischemia. Moreover, upregulation of Epac1 occurs during organ development and in diseases such as myocardial hypertrophy, diabetes, and Alzheimer's disease. We report here that hypoxia upregulated Epac1 through HIF-1α induction in the CD34-immunosorted human umbilical cord blood hematopoietic stem cells (hUCB³⁴). Importantly, implantation of hUCB³⁴ subjected to hypoxia-preconditioning (HP-hUCB³⁴) improved stroke outcome, more than did implantation of untreated hUCB³⁴, in rodents subjected to cerebral ischemia, and this required Epac1-to-matrix metalloprotease (MMP) signaling. This improved therapeutic efficacy correlated with better engraftment and differentiation of these cells in the ischemic host brain. In addition, more than did implantation of untreated HP-hUCB³⁴, implantation of HP-hUCB³⁴ improved cerebral blood flow into the ischemic brain via induction of angiogenesis, facilitated proliferation/recruitment of endogenous neural progenitor cells in the ischemic brain, and promoted neurite outgrowth following cerebral ischemia. Consistent with our proposed role of Epac1-to-MMP signaling in hypoxia-preconditioning, the above mentioned effects of implanting HP-hUCB³⁴ could be abolished by pharmacological inhibition and genetic disruption/deletion of Epac1 or MMPs. We have discovered a HIF-1α-to-Epac1-to-MMP signaling pathway that is required for the improved therapeutic efficacy resulting from hypoxia preconditioning of hUCB³⁴ in vitro prior to their implantation into the host brain in vivo.

First drug to improve heart failure mortality in over a decade

You will want to read this if you are taking statins. Your doctor should know about this side effect of statins.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=131385&CultureCode=en
Coenzyme Q10 decreases all cause mortality by half, according to the results of a multicentre randomised double blind trial presented today at Heart Failure 2013 congress. It is the first drug to improve heart failure mortality in over a decade and should be added to standard treatment, according to lead author Professor Svend Aage Mortensen (Copenhagen, Denmark).
Heart Failure 2013 is being held from 25-28 May in Lisbon, Portugal. It is the main annual meeting of the Heart Failure Association of the European Society of Cardiology (1).
Coenzyme Q10 (CoQ10) occurs naturally in the body and is essential to survival. CoQ10 works as an electron carrier in the mitochondria, the powerhouse of the cells, to produce energy and is also a powerful antioxidant. It is the only antioxidant that humans synthesise in the body.
CoQ10 levels are decreased in the heart muscle of patients with heart failure, with the deficiency becoming more pronounced as heart failure severity worsens. Statins are used to treat many patients with heart failure because they block the synthesis of cholesterol, but these drugs also block the synthesis of CoQ10, which further decreases levels in the body.
Double blind controlled trials have shown that CoQ10 improves symptoms, functional capacity and quality of life in patients with heart failure with no side effects. But until now, no trials have been statistically powered to address effects on survival.

More at link.

Gamma Aminobutyric Acid Receptor Agonists for Acute Stroke

Now if we just had some doctors with initiative, we could be trying out this along with my earlier 177 hyperacute options and actually save trillions of neurons from dying. Or just a very loud mouth type A personality that won't take doing nothing for an answer. I bet it will be the type A personality that advances stroke rehab rather than any doctor, but I'm willing to be proven wrong. 

Gamma Aminobutyric Acid Receptor Agonists for Acute Stroke

Introduction

Gamma aminobutyric acid (GABA) receptor agonists have shown to be effective in reducing infarct size and improving functional outcome in animal models of cerebral ischemia. However, the sedation effects of GABA receptor agonists limited the application in acute stroke patients because of the potential risk of stupor.

Materials and Methods

Objective

The aim of this study is to determine the efficacy and safety of GABA receptor agonists in the treatment of acute stroke.

Types of Studies

Randomized controlled trials.

Types of Participants

Acute stroke patients within 12 hours after stroke onset.

Types of Interventions

GABA receptor agonists in comparison with placebo.

Primary Outcomes

Death or dependency, defined as a Barthel Index score of ≤60, or the modified Rankin Scale graded 3 to 5, and adverse events.

Secondary Outcomes

Functional independence, defined as Barthel Index score >60, or modified Rankin Scale <3, and neurological function measured by other stroke scales.

Results

We included 5 trials with 3838 randomized patients. The methodological quality of the included trials was generally good, with low risk of bias. Four trials measured death and dependency at 3 months in chlormethiazole versus placebo without significant difference (2909 patients; risk ratio [RR], 1.03, 95% confidence interval [CI], 0.95–1.11). One trial measured this outcome between diazepam and placebo (849 patients; RR, 0.94; 95% CI, 0.82–1.07). In the subgroup analysis of total anterior circulation syndrome, a higher percentage of functional independence was found in the chlormethiazole group (635 patients; RR, 1.33; 95% CI, 1.09–1.64). The frequent adverse events related to chlormethiazole were somnolence (2527 patients; RR, 4.56, 95% CI, 3.50–5.95) and rhinitis (2527 patients; RR, 4.75, 95% CI

Tim Curry’s Stroke Major, But’s He’s Recovering at Home; Can Speak, Might Sing

I'll only point out 1 bone of contention.
http://www.denofgeek.us/movies/tim-curry/121986/tim-curry%E2%80%99s-stroke-major-but%E2%80%99s-he%E2%80%99s-recovering-at-home-can-speak-might-sing
According to published reports, Tim Curry is recovering after suffering a major stroke last night. Curry’s agent said he’s back at home recovering and, contrary to earlier reports, he has not lost his ability to speak.
Tim Curry’s stroke happened last night at his LA home. Sources say Tim Curry’s stroke was a major one, but he is expected to recover fully. Marcia Hurwitz, Tim Curry’s long-time agent, told the press that "Tim is doing great. He absolutely can speak and is recovering at this time and in great humor."

Whomever is saying fully recover has no clue what they are talking about. Nobody is doing any kind of damage diagnosis today and there is no understanding of what damage continues to occur during the first week due to the neuronal cascade of death. Unless it was not major and was only a TIA.

Wrong, wrong, wrong.

Tim Curry’s Stroke Occured Last July, Not Thursday

Dopamine restores reward prediction errors in old age

From my reading of this our doctors should be concerned and be using a protocol that restores dopamine prior to getting our regular therapy.
http://www.nature.com/neuro/journal/v16/n5/full/nn.3364.html

Abstract

Senescence affects the ability to utilize information about the likelihood of rewards for optimal decision-making. Using functional magnetic resonance imaging in humans, we found that healthy older adults had an abnormal signature of expected value, resulting in an incomplete reward prediction error (RPE) signal in the nucleus accumbens, a brain region that receives rich input projections from substantia nigra/ventral tegmental area (SN/VTA) dopaminergic neurons. Structural connectivity between SN/VTA and striatum, measured by diffusion tensor imaging, was tightly coupled to inter-individual differences in the expression of this expected reward value signal. The dopamine precursor levodopa (L-DOPA) increased the task-based learning rate and task performance in some older adults to the level of young adults. This drug effect was linked to restoration of a canonical neural RPE. Our results identify a neurochemical signature underlying abnormal reward processing in older adults and indicate that this can be modulated by L-DOPA