Cold weather linked to increased stroke risk in atrial fibrillation patients

Ask your doctor to resolve between these two studies.
The risk of heading to the ER for certain conditions, such as heart disease, diabetes, stroke, kidney disease and low blood pressure rises slightly as temperature and humidity increase, according to a new 
 Cold weather linked to increased stroke risk in atrial fibrillation patients

Cold weather is associated with increased risk of ischaemic stroke in patients with atrial fibrillation, according to research presented at ESC Congress today by Dr Tze-Fan Chao, cardiologist at Taipei Veterans General Hospital and the National Yang-Ming University in Taiwan.1 The study in nearly 290 000 patients suggests that cool climate may be an underrated issue for health that deserves more attention.
“Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and it increases the risk of ischaemic stroke by four- to five-fold,” said Dr Chao. “During AF, the electrical activity of the left atrium is disordered and the contraction is ineffective which results in stasis of blood in the atrium. The blood pools and becomes sluggish and can result in the formation of blood clots. If a clot leaves the heart and travels to the brain, it can cause a stroke by blocking the flow of blood through cerebral arteries.”
The autumn/winter season has been associated with a higher incidence and mortality rate of myocardial infarction, stroke and congestive heart failure. A greater plasma fibrinogen level and factor VII clotting activity in the winter have been reported as possible mechanisms.
“The elevation and activation of these coagulation factors may lead to a pro-coagulant status in cool climates which may promote the formation of blood clots within the left atrium and increase the risk of stroke for AF patients,” said Dr Chao. “However until now it was unclear whether the risk of ischaemic stroke was higher in AF patients during cool seasons or on days with a lower temperature.”
The study investigated this issue in 289 559 new-onset AF patients from the “National Health Insurance Research Database” in Taiwan during 2000 to 2011. Average daily temperatures in six regions of Taiwan were obtained from the Central Weather Bureau and average temperatures of each month and season were calculated. Taiwan is a small island and the differences in temperature between different regions were not large (Figure 1). The researchers therefore averaged the temperatures in the six regions to calculate the country average. The risk of ischaemic stroke was estimated for each month and season.
Among the Taiwan AF cohort, 34 991 patients suffered from an ischaemic stroke during the mean follow up of three years. The risk of ischaemic stroke was higher among the months with a lower average temperature (Figure 2). In addition, the incidence of ischaemic stroke was highest in winter and lowest in summer (Figure 3). Compared to summer, the risk of ischaemic stroke increased by 10% in spring and 19% in winter. Stroke risk did not differ significantly between summer and autumn.
“Our study shows a clear association between temperature and risk of ischaemic stroke in patients with AF,” said Dr Chao. “Risk may increase in cold weather because of the pro-coagulant status.”
A 5 °C decrease in daily temperature within 14 days before the stroke occurred was associated with an increased risk of stroke with an odds ratio of 1.128 (95% confidence interval [CI] = 1.061–1.199, p<0.001). Dr Chao said: “This suggests that there may be an opportunity to predict strokes in AF patients before they happen and put preventative measures in place such as adequate anticoagulants and reducing cold exposure through protective clothing and heating homes in winter.”
When the average temperature was below 20 °C the risk of ischaemic stroke significantly increased compared to days with an average temperature of 30 °C. “This may be because of the increased coagulability and plasma viscosity,” said Dr Chao.
He concluded: “In this large-scale nationwide AF registry, the risk of ischaemic stroke in AF patients was higher during cool months and seasons. The results imply that the interaction between humans and the environment may play an important role in AF-related stroke and remind us that cool climate may be an underrated issue for health which deserves more attention.”

Research in mice shows potential value of antidepressant in some stroke victims

Well shit, this has been known since January, 2013, wrong, since 2011.
Antidepressants may help people recover from stroke even if they are not depressed
What the fuck is it going to take to create a stroke protocol on this and help survivors?.
Our stroke associations have obviously done absolutely nothing.
You as a stroke survivor are fucking screwed since  no one is willing to do anything useful for survivors. You may as well  contact each stroke association president and ream them out for their absolute incompetence. Maybe schadenfreude will occur to those presidents. We can only hope.
If your hospital doesn't do something about this in the next month you need to call the board of directors and have them fire the president and stroke department head. This needs to be a fireable offense.
Matt Lopez, president of the NSA?
Dr. Mariel Jessup, president of the ASA?
WSO President - Steve Davis (Australia)?  
 http://medicalxpress.com/news/2015-08-mice-potential-antidepressant-victims.html
Working with mice, researchers at Johns Hopkins have added to evidence that a commonly prescribed antidepressant called fluoxetine helps stroke victims improve movement and coordination, and possibly why.Specifically, the researchers say, their experiments suggest the drug, often sold under the trade name Prozac, prolongs the time after a stroke during which physical therapy remains effective for recovering lost motor function.

The study, which may help explain the benefit of selective serotonin reuptake inhibitors already seen in stroke patients, holds potentially great value for those too ill immediately after an ischemic stroke to start the intensive rehabilitation therapy needed to recover lost motor functions. Ischemic strokes are marked by the sudden loss of blood circulation to the brain caused by a clot.
"For rehabilitation to be effective, it needs to start as soon after a stroke as possible," says Steven Zeiler, M.D., Ph.D., assistant professor of neurology at the Johns Hopkins University School of Medicine and lead author of the study reported in the October issue of the journal Stroke. "But with this study, we've shown that in mice, we can extend the time period during which rehabilitative intervention has an effect on meaningful recovery."
An estimated 65 percent of stroke survivors experience some weakness or paralysis of their limbs, and difficulty in walking and moving due to the death of brain cells from lack of blood flow. Rehabilitation involves retraining other parts of the brain to take over and restore lost functions. Zeiler worked with John Krakauer, M.D., who directs the Brain, Learning, Animation and Movement Lab, to show that in mice, such behavioral efforts work best when they begin early and at high dosages. Numerous research studies have reached similar conclusions, Zeiler says.
For the current study, his team tested whether mice with induced strokes given fluoxetine would get the same recovery results even when rehab was delayed.
A 2011 study of patients who took fluoxetine after an ischemic stroke—called "Fluoxetine for motor recovery after acute ischemic stroke," or FLAME—suggested that the strategy could work. "We took the results of the success found in the FLAME study and reverse-engineered it to look at what fluoxetine may be doing," says Zeiler. "Nobody knows how fluoxetine worked in those patients' stroke recovery—only that it did and it does."
The mouse model the researchers used involved training mice to do a task they don't normally do: reach through a slit to grab a food pellet. "As primates, we make this motion all the time," says Zeiler, "but quadrupeds, like cats, dogs and mice, aren't so good at it." Once the trained mice became good at it, the researchers induced a stroke in the motor area that affected the mice's ability to do that task.
To test whether the mice properly modeled human stroke patients, Zeiler started rehab with some of the mice immediately after the induced stroke. As with human stroke patients, early intervention made a difference: Those mice soon recovered the lost motor function. Mice for which rehab was delayed by a week showed incomplete recovery, gaining back a little less than one-half of their former ability.
"For patients," says Zeiler, "incomplete recovery means weakness or a loss of control in the affected body part or region." For the mice, it meant that they knocked the food pellet from the holder, dropped it or otherwise lost control of it.
When the researchers administered fluoxetine daily to the mice beginning 24 hours after inducing stroke, however, the mice recovered the ability to do the learned task even if they started rehab after a week's delay.
Zeiler emphasizes that the precise cause of fluoxetine's effect on stroke recovery is not yet known, but he says that after looking at brain tissue from his study's mice, he thinks the drug changed the way their brains responded to retraining. "We believe the drug is changing plasticity," says Zeiler, "changing the way individual neurons are responding to sensory input after the stroke."
"There are some who believe fluoxetine can reduce the amount of brain tissue that dies after a stroke," says Zeiler, but his team's findings do not bear that out. "In fact," Zeiler says, "there was more—not less—brain tissue death in the animals that got fluoxetine than in those that did not. We didn't predict that, but the fact that the animals actually got better—despite increased cell death—tells us that fluoxetine is having some pretty amazing effects."
"Time still matters; it's key," cautions Zeiler. The mice that fully recovered motor function were started on fluoxetine immediately after the induced stroke; if fluoxetine administration was delayed by one week after stroke, instead of 24 hours, the mice did not fully recover.
Like all drugs, Zeiler notes, fluoxetine can have negative side effects. Still, Zeiler says, stroke doctors at Johns Hopkins recommend it for stroke patients, especially those who suffer motor loss. "But it's not something that a patient would be prescribed forever," he adds.

Coffee linked with increased cardiovascular risk in young adults(18-45) with mild hypertension

Well, I'm obviously no longer young and my coffee consumption is needed for many reasons.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=155759&CultureCode=en
Coffee drinking is associated with increased risk of cardiovascular events (mainly heart attacks) in young adults (18-45) with mild hypertension, according to research presented at ESC Congress today by Dr Lucio Mos, a cardiologist at Hospital of San Daniele del Friuli in Udine, Italy.1 The 12 year study in more than 1 200 patients found that heavy coffee drinkers had a four-fold increased risk while moderate drinkers tripled their risk. Future prediabetes attenuated the associations suggesting that the effect of coffee on cardiovascular events may be mediated by its long term influence on blood pressure and glucose metabolism.
“There is controversy surrounding the long term cardiovascular and metabolic effects of coffee consumption in patients with hypertension,” said Dr Mos. “Our study was designed to evaluate whether coffee drinking had an effect on the risk of cardiovascular events, and if the association was mediated by effects on blood pressure and glucose metabolism.”
The study included 1 201 non-diabetic patients aged 18 to 45 years from the prospective HARVEST2 study who had untreated stage 1 hypertension (systolic blood pressure between 140 and 159 mmHg and/or diastolic blood pressure between 90 and 99 mmHg). Coffee consumption was categorised by the number of caffeine-containing cups per day: non-drinkers (0), moderate (1–3) and heavy drinkers (4 or more). Among the participants, 26.3% were abstainers, 62.7% were moderate and 10.0% were heavy coffee drinkers. Coffee drinkers were older and had a higher body mass index than abstainers.
There was a linear relationship between coffee use and risk of hypertension needing treatment. The association reached statistical significance for heavy drinkers (figure 1). As type 2 diabetes often develops in hypertensive patients at a later stage, the study examined the long term effect of coffee drinking on the risk of developing prediabetes. A linear relationship was found, with a 100% (30% to 210%) increased risk of prediabetes in the heavy coffee drinkers (figure 2).
However, the risk of prediabetes related to coffee consumption differed according to the CYP1A2 genotype, which determines whether individuals are fast or slow caffeine metabolisers. The risk of prediabetes was increased significantly only in slow caffeine metabolisers, with a hazard ratio (HR) of 2.78 (95% confidence interval 1.32-5.88, p=0.0076) for heavy coffee drinkers.
“Drinking coffee increases the risk of prediabetes in young adults with hypertension who are slow caffeine metabolisers,” said Dr Mos. “Slow caffeine metabolisers have longer exposure to the detrimental effects of caffeine on glucose metabolism. The risk is even greater if they are overweight or obese, and if they are heavy coffee drinkers. Thus, the effect of coffee on prediabetes depends on the amount of daily coffee intake and genetic background.”
During the 12.5 year follow-up there were 60 cardiovascular events. Of these about 80% were heart attacks and the remainder included strokes, peripheral artery disease and kidney failure. In multivariable analyses including other lifestyle factors, age, sex, parental cardiovascular morbidity, body mass index, total blood cholesterol, 24 hour ambulatory blood pressure, 24 hour ambulatory heart rate and follow-up changes in body weight, both coffee categories were independent predictors of cardiovascular events with HRs of 4.3 (1.3-13.9) for heavy coffee drinkers and 2.9 (1.04-8.2) for moderate drinkers.
Inclusion of hypertension development in the analysis attenuated the strength of the association between coffee and cardiovascular events with HRs of 3.9 (1.2-12.5) for heavy and of 2.8 (0.99-7.8) for moderate drinkers.  When future prediabetes was also incorporated, the relationship was of borderline significance for heavy coffee drinkers (HR, 3.2, 95%CI, 0.94-10.9) and was no longer significant for moderate drinkers (HR, 2.3, 95%CI, 0.8-6.5).
Dr Mos concluded: “Our study shows that coffee use is linearly associated with increased risk of cardiovascular events in young adults with mild hypertension. This relationship seems to be at least partially mediated by the long term effect of coffee on blood pressure and glucose metabolism. These patients should be aware that coffee consumption may increase their risk of developing more severe hypertension and diabetes in later life and should keep consumption to a minimum.”

Midday naps associated with reduced blood pressure and fewer medications

So your midday naps are good for you, but I bet your doctor won't be prescribing them.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=155758&CultureCode=en
Midday naps are associated with reduced blood pressure levels and prescription of fewer antihypertensive medications, according to research presented at ESC Congress today by Dr Manolis Kallistratos, a cardiologist at Asklepieion Voula General Hospital in Athens, Greece.1
“Although William Blake affirms that it is better to think in the morning, act at noon, eat in the evening and sleep at night, noon sleep seems to have beneficial effects,” said Dr Kallistratos. “Two influential UK Prime Ministers were supporters of the midday nap. Winston Churchill said that we must sleep sometime between lunch and dinner while Margaret Thatcher didn’t want to be disturbed at around 3:00 pm.  According to our study they were right because midday naps seem to lower blood pressure levels and may probably also decrease the number of required antihypertensive medications.”
He added: “Μidday sleep is a habit that nowadays is almost a privileged due to a nine to five working culture and intense daily routine. However the real question regarding this habit is: is it only a custom or is it also beneficial?”
The purpose of this prospective study was to assess the effect of midday sleep on blood pressure (BP) levels in hypertensive patients. The study included 386 middle aged patients (200 men and 186 women, average age 61.4 years) with arterial hypertension. The following measurements were performed in all patients: midday sleep time (in minutes), office BP, 24 hour ambulatory BP, pulse wave velocity,2 lifestyle habits, body mass index (BMI) and a complete echocardiographic evaluation including left atrial size.3 BP measurements were reported as diastolic and systolic BP.4
After adjusting for other factors that could influence BP such as age, gender, BMI, smoking status, salt, alcohol, exercise and coffee, the researchers found that midday sleepers had 5% lower average 24 hour ambulatory systolic BP (6 mmHg) compared to patients who did not sleep at all midday. Their average systolic BP readings were 4% lower when they were awake (5 mmHg) and 6% lower while they slept at night (7 mmHg) than non-midday sleepers (Figure 1).
Dr Kallistratos said: “Although the mean BP decrease seems low, it has to be mentioned that reductions as small as 2 mmHg in systolic blood pressure can reduce the risk of cardiovascular events by up to 10%.”
The researchers also found that in midday sleepers pulse wave velocity levels were 11% lower and left atrium diameter was 5% smaller. “These findings suggest that midday sleepers have less damage from high blood pressure in their arteries and heart,” said Dr Kallistratos.
The duration of midday sleep was associated with the burden of arterial hypertension. Patients who slept for 60 minutes midday had 4 mmHg lower average 24 hour systolic BP readings and a 2% higher dipping status5 compared to patients who did not sleep midday. Dippers had an average of 17 minutes more midday sleep than non-dippers.
Dr Kallistratos said: “Our study shows that not only is midday sleep associated with lower blood pressure, but longer sleeps are even more beneficial. Midday sleepers had greater dips in blood pressure while sleeping at night which is associated with better health outcomes. We also found that hypertensive patients who slept at noon were under fewer antihypertensive medications compared to those who didn’t sleep midday.”
He concluded: “We found that midday sleep is associated with lower 24 hour blood pressure, an enhanced fall of BP in night, and less damage to the arteries and the heart. The longer the midday sleep, the lower the systolic BP levels and probably fewer drugs needed to lower BP.”

New Alternatives to Statins Add to a Quandary on Cholesterol

A well thought out article on statins.  Except that they still are going after secondary issues rather than the primary one, stopping the inflammation in your arteries that collects cholesterol.
Stopping inflammation would make much more sense, but that won't occur now because statins are a huge profit center for the drug industry.
Video here:
Stopping the original inflammation that starts the process of plaque formation

http://www.nytimes.com/2015/08/30/health/new-alternatives-to-statins-add-to-a-quandary-on-cholesterol.html?emc=edit_th_20150830&nl=todaysheadlines&nlid=59279641
Well worth being one of the 10 free articles a month you get from the NYTimes.

Doctors have long faced a conundrum in prescribing statins to lower cholesterol and heart attack risk: The drugs are cheap and effective for most people, and large, rigorous clinical trials have found minimal side effects. But as many as 25 percent of those who try them complain of muscle pain. Others stop taking the drugs because, they say, they cause a hazy memory or sleep problems, among other side effects not documented in studies.

Now, with the approval on Thursday of the second in a powerful — and very expensive — new class of cholesterol-lowering drugs, the dilemma confronting doctors just got trickier. Should the people who need to lower their cholesterol, but say they cannot tolerate statins, be prescribed new drugs that cost more than $14,000 a year, potentially adding billions of dollars to the nation’s medical bill?

Doctors say their first responsibility is to patients, but it is hard for them or their patients to forget the price of drugs meant to be taken for a lifetime. The new drugs are approved for use by people with heart disease who cannot control their LDL, the dangerous cholesterol, by other means. Doctors say they try to work with patients to ensure that all who can safely take statins, many of which cost pennies a day, do so, but a substantial portion of patients insist the side effects are too severe.

Mre at link.

A case to be made: theoretical and empirical arguments for the need to consider fatigue in post-stroke motor rehabilitation

Well, DUH! When you are fatigued you can't do the millions of repetitions needed for recovery.

A case to be made: theoretical and empirical arguments for the need to consider fatigue in post-stroke motor rehabilitation

Annette Sterr Ph.D. ¹, Leonardo Furlan^2
1 School of Psychology, University of Surrey, Guildford, UK; Department of Neurology, University of Sao Paulo, Sao Paulo, Brazil,
² School of Psychology, University of Surrey, Guildford, United Kingdom

Date of Acceptance	29-May-2015
Date of Web Publication	26-Aug-2015

Correspondence Address:
Annette Sterr
School of Psychology, University of Surrey, Guildford, UK; Department of Neurology, University of Sao Paulo, Sao Paulo, Brazil


Source of Support: None, Conflict of Interest: None
DOI: 10.4103/1673-5374.162689

How to cite this article: Sterr A, Furlan L. A case to be made: theoretical and empirical arguments for the need to consider fatigue in post-stroke motor rehabilitation. Neural Regen Res 2015;10:1195-7

How to cite this URL: Sterr A, Furlan L. A case to be made: theoretical and empirical arguments for the need to consider fatigue in post-stroke motor rehabilitation. Neural Regen Res [serial online] 2015 [cited 2015 Aug 29];10:1195-7. Available from: http://www.nrronline.org/text.asp?2015/10/8/1195/162689

Motor rehabilitation after hemiparetic stroke is essential to soften physical disability (Furlan, 2014). Nevertheless, current interventions are mostly designed for well recovered individuals and often exclude stroke survivors with rather limited motor ability (Sterr and Conforto, 2012). Given that, and further advancing our research agenda in this arena (Sterr et al., 2002; Sterr and Freivogel, 2003, 2004; Sterr, 2004; Sterr et al., 2006; Sterr and Saunders, 2006), we recently tested the efficacy of a 2-week modified constraint-induced (CI) therapy program in chronic stroke individuals with very low-functioning upper limb hemiparesis (Sterr et al., 2014a). We tested the influence of both the intensity of daily motor training (90 vs. 180 minutes) and the restraint of the less affected upper limb (restraint vs. no restraint) on treatment outcomes. Sixty-five individuals were randomly assigned to four experimental conditions (90 minutes of training with or without restraint, and 180 minutes of training with or without restraint). They were assessed at baseline and after the intervention (2 weeks before, immediately before and after, 6, and 12 months after). Across the cohort, motor function improved significantly, and treatment benefits were largely sustained over the 12 months of follow-up. Analysis of the different treatment variants, however, revealed interesting yet unexpected findings, particularly with regards to the relationship between intensity (amount) of daily training and motor outcomes. As suggested by previous work (Sterr et al., 2002), longer sessions of daily training were expected to yield better outcomes than short sessions, a finding in line with the theory that massed practice is essential for neuroplasticity processes driving the functional improvements induced by CI therapy. However, this was not entirely the case. While we found some differences suggesting greater benefit of longer training sessions, the picture was not as clear as one might expect. This pointed to an interaction between training intensity and motor outcomes in low-functioning chronic stroke that appears to be different from that seen in less severe chronic hemiparesis, where the concept of 'the more the better' often holds true ([Figure 1]). We argued that this intensity-outcome relationship is moderated by variables that highly depend on the level of residual recovery. A key candidate for this moderation is fatigue. Fatigue is identified as rather common, yet obscure problem in stroke survivors (Wu et al., 2015). Post-stroke fatigue is multifactorial and seems to result from a complex interaction among biological, psychosocial, and behavioral factors (Wu et al., 2015). Here, we discuss the role of fatigue in motor rehabilitation of low-functioning chronic stroke using the framework recently suggested by Kluger et al. (2013). Although relatively different from, yet not antithetic to other fatigue models (e.g., Wu et al., 2015), we believe their framework provides conceptual and mechanistic support to our hypothesis. According to that framework, neurological, including post-stroke fatigue encompasses two domains: Perception of fatigue and fatigability. Perception of fatigue refers to a subjective sense of effort or exhaustion, whereas fatigability is related to an objective decline in performance. Although these two types of fatigue might be largely interrelated (e.g., an increased sense of effort would usually contribute to impair performance), they might also act independently and still significantly affect the individual's engagement with activities posing high motor and/or cognitive demands. This is because those two types of fatigue are likely to be caused by different, yet potentially interacting factors. For instance, perception of fatigue could be induced by homeostatic (e.g., metabolic stimuli, such as depletion of energy reserves in skeletal muscle and/or brain tissue) and/or psychological (e.g., decreased motivation) mechanisms, while fatigability could occur due to declines in skeletal muscle force production and/or deficits in task-related neural processing (Kluger et al., 2013). Based on that, we propose that low-functioning chronic stroke survivors are highly susceptible to get into a complex fatigued state, which renders motor training ineffective. This state is more likely to be reached by individuals undergoing longer training sessions. Essentially, we elaborate here on the possibility that a combination of general deconditioning and compromised neural processing might greatly increase both perception of fatigue and fatigability in those individuals, which substantially reduces their engagement with motor training and thereby decreases the likelihood for neuroplasticity processes driving behavioral improvements.
Conclusion: We believe the results from our study, when interpreted under the perspective presented in this article, harbor important implications for post-stroke motor rehabilitation research. Two of the many challenges in this field have been to define the optimal intensity of motor training-based interventions (Cooke et al., 2010) and to account for potential individual differences in motor outcomes after such interventions. Taking critical modulators such as fatigue into consideration is very important here. This is because not only it might explain individual differences to some extent, but also it will contribute to prevent misconceptions around the intensity-outcome relationship of those interventions. Because fatigue is very likely to be more pronounced in low-functioning chronic stroke, studies with this group have an even stronger mandate to take it into consideration when both, seeking for optimal training intensity-related parameters as well as interpreting motor outcome measures.

Safety of Statin Pretreatment in Intravenous Thrombolysis for Acute Ischemic Stroke

I guess I'm supposed to be smart enough to understand what statin pretreatment is since it is never explained.
http://www.ncbi.nlm.nih.gov/pubmed/26173726

Tsivgoulis G¹, Kadlecová P², Kobayashi A², Czlonkowska A², Brozman M², Švigelj V², Csiba L², Kõrv J², Demarin V², Vilionskis A², Jatuzis D², Katsanos AH², Rudolf J², Krespi Y², Mikulik R².

Author information

Abstract

BACKGROUND AND PURPOSE:

A recent meta-analysis investigating the association between statins and early outcomes in acute ischemic stroke (AIS) patients treated with intravenous thrombolysis (IVT) indicated that prestroke statin treatment was associated with increased risk of 90-day mortality and symptomatic intracranial hemorrhage. We investigated the potential association of statin pretreatment with early outcomes in a large, international registry of AIS patients treated with IVT.

METHODS:

We analyzed prospectively collected data from the Safe Implementation of Treatments in Stroke-East registry (SITS-EAST) registry on consecutive AIS patients treated with IVT during an 8-year period. Early clinical recovery within 24 hours was defined as reduction in baseline National Institutes of Health Stroke Scale score of ≥10 points. Favorable functional outcome at 3 months was defined as modified Rankin Scale scores of 0 to 1. Symptomatic intracranial hemorrhage was diagnosed using National Institute of Neurological Disorders and Stroke, European-Australasian Acute Stroke Study-II and SITS definitions.

RESULTS:

A total of 1660 AIS patients treated with IVT fulfilled our inclusion criteria. Patients with statin pretreatment (23%) had higher baseline stroke severity compared with cases who had not received any statin at symptom onset. After adjusting for potential confounders, statin pretreatment was not associated with a higher likelihood of symptomatic intracranial hemorrhage defined by any of the 3 definitions. Statin pretreatment was not related to 3-month all-cause mortality (odds ratio, 0.92; 95% confidence interval, 0.57-1.49; P=0.741) or 3-month favorable functional outcome (odds ratio, 0.81; 95% confidence interval, 0.52-1.27; P=0.364). Statin pretreatment was independently associated with a higher odds of early clinical recovery (odds ratio, 1.91; 95% confidence interval, 1.25-2.92; P=0.003).

CONCLUSIONS:

Statin pretreatment seems not to be associated with adverse outcomes in AIS patients treated with IVT. The effect of statin pretreatment on early functional outcomes in thrombolysed AIS patients deserves further investigation.

Alzheimer’s disease thought to be accelerated by an abnormal build-up of fat in the brain

What is your doctor doing with this discovery?
What is your doctor doing to prevent your 33% dementia chance post-stroke from an Australian study? ANYTHING AT ALL? Or is your doctor expecting you to figure this out on your own?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=155778&CultureCode=en 

People with Alzheimer’s disease have fat deposits in the brain. For the first time since the disease was described 109 years ago, researchers affiliated with the University of Montreal Hospital Research Centre (CRCHUM) have discovered accumulations of fat droplets in the brain of patients who died from the disease and have identified the nature of the fat.
This breakthrough, published today in the journal Cell Stem Cell, opens up a new avenue in the search for a medication to cure or slow the progression of Alzheimer’s disease. "We found fatty acid deposits in the brain of patients who died from the disease and in mice that were genetically modified to develop Alzheimer’s disease. Our experiments suggest that these abnormal fat deposits could be a trigger for the disease", said Karl Fernandes, a researcher at the CRCHUM and a professor at University of Montreal.
Over 47.5 million people worldwide have Alzheimer’s disease or some other type of dementia, according to the World Health Organization. Despite decades of research, the only medications currently available treat the symptoms alone.
This study highlights what might prove to be a missing link in the field. Researchers initially tried to understand why the brain’s stem cells, which normally help repair brain damage, are unresponsive in Alzheimer’s disease. Doctoral student Laura Hamilton was astonished to find fat droplets near the stem cells, on the inner surface of the brain in mice predisposed to develop the disease. "We realized that Dr. Alois Alzheimer himself had noted the presence of lipid accumulations in patients’ brains after their death when he first described the disease in 1906. But this observation was dismissed and largely forgotten due to the complexity of lipid biochemistry", said Laura Hamilton.
The researchers examined the brains of nine patients who died from Alzheimer’s disease and found significantly more fat droplets compared with five healthy brains. A team of chemists from University of Montreal led by Pierre Chaurand then used an advanced mass spectrometry technique to identify these fat deposits as triglycerides enriched with specific fatty acids, which can also be found in animal fats and vegetable oils.
"We discovered that these fatty acids are produced by the brain, that they build up slowly with normal aging, but that the process is accelerated significantly in the presence of genes that predispose to Alzheimer’s disease", explained Karl Fernandes. In mice predisposed to the disease, we showed that these fatty acids accumulate very early on, at two months of age, which corresponds to the early twenties in humans. Therefore, we think that the build-up of fatty acids is not a consequence but rather a cause or accelerator of the disease."
Fortunately, there are pharmacological inhibitors of the enzyme that produces these fatty acids. These molecules, which are currently being tested for metabolic diseases such as obesity, could be effective in treating Alzheimer’s disease. "We succeeded in preventing these fatty acids from building up in the brains of mice predisposed to the disease. The impact of this treatment on all the aspects of the disease is not yet known, but it significantly increased stem cell activity," explained Karl Fernandes. "This is very promising because stem cells play an important role in learning, memory and regeneration."
This discovery lends support to the argument that Alzheimer’s disease is a metabolic brain disease, rather like obesity or diabetes are peripheral metabolic diseases. Karl Fernandes’ team is continuing its experiments to verify whether this new approach can prevent or delay the problems with memory, learning and depression associated with the disease.

Survivors of Childhood Cancer Have High-Risk of Recurrent Stroke

Once again the fixation on preventing stroke shows up. We should be having a multi-pronged approach. But this isn't going to occur until we get a great stroke association.
1. Replace the 88% failure rate of tPA
2. Solve the neuronal cascade of death.
3. Solve all the problems in stroke.
http://dgnews.docguide.com/survivors-childhood-cancer-have-high-risk-recurrent-stroke?
New evidence suggests that childhood cancer survivors who have experienced a stroke have double the risk of suffering a second stroke, when compared with non-cancer stroke survivors.
The study, published in the online edition of the journal Neurology, found that the main predictors of recurrent stroke were cranial radiation therapy, hypertension, and older age at first stroke -- factors that could help physicians identify high-risk patients.
The findings provide strong evidence for adjusting secondary stroke prevention strategies in these patients, and to aggressively detect and treat modifiable stroke risk factors, such as hypertension.
“We are at a point where more children are surviving cancer because of life-saving interventions,” said Sabine Mueller, MD, Pediatric Brain Tumor Center at the University of California at San Francisco, San Francisco, California. “Now, we are facing long-term problems associated with these interventions.”
The researchers analysed retrospective data from the Childhood Cancer Survivor Study (CCSS), which has followed 14,358 survivors diagnosed between 1970 and 1986 in the United States and Canada to track long-term outcomes of cancer treatment. All of the recruits were diagnosed with cancer before age 21.
To assess stroke recurrence rates, the researchers sent a second survey to participants who had reported a first stroke, asking them to confirm their first stroke and report if and when they had had another. The researchers analysed the respondent demographics and cancer treatments to identify any potential predictors of recurrent strokes.
Of the 271 respondents who reported having had a stroke, 70 also reported a second one. Overall, the rate of recurrence within the first 10 years after an initial stroke was 21%, which is double the rate of the general population of stroke survivors. The rate was even higher -- 33% for patients who had received cranial radiation therapy.
Previous research has shown that radiation therapy targeting the head is a strong predictor of a first stroke. In an earlier study, the authors found that children treated for brain tumours were 30 times more likely to suffer a stroke compared with their siblings. While the exact mechanisms are unclear, the scientists think high-dose radiation causes the blood vessels to constrict and encourage blockage.
“If they have 1 stroke, it’s not actually surprising that they have a high risk of getting another stroke,” said Heather Fullerton, MD, University of California at San Francisco. “You might use aspirin after the first stroke to try to reduce blood clots, but you’re not making those diseased blood vessels go away.”
The findings have significant implications for medical follow-up in childhood cancer patients. The authors said that current survivor screening guidelines do not recommend checking for diseased blood vessels, even though the signs are visible in standard MRIs.
“The radiologists are so focused on looking in the brain area where the tumour used to be that they’re not looking at the blood vessels,” said Dr. Fullerton.
Based on the findings, the University of California San Francisco has updated protocols for monitoring patients to include screening for both blood vessel injury and modifiable stroke risk factors, but it is not required on a national level.
“If we could identify high-risk patients, we could recommend they be followed by a paediatric stroke specialist,” said Dr. Mueller. “That will be huge in providing effective follow-up care for these children.”
SOURCE: University of California, San Francisco

Regulation of Intracellular Structural Tension by Talin in the Axon Growth and Regeneration

We need axon growth so DEMAND your doctor run a clinical trial to see if this would work in humans and what the dosing would be.
http://link.springer.com/article/10.1007/s12035-015-9394-9

• Wang Dingyu,
• Meng Fanjie,
• Ding Zhengzheng,
• Huang Baosheng,
• Yang Chao,
• Pan Yi,
• Wu Huiwen,
• Guo Jun,
• Hu Gang

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Abstract

Intracellular tension is the most important characteristic of neuron polarization as well as the growth and regeneration of axons, which can be generated by motor proteins and conducted along the cytoskeleton. To better understand this process, we created Förster resonance energy transfer (FRET)-based tension probes that can be incorporated into microfilaments to provide a real-time measurement of forces in neuron cytoskeletons. We found that our probe could be used to assess the structural tension of neuron polarity. Nerve growth factor (NGF) upregulated structural forces, whereas the glial-scar inhibitors chondroitin sulfate proteoglycan (CSPG) and aggrecan weakened such forces. Notably, the tension across axons was distributed uniformly and remarkably stronger than that in the cell body in NGF-stimulated neurons. The mechanosensors talin/vinculin could antagonize the effect of glial-scar inhibitors via structural forces. However, E-cadherin was closely associated with glial-scar inhibitor-induced downregulation of structural forces. Talin/vinculin was involved in the negative regulation of E-cadherin transcription through the nuclear factor-kappa B pathway. Collectively, this study clarified the mechanism underlying intracellular tension in the growth and regeneration of axons which, conversely, can be regulated by talin and E-cadherin.

Effects of Ginko biloba leaf extract on the neurogenesis of the hippocampal dentate gyrus in the elderly mice

Don't start on this just because it works on mice. Ask your doctor to run a clinical trial on this. No pharma company is going to sponsor such research.
http://link.springer.com/article/10.1007/s12565-015-0297-7

• Noura M. S. Osman,
• Ayman S. Amer,
• Soha Abdelwahab

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Abstract

Aging is associated with reduced hippocampal neurogenesis, which may in turn contribute to cognitive impairment. We assessed the effect of Ginkgo biloba (Gb) on hippocampal neurogenesis in elderly male mice using immunohistochemistry. We used anti-caspase-3 as a marker of apoptosis, anti-GFAP as a marker of neural stem cells, anti-Ki-67 as a specific marker for cellular proliferation and anti-doublecortin (DCX) to detect newly born neurons in the hippocampal dentate gyrus (DG) of aged male mice. The 24-month-old male mice were divided into two groups: a control group treated with distilled water and a group fed with Gb at a dose of 100 mg/kg once daily for 28 days. A sharp decrease in apoptotic cells in Gb-treated compared to nontreated mice was observed by anti-csapase-3 immunostaining. A large number of GFAP+ve cells was found in the subgranular zone of the DG of Gb-treated mice, suggesting an increase in the pool of neural stem cells by Gb treatment. There was also an increase in Ki-67 immunoreactive cells, indicating increased cell proliferation in the DG in the Gb-treated compared to nontreated group. A significant increase in newborn DCX+ve neurons with well-developed tertiary dendrites was also found in the Gb-treated compared to nontreated group. Using Western blot analysis, the expression of DCX protein in the Gb group was also significantly increased compared to the control. The results support a beneficial role of Gb on hippocampal neurogenesis in the context of brain aging.

St. Luke’s Baptist Hospital Receives Comprehensive Stroke Center Certification from DNV GL Healthcare - San Antonio, Texas

You'll notice that nowhere in here do they refer to RESULTS.  We don't give a shit about care, care and processes doesn't solve any of the problems in stroke. Call that hospital CEO(Graham Reeve, President and CEO) and demand to know what the RESULTS are; tPA efficacy, 30 day deaths, 100% recovery. Accreditation means nothing here, except it looks good on paper.
Big f*cking  Whoopee.
The puffery piece here:
http://www.businesswire.com/news/home/20150826005251/en/St.-Luke%E2%80%99s-Baptist-Hospital-Receives-Comprehensive-Stroke#.Vd5qKkbDOao

Considerations for the optimization of induced white matter injury preclinical models

It should be a simple matter to calculate how much white matter was damaged during your stroke.
1. Locate the epicenter
2. calculate the radius of gray matter damage from the regular scans, after the neuronal cascade of death is finished.
3. extrapolate that radius into the white matter.
This is not rocket science, Considering the large radius of my infarct, my white matter damage must be massive. Yet, there is absolutely no intervention or protocol for recovering from such damage. What should be occurring is using interventions that;
1. accelerate dendritic branching and
2.  axon pathfinding.
If I remember correctly I've written 17 posts on dendritic branching and 15 posts on axon pathfinding.
Your doctor, if any good at all, should know of all of these and have created stroke protocols for them.
http://journal.frontiersin.org/article/10.3389/fneur.2015.00172/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w35-2015

Abdullah Shafique Ahmad^1†, Irawan Satriotomo^1†, Jawad Fazal¹, Stephen E. Nadeau^2,3 and Sylvain Doré^{1,2,3,4,5,6,7,8}*

• ¹Department of Anesthesiology, Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, USA
• ²Research Service, Brain Rehabilitation Research Center, Malcom Randall Veterans Affairs Medical Center, Gainesville, FL, USA
• ³Department of Neurology, University of Florida, Gainesville, FL, USA
• ⁴Department of Neuroscience, University of Florida, Gainesville, FL, USA
• ⁵Department of Neurology, University of Florida, Gainesville, FL, USA
• ⁶Department of Pharmaceutics, University of Florida, Gainesville, FL, USA
• ⁷Department of Psychology, University of Florida, Gainesville, FL, USA
• ⁸Department of Psychiatry, University of Florida, Gainesville, FL, USA

White matter (WM) injury in relation to acute neurologic conditions, especially stroke, has remained obscure until recently. Current advances in imaging technologies in the field of stroke have confirmed that WM injury plays an important role in the prognosis of stroke and suggest that WM protection is essential for functional recovery and post-stroke rehabilitation. However, due to the lack of a reproducible animal model of WM injury, the pathophysiology and mechanisms of this injury are not well studied. Moreover, producing selective WM injury in animals, especially in rodents, has proven to be challenging. Problems associated with inducing selective WM ischemic injury in the rodent derive from differences in the architecture of the brain, most particularly, the ratio of WM to gray matter in rodents compared to humans, the agents used to induce the injury, and the location of the injury. Aging, gender differences, and comorbidities further add to this complexity. This review provides a brief account of the techniques commonly used to induce general WM injury in animal models (stroke and non-stroke related) and highlights relevance, optimization issues, and translational potentials associated with this particular form of injury.

Introduction

The human brain comprises both gray matter and white matter (WM), with the latter constituting roughly 60% of the total volume. Gray matter consists of neuronal cell bodies, their dendrites and axons, glial cells, and blood vessels (1). On the other hand, WM consists of myelinated and unmyelinated axons that connect various gray matter areas of the brain and support communication between neurons, as well as convey information among the network of efferent and afferent axonal fibers. Disruption of these conduction pathways may cause motor and sensory dysfunction, neurobehavioral syndromes, and cognitive impairment (2–4). In clinical settings, WM injury can occur at any time in the life span, such as with the development of periventricular leukomalacia due to hypoxic ischemic injury in infants, cardiac arrest and stroke in adults, and vascular dementia in the elderly (5–8). WM injury is the major cause of paresis in all types of stroke (9). Most obviously this is true for lacunar infarcts, which comprise about 25% of all strokes, and for lower extremity paresis in large vessel distribution strokes (except in the rare circumstance that the anterior cerebral artery territory is involved). However, because anterior circulation large vessel strokes are almost always due to clots embolizing or propagating to the carotid T-junction or the proximal middle cerebral artery, and because infarcts in both locations cause ischemia in the posterior periventricular WM, through which corticospinal and corticobulbar pathways pass, ischemic WM injury also accounts for most upper extremity paresis in large vessel distribution strokes. Furthermore, the site of periventricular WM lesions that cause paresis is also the site of crossing callosal fibers. Damage to these may contribute to apraxia after left brain stroke and may interfere with language recovery after stroke.

Thus, the extent to which WM injuries contribute to neurological impairment after stroke and the frequency with which WM damage contributes to other neurologic disorders highlights the need for therapeutic intervention strategies aimed at ameliorating WM damage or promoting WM recovery, as well as the need to dissect the molecular mechanisms involved in the pathophysiology of this injury. This review focuses essentially on techniques reported to induce WM injury. For other topics such as WM injury induced by traumatic brain injury, the pathophysiology of WM injury, WM hypersensitivity, and genetics variants leading to stroke and WM injury, which are beyond the scope of this paper, see reviews (10–17) and original research articles (18–20).

Lots more to read.

Improvement in touch sensation after stroke is associated with resting functional connectivity changes

I don't give a shit what your conclusions are, you should not have any stroke research funded without coming up with a translational plan to put your results into a stroke protocol. Worthless crap.
http://journal.frontiersin.org/article/10.3389/fneur.2015.00165/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w35-2015

Louise C. Bannister^1,2,3, Sheila G. Crewther², Maria Gavrilescu^1,4 and Leeanne M. Carey^1,3,5*

• ¹Neurorehabilitation and Recovery, Stroke Division, Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia
• ²School of Psychology and Public Health, College of Science, Health and Engineering, La Trobe University, Melbourne, VIC, Australia
• ³Occupational Therapy, School of Allied Health, College of Science, Health and Engineering, La Trobe University, Melbourne, VIC, Australia
• ⁴Defence Science and Technology Organisation, Melbourne, VIC, Australia
• ⁵Florey Department of Neuroscience and Mental Health, The University of Melbourne, Melbourne, VIC, Australia

Background: Distributed brain networks are known to be involved in facilitating behavioral improvement after stroke, yet few, if any, studies have investigated the relationship between improved touch sensation after stroke and changes in functional brain connectivity.

Objective: We aimed to identify how recovery of somatosensory function in the first 6 months after stroke was associated with functional network changes as measured using resting-state connectivity analysis of functional magnetic resonance imaging (fMRI) data.

Methods: Ten stroke survivors underwent clinical testing and resting-state fMRI scans at 1 and 6 months post-stroke. Ten age-matched healthy participants were included as controls.

Results: Patients demonstrated a wide range of severity of touch impairment 1 month post-stroke, followed by variable improvement over time. In the stroke group, significantly stronger interhemispheric functional correlations between regions of the somatosensory system, and with visual and frontal areas, were found at 6 months than at 1 month post-stroke. Clinical improvement in touch discrimination was associated with stronger correlations at 6 months between contralesional secondary somatosensory cortex (SII) and inferior parietal cortex and middle temporal gyrus, and between contralesional thalamus and cerebellum.

Conclusion: The strength of connectivity between somatosensory regions and distributed brain networks, including vision and attention networks, may change over time in stroke survivors with impaired touch discrimination. Connectivity changes from contralesional SII and contralesional thalamus are associated with improved touch sensation at 6 months post-stroke. These functional connectivity changes could represent future targets for therapy.

Introduction

Somatosensory impairment is common after stroke, occurring in 50–80% of stroke survivors (1, 2). However, investigations of the neural correlates of clinical somatosensory improvement after stroke are scarce (3). In particular, knowledge of how brain networks are interrupted is limited, but is critical to better understand the nature of the clinical deficit and post-stroke recovery (4).

Stroke impacts not only the focal lesion site but also on remote brain regions (5, 6). Lesions have important remote effects on the function of connected neural networks that are structurally intact, i.e., physiological changes in distant but functionally related brain areas (4, 7, 8). These remote effects contribute significantly to the observed behavioral deficits and recovery potential (4, 8). Further, changes in brain networks (across both hemispheres and function-specific networks) have been shown to be important in recovery of motor and attention functions (4, 6). A significant challenge is to identify the brain networks and processes that mediate functional improvement so that rehabilitation strategies can be aimed at the appropriate targets (9).

Only a few studies have investigated changes in the brain over time in association with somatosensory recovery (3, 10–13). These studies have primarily involved identification of brain regions associated with task-related brain activation. A few studies have reported that somatosensory recovery is associated with patterns of activation in primary somatosensory (SI) cortex that resembles those seen in healthy controls. For example, return of ipsilesional SI activation has been shown to be associated with improved somatosensory perception (10–12). Staines et al. (12) found that enhanced primary somatosensory cortex activation using functional MRI in the stroke-affected hemisphere occurred in conjunction with improved touch detection in four patients with thalamocortical strokes. Likewise, Wikström et al. (10) reported that increased amplitude of early somatosensory evoked fields in the ipsilesional SI in response to median nerve simulation was associated with recovery of two-point discrimination (the ability to discern that two nearby objects touching the skin are truly two distinct points, not one) in stroke patients.

While relative “normalization” of brain activity in primary and secondary (SII) somatosensory regions in both hemispheres seems to underlie good clinical recovery, patients with more severe impairments have been shown to recruit attention and multisensory brain regions to a greater degree than that seen in healthy controls, in order to accomplish successful task performance (3, 11, 14–17). In an early positron emission tomography (PET) study of five patients after subcortical stroke, Weder et al. (14) reported activation across bilateral sensorimotor cortex and distributed regions, such as premotor cortex and cerebellum, with worse performance on a tactile shape discrimination task found to correlate with bilateral sensorimotor cortex activation. Tecchio et al. (16) used magnetoencephalography (MEG) to study 18 patients at the acute (5 days) and post-acute (6 months) stages after stroke. They reported that excessive interhemispheric asymmetry correlated with a greater degree of clinical improvement over time in those patients who showed partial recovery. Taskin et al. (15) reported reduced activation of ipsilesional SI with preserved responsiveness of SII in six patients who had suffered thalamic strokes. More recently, in 19 patients, a study into the relationship between touch impairment and interruption to cortical and subcortical somatosensory areas revealed that the neural correlates of touch impairment in patients with interruption to subcortical somatosensory areas (e.g., thalamus), involved a distributed network of ipsilesional SI and SII, contralesional thalamus, and attention-related frontal and occipital regions (3).

Use of task-based brain activation paradigms can be challenging for stroke patients who may have difficulty performing a given task, and inability to perform the task may impact on the validity of the results (18). Resting-state functional connectivity analysis of functional magnetic resonance imaging (fMRI) data has more recently been employed as a way of assessing activity in the brain over time and across different networks of the brain (19, 20). Resting-state functional connectivity reveals intrinsic, spontaneous networks that elucidate the functional architecture of the human brain at rest (task-independent). Functional connectivity is defined as the statistical association (or temporal correlation) among two or more anatomically distinct regions (21). Data are analyzed for coherence across the whole brain and/or in relation to particular regions of interest (ROIs). Evidence suggests that this measure is indicative of behaviorally relevant brain networks without requiring task performance (22). Consistent resting-state networks, with sharp transitions in correlation patterns, are reliably detected in individual and group data (23, 24).

In stroke patients, use of this technique has revealed disruption of functional connectivity of brain networks, even within structurally intact brain regions (6, 25, 26). Changes in functional connectivity have been described in motor recovery under resting-state and task-related conditions (27). Further, changes in functional connectivity over time have been found to occur in conjunction with behavioral change, both in healthy individuals (22) and in stroke patients (7, 25). For example, He and colleagues (25) reported that in patients with spatial neglect, dorsal attention network connectivity was disrupted early after stroke, but appeared to have improved to similar levels as controls by 9 months post-stroke, in conjunction with behavioral improvement. This supports the interpretation that different networks or areas of the brain may dynamically change and assume different roles to allow behavior to occur.

The aim of the current study was to identify longitudinal changes in functional connections of the somatosensory network in stroke patients with somatosensory impairment, and to establish if and how these correlations are associated with improvement in touch discrimination.

The importance of interhemispheric functional connectivity in behavioral performance and recovery has been highlighted from studies using resting-state fMRI (rsfMRI) with animal and human stroke populations (7, 25, 28). The most consistent finding is of changes in interhemispheric functional connectivity between homotopic areas, such as ipsilesional and contralesional primary motor cortex (7). Longitudinal changes have also been reported. Decreased interhemispheric functional connectivity of the ipsilesional sensorimotor cortex has been reported early after stroke, with return to more normal levels during the recovery process (7, 29, 30). These findings are not surprising given that interhemispheric connections are implicated in sensory (31) and cognitive processing (32) and in models of motor and somatosensory recovery (33–37). Thus, changes in interhemispheric functional connectivity in stroke patients and associations between these changes and behavioral improvement are expected. We hypothesized that over time, stroke patients would exhibit return to a more “typical” pattern of interhemispheric functional connectivity between homologous cortical somatosensory regions, and that stronger interhemispheric resting-state functional correlations between homologous SI and SII regions at 6 months than at 1 month post-stroke would be associated with clinical improvement.

Increased connectivity with distributed networks has also been reported in recovery after stroke. First, the visual system drives human attention and planning (38, 39), and a rich history of evidence for cross-modal plasticity between the visual and somatosensory systems exists (40). Recruitment of visual areas has been reported in previous studies of motor recovery after stroke (30, 41) as well as in patients with somatosensory impairment after stroke (3). Second, greater recruitment of attention systems is known to be necessary (42) to compensate for the impairment of function-specific brain areas due to aging or injury (43, 44). In stroke patients, increased attention has been shown to be required to accomplish previously simple tasks, such as walking, and attention skills have been shown to predict outcome after stroke (42, 45). Increased activation of frontoparietal attention areas, such as inferior parietal cortex (IPC), has been reported to occur in recovering stroke patients with motor problems (46–48). Thus, greater functional connections with frontoparietal attention networks could be expected in stroke patients with somatosensory impairment. As such, we predicted that stronger thalamocortical and cortico-cortical functional correlations with frontoparietal visual attention networks at 6 months post-stroke would be associated with clinical improvement.

More at link, not that it will help any survivor.

Image more to save more

The only thing I can think of here is that the researchers are basically recommending that they cherry pick the patients to a vast extent to make sure their clinical trials succeed. You will need to make sure you have the 'correct' stroke so that the interventions available actually work. Rather than working with real-life strokes and figuring out how to solve them. Lazy bastards. What do you expect when you don't have stroke survivors running the strategy and research teams?
http://journal.frontiersin.org/article/10.3389/fneur.2015.00156/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w35-2015

Aaron P. Tansy¹*, Jason D. Hinman², Kwan L. Ng², Mateo Calderon-Arnulphi², Royya Modir³, Fiona Chatfield² and David S. Liebeskind²

• ¹Department of Neurology, Mount Sinai Comprehensive Stroke Center, New York, NY, USA
• ²University of California Los Angeles Comprehensive Stroke Center, Los Angeles, CA, USA
• ³University of California San Diego Comprehensive Stroke Center, San Diego, CA, USA

Recent successful endovascular stroke trials have provided unequivocal support for these therapies in selected patients with large-vessel occlusive acute ischemic stroke. In this piece, we briefly review these trials and their utilization of advanced neuroimaging techniques that played a pivotal role in their success through targeted patient selection. In this context, the unique challenges and opportunity for advancement in current stroke networks’ routine delivery of care created by these trials are discussed and recommendations to change current national stroke system guidelines are proposed.

Recent clinical trials have endorsed a variety of advanced neuroimaging approaches to reiterate the now unequivocal superiority of combined thrombolytic and endovascular therapy for improving outcomes in acute ischemic stroke (AIS) patients with large-vessel occlusion (LVO). Heralding a new era, this momentous advance in treatment has, on the one hand, created a novel challenge to current routine clinical practice and, on the other, a tremendous opportunity to modernize current stroke systems of care: the necessary and inevitable incorporation of advanced imaging techniques into acute stroke. Such integration and utilization, as these trials have demonstrated, holds the key for stroke care providers to save more brain and more stroke patients.

Advanced imaging, specifically vascular imaging, was an essential component of the recent landmark clinical trials and their success. Multicenter Randomized Clinical Trial of Endovascular treatment for AIS in the Netherlands (MR CLEAN), Trial and Cost Effectiveness Evaluation of Intra-arterial Thrombectomy in Acute Ischemic Stroke (THRACE), and Assess the Penumbra System in the Treatment of Acute Stroke (THERAPY) all required imaging evidence of LVO for enrollment (1–3). Even more selectively, THERAPY limited inclusion to LVOs of at least 8 mm in measured length (3). Extending the Time for Thrombolysis in Emergency Neurological Deficits-Intra-Arterial (EXTEND-IA) required not only detection of LVO but also an a priori determined favorable perfusion/ischemic mismatch profile within the affected vascular territory (4). Endovascular treatment for small core and proximal occlusion ischemic stroke (ESCAPE) required presence of LVO and excluded those with poor Alberta Stroke Program Early CT Score (ASPECTS) scores and poor collateral circulation (5, 6). Similarly, Solitaire™ FR as primary treatment for acute ischemic stroke (SWIFT-PRIME) and endovascular revascularization with solitaire device versus best medical therapy in anterior circulation stroke within 8 h (REVASCAT) required presence of LVO and excluded those with unfavorable ASPECTS scores (7, 8).

As a consequence of these trials’ requisite inclusion of vascular imaging, their image profiles reflected a more comprehensive, informative assessment of acute stroke than those obtained in routine clinical practice: one not only of tissue status but also of vascular status. More importantly, because these trials enrolled patients with LVO across a wide range of clinical scenarios, their results demonstrated that acute stroke imaging profiles enhanced with vascular status invaluably expanded eligibility for and established treatment of LVO-AIS in its diverse array of clinical impairment beyond what routine practice has offered.

The notion that imaging which reflects both tissue and vascular status may be of great benefit is not new to the field of stroke. An abundance of evidence has progressively mounted to modernize acute stroke management through approaches that provide such information. For one, ASPECTS scoring is a validated method for assessing tissue status using either CT or MR imaging (9) and indicates the likelihood of a favorable response to treatment (5). Vascular status, although less established, has been shown also to play a significant role in AIS (10–12). Collateral flow, in particular, appears to impact acute stroke treatment response: both clinical and radiographic outcomes across all AIS and treatments are better in those with existing collateral flow than in those without (10, 13). As a consequence, the development and utilization of ASPECTS collateral scoring in acute stroke assessment and treatment guidance has been promoted within the stroke community. Furthermore, perfusion-based methods have garnered continued support for assessment of tissue and vascular status in acute stroke (12, 14). Evaluating therapeutic responsiveness for hypoperfusion of an affected territory in LVO, perfusion-based imaging trials have required vascular imaging to determine LVO status for eligibility selection. In fact, EXTEND-IA, where a small ischemic core (<70 cm³), a region of hypoperfusion, and a vascular occlusion were required for entry, demonstrated a high-revascularization rate (4) and the lowest NNT (3) of any of the recent trials, supporting the idea that collateral flow and tissue perfusion remain tightly linked to the success of endovascular therapy (15, 16). Even more importantly, ongoing trials utilizing perfusion- and vascular-based imaging have demonstrated promising early results that further encourage and justify continued investigation of imaging profiles in LVO-AIS that may be most responsive to recanalization therapies (17).

In essence then, advanced stroke imaging has changed how providers can now utilize diagnostic methods to inform treatment decision-making, whereas before it allowed for exclusion of pathology (i.e., hemorrhage) (18), it now allows for active detection of it (i.e., LVO, ischemic changes). This revolution in applicability affords, somewhat paradoxically, the opportunity to deliver more and better care, but only at the expense of improved diagnostic certainty not obtained in routine clinical practice. As a consequence, the modernization of acute stroke through utilization of advancing neuroimaging requires a re-evaluation of acute stroke triage and available diagnostic resources within the hub-and-spoke model.

Current stroke systems of care predominantly implement a hub-and-spoke model that links multiple primary stroke centers (PSCs) with a comprehensive stroke center (CSC) (19). This model provides proven excellence in stroke care for uncomplicated cases at all sites through compliance with established best-care practice, but also allows for a higher level of care for more complicated cases at CSCs when necessary (20). Best-care practice required for PSC designation includes immediate neuroimaging availability for determination of thrombolysis eligibility, largely achieved with non-contrast CT. However, more advanced neuroimaging approaches, such as multimodal CT or MRI to ascertain vascular and perfusion status, are presently not required.

Consequently, these requirements already provide challenge to current consensus positions on early management of LVO-AIS. The 2013 AHA/ASA Guidelines for the Early Management of Patients with AIS include the following recommendations: intracranial vascular imaging when endovascular therapy is considered (Class I, LOE A) and perfusion-based methods for reperfusion therapies when event duration exceeds thrombolytic eligibility windows (Class IIb, LOE B) (19). This challenge is only magnified by the fact that the vast majority of patients receive their initial acute stroke evaluation at PSCs: according to the “Get with the Guidelines” registry data from 2014, over 70%. Furthermore, although LVO comprises only a minority of this population, it carries the highest rates of disability making its rapid identification and treatment crucial (21). As a consequence, efficient triage and selection of LVO-AIS for potential combined or endovascular monotherapy cannot rely on nor succeed with the existing imaging standards of PSCs. Because advanced imaging has now become a key determinant in stroke treatment best-practice, incorporation of such methods, particularly vascular imaging, and their rapid expert interpretation have become a necessity of all designated stroke centers.

Without updating this requirement for PSC designation, the current framework within which stroke care is delivered faces significant challenges. For one, currently designated PSCs without at least vascular imaging capability and vascular neurology expertise available for its interpretation run the grave risk of becoming obsolete. Although these sites can administer thrombolytic therapy and clinically infer presence of LVO, without vascular imaging and its expert evaluation, they can no longer provide a definitive, complete assessment of acute stroke rendering them ineffective within an acute stroke system of care. In fact, a recent analysis of over 11,000 patients in the SITS-International Stroke Thrombolysis Register demonstrated that an NIHSS of 11 was moderately predictive of LVO, though the sensitivity of this measure was only 64.5% (22), in line with prior studies suggesting that this widely used and PSC-certification-required initial triage assessment tool is not adequate to identify all patients with LVO (23). Thus, this handicap will have many downstream effects within acute stroke networks diminishing stroke care delivery overall: a priori bypassing of centers without access to vascular imaging and/or additional transfer to those with it leading to the disuse of certain centers and an overburdening on and stressing of a network’s remaining available sites, services, and resources to accommodate this need.

With these concepts in mind, we suggest that PSC certification (or re-certification) mandate the following new key elements: (1) immediate availability of vascular imaging with either contrast-enhanced CT angiography or time of flight magnetic resonance angiography for all patients presenting with acute stroke; (2) immediate availability of vascular neurology expertise via in-person or telemedicine for clinical and radiologic evaluation of acute stroke; and (3) in-place protocols within acute stroke networks of care for rapid identification, stabilization, and transfer of LVO-AIS patients to CSCs or facilities of equivalence in care.

The colossal efforts to advance acute stroke care have yielded a tremendous opportunity that should not be forsaken. More imaging, incorporating non-invasive angiography and multimodal CT or MRI, beyond the current standard of non-contrast CT at PSCs will facilitate triage of stroke patients for current state-of-the-art therapies to save more brain and to extend this opportunity to more patients at greatest risk of long-term disability. Such modernization of stroke systems of care through incorporation of advanced imaging methods and their timely interpretation in clinical context is not just an opportunity, but an inevitable next step that recent trial success has galvanized with a clear message: we must image more to save more.

Which means even fewer stroke centers will have such ability and only those within a deliverable radius in the correct elapsed time will be helped. We are basically going backwards in helping stroke survivors, eventually these head-in-the sand medical professionals will realize that stopping the neuronal cascade of death will help all survivors. But don't count on that happening for another 50 years.