Effects of Single or Multiple Sessions of Whole Body Vibration in Stroke: Is There Any Evidence to Support the Clinical Use in Rehabilitation?

Once again more studies and followup needed. No problems with that, stroke patients can wait forever while the stroke medical world twiddles their thumbs.  In the meantime another 10 million yearly stroke survivors  will have no useful therapy.

Effects of Single or Multiple Sessions of Whole Body Vibration in Stroke: Is There Any Evidence to Support the Clinical Use in Rehabilitation?

Cosimo Costantino
,1 Federica Petraglia,2 Laura Luigia Sabetta,3 and Riccardo Giumelli2

1Department of Medicine and Surgery, University of Parma, Italy
2Physical Medicine and Rehabilitation Residency Program, University of Parma, Italy
3Pre-Med Student, University of Parma, Italy

Correspondence should be addressed to Cosimo Costantino; cosimo.costantino@unipr.it

Received 30 January 2018; Revised 23 April 2018; Accepted 25 May 2018; Published 30 July 2018

Academic Editor: Mario Bernardo-Filho

Copyright © 2018 Cosimo Costantino et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract

Background and Purpose. Recently new technologies and new techniques, such as Whole Body Vibration (WBV), have been introduced by the health and fitness industry to pursue therapeutic or physical performance goals. The aim of this systematic review is to investigate the effectiveness of single or multiple WBV sessions alone or in association with traditional rehabilitation, compared to traditional rehabilitation therapy or with sham therapy in poststroke patients. Methods. Randomized Control Trials and controlled clinical trials written in English between January 1st, 2003, and December 31st, 2017, were selected from PubMed, Cochrane-Central-Register-of-Controlled-Trials, and Physiotherapy-Evidence-Database (PEDro). The single WBV session and multiple sessions’ effects were assessed. Study characteristics, study population, intervention protocols, effects of WBV sessions, and adverse events were investigated with a descriptive analysis. Results. The search reported 365 articles and after screening and removal of duplicates, 11 manuscripts with PEDro score≥6/10 were selected (391 poststroke patients). Study characteristics, study population, intervention protocols (frequencies, amplitude of vibration, and peak acceleration), effects of a single or multiple WBV sessions, and adverse events were analyzed. They have been investigated with particular attention to bone turnover, structure and muscle functions, spasticity, postural control and risk of falls, functional mobility, somatosensory threshold, and activity and participation. Comparing WBV group with control group no significant benefits emerged. Discussion. This systematic review included studies involving participants with non homogeneous characteristics, just considering the incorporation of studies on individuals with chronic and postacute stroke. Despite these limits, WBV treatment has no significant risks for patients and shows interesting effects of WBV treatment in Structure and muscle functions, Spasticity and Postural control. Conclusions. Even though treatment with WBV appears safe and feasible, there is insufficient evidence to support its clinical use in poststroke rehabilitation at this point. More studies assessing other functional tests and with more specific treatment protocols are needed.
1. Introduction

Recently new technologies and new techniques, such as Whole Body Vibration (WBV), have been introduced by the health and fitness industry to pursue therapeutic or physical performance goals. Basic neurophysiological studies have shown that vibration can alter sensory and motor function by mostly activating the primary spindle endings, although secondary spindle endings, such as Golgi tendon organs, Pacinian, and Meissner corpuscles can also be activated [1]. Several types of Whole Body Vibration platforms can be found in literature [2–4].

Currently, there are three commercial typologies of vibration platforms. The first one, Galileo®, has a teeterboard that produces asynchronous sinusoidal side-alternating vertical vibrations.

The second type of commercial machines (Bodypulse®, Power Plate®, Soloflex®, Nemes®, Vibra Pro®, Vibra Fit®, Fitvibe®, PneuVibe®, and VibroGym®) produces vertical synchronous vibrations. The third type, called Extream 1000 AMH International Inc., Korea, is a slipping platform that produces horizontal vibrations [5].

Key descriptors of vibration devices include the frequency (number of complete movement cycles per second, measured in hertz), the amplitude (displacement of oscillatory motion, measured in mm), the acceleration (measured in m/s2 or g), and the duration (exposure time) of the vibration exposure [6]. The intensity of vibration is determined by varying both frequency and amplitude; accordingly it may be possible to get a training program tailored to the needs of the person, or to adapt it to different goals.

The vibration devices can differ with frequency ranges from 0 to 60 Hz, amplitudes from 0 to 12 millimeters, and peak acceleration from 0 to 20,1 g. In a typical session, the user stands on the device doing static or dynamic exercises while the platform produces sinusoidal oscillations. In most cases, the vibration session consists of several bouts of vibration exposure (each lasting from less than a minute to several minutes) separated by rest periods.

The growing interest in vibrations started from animal research in the 1990s and early 2000s when a correlation between vibration and bone deposition was reported [7, 8].

Other studies demonstrated that WBV training causes a continuous proprioceptive stimulation which increases neuromuscular receptivity [9]. Many studies have highlighted the possibility of WBV training to improve sport performance, increasing range of motion, and to be a beneficial supplementary training technique in strength programs for athletes [10–16].

Others studies have explored WBV applications in different clinical frameworks such as Osteoarthritis [17], Cognitive Function [18, 19], Postmenopausal Women [20, 21], Spinal Cord Injury [22], Rheumatoid arthritis [23], Multiple Sclerosis [24], Parkinson’s disease [25], Down Syndrome [26], Metabolic Syndrome [27], Osteoporosis [28], Chronic Obstructive Pulmonary Disease [29], and other medical conditions [30].

The aim of this systematic review is to investigate the effectiveness of single or multiple WBV sessions, alone or in association with traditional rehabilitation, compared to traditional rehabilitation therapy or with sham therapy in patients with a stroke.

More at link.

Human Recombinant Hyaluronidase Injections For Upper Limb Muscle Stiffness in Individuals With Cerebral Injury: A Case Series

Having never heard of this before I have zero clue on it. A great stroke association would have complete documentation on it with efficacy and protocols. But we have fucking failures of stroke associations instead.Or is hyaluronan just the aftereffects of contracturre?
http://www.ebiomedicine.com/article/S2352-3964%2816%2930197-9/abstract

Preeti RaghavanPress enter key for correspondence information^1,Press enter key to Email the author

,

Ying Lu

,

Mona Mirchandani

,

Antonio Stecco

¹Dr. Preeti Raghavan confirms that she had full access to all the data in the study and had final responsibility for the decision to submit for publication.

Open Access

DOI: http://dx.doi.org/10.1016/j.ebiom.2016.05.014

• Abstract

• Full Text
• Images
• References
• Supplemental Materials

Highlights

• •The accumulation of hyaluronan within muscles contributes to the development of muscle stiffness after neurologic injury.
• •Intramuscular injection of hyaluronidase reduces muscle stiffness and increases passive and active movement.
• •The injections did not produce weakness or clinically significant adverse effects in the reported case series.

Muscle stiffness contributes to disability after neurologic injury. However both the cause of the muscle stiffness and its treatment remain to be established. We propose that the accumulation of hyaluronan within muscles promotes the development of muscle stiffness. We report that the enzyme hyaluronidase, which hydrolyzes hyaluronan, reduces muscle stiffness and increases both passive and active movement in individuals with spastic paralysis after cerebral injury. The treatment takes effect within days to 2 weeks, lasts for at least three months, does not produce weakness, and is safe without clinically significant adverse effects. These results present a promising treatment for a widespread problem.

Abstract

Spasticity, muscle stiffness and contracture cause severe disability after central nervous system injury. However, current treatment options for spasticity produce muscle weakness which can impede movement, and do not directly address muscle stiffness. Here we propose that the accumulation of hyaluronan within muscles promotes the development of muscle stiffness, and report that treatment with the enzyme hyaluronidase increases upper limb movement and reduces muscle stiffness without producing weakness. 20 patients with unilateral upper limb spasticity received multiple intramuscular injections of human recombinant hyaluronidase with saline at a single visit. The safety and efficacy of the injections, passive and active movement, and muscle stiffness at eight upper limb joints were assessed at four time points: pre-injection (T0), within 2 weeks (T1), within 4–6 weeks (T2), and within 3–5 months post-injection (T3). There were no clinically significant adverse effects from the injections. Passive movement at all joints, and active movement at most joints increased at T1, and persisted at T2 and T3 for most joints. The modified Ashworth scores also declined significantly over time post-injection. Hyaluronidase injections offer a safe and potentially efficacious treatment for muscle stiffness in neurologically impaired individuals. These results warrant confirmation in placebo-controlled clinical trials.

Evidence for the efficacy of melatonin in the treatment of primary adult sleep disorders

More research needed before this can replace the feeding of sleeping pills while in the hospital.
http://www.smrv-journal.com/article/S1087-0792%2816%2930054-5/abstract?rss=yes

F. Auld

,

E.L. Maschauer

,

I. Morrison

,

D.J. Skene

,

R.L. RihaPress enter key for correspondence informationPress enter key to Email the author

DOI:

References

Supplemental Materials

Summary

Melatonin is a physiological hormone involved in sleep timing and is currently used exogenously in the treatment of primary and secondary sleep disorders with empirical evidence of efficacy, but very little evidence from randomised, controlled studies. The aim of this meta-analysis was to assess the evidence base for the therapeutic effects of exogenous melatonin in treating primary sleep disorders.
An electronic literature review search of MEDLINE (1950-present) EMBASE (1980- present), PsycINFO (1987- present), and SCOPUS (1990- present), along with a hand-searching of key journals was performed in July 2013 and then again in May 2015. This identified all studies that compared the effect of exogenous melatonin and placebo in patients with primary insomnia, delayed sleep phase syndrome, Non 24-hour sleep wake syndrome in people who are blind, and REM-Behaviour Disorder. Meta-analyses were performed to determine the effect of magnitude in studies of melatonin in improving sleep.
A total of 5030 studies were identified; of these citations, 13 were included for review based on the inclusion criteria of being: double or single-blind, randomised and controlled. Results from the meta-analyses showed the most convincing evidence for exogenous melatonin use was in reducing sleep onset latency in primary insomnia (p=0.002), delayed sleep phase syndrome (p<0.0001), and regulating the sleep-wake patterns in blind patients compared with placebo.
These findings highlight the potential importance of melatonin in treating certain first degree sleep disorders. The development of large-scale, randomised, controlled trials is recommended to provide further evidence for therapeutic use of melatonin in a variety of sleep difficulties.

Methylene blue shows promise for improving short-term memory

Having red blood cells release more oxygen sounds like a great way to treat the initial aftermath of the stroke. But this won't be followed up because we have NO stroke leadership to go to to update our stroke strategy. You're fucking screwed forever as a survivor.
http://medicalxpress.com/news/2016-06-methylene-blue-short-term-memory.html
A single oral dose of methylene blue results in an increased MRI-based response in brain areas that control short-term memory and attention, according to a new study published online in the journal Radiology.
Methylene blue is used to treat methemoglobinemia, a blood disorder in which oxygen is unable to release effectively to body tissues, and as a surgical stain.
Animal studies have shown a single low dose of methylene blue enhances long-term contextual memory—the conscious recall of the source and circumstances of a specific memory—and extinction memory, a process in which a conditioned response from stimuli gradually diminishes over time.
"Although the memory-enhancing effects of methylene blue were shown in rodents in the 1970s, the underlying neuronal changes in the brain responsible for memory improvement and the effects of methylene blue on short-term memory and sustained-attention tasks have not been investigated," said study author Timothy Q. Duong, Ph.D., from the University of Texas Health Science Center at San Antonio, Texas. "Our team decided to conduct the first multi-modal MRI study of methylene blue in humans."
Twenty-six healthy participants, between the ages of 22 and 62, were enrolled in a double-blinded, randomized, placebo-controlled clinical trial to measure the effects of methylene blue on the human brain during working-memory and sustained-attention tasks. This study was approved by the local ethical committee.
The participants underwent functional MRI (fMRI) before and one hour after low-dose methylene blue or placebo administration to evaluate the potential effects of methylene blue on cerebrovascular reactivity during tasks. Mean cerebral blood flow was measured pre- and post-intervention.
The results showed methylene blue increased response in the bilateral insular cortex—an area deep within the brain associated with emotional responses—during a task that measured reaction time to a visual stimulus. The fMRI results also showed an increased response during short-term memory tasks involving the brain's prefrontal cortex, which controls processing of memories, the parietal lobe, primarily associated with the processing of sensory information, and the occipital cortex, the visual processing center of the brain. In addition, methylene blue was associated with a 7 percent increase in correct responses during memory retrieval.
The findings suggest that methylene blue can regulate certain brain networks related to sustained attention and short-term memory after a single oral low dose.
"This work certainly provides a foundation for future trials of methylene blue in healthy aging, cognitive impairment, dementia and other conditions that might benefit from drug-induced memory enhancement," Dr. Duong said.

Explore further: Memory-enhancing drug may improve exposure therapy for PTSD patients

Journal reference: Radiology
Provided by: Radiological Society of North America

Indicator of chronic fatigue syndrome found in gut bacteria

Physicians are also mystified by stroke fatigue. Would looking into this help solve the stroke problem? But we have NO stroke leader to bring this idea to, so it will die on the vine. Survivors are screwed as they always will be until we kill off the current fucking failures of stroke associations. 
http://www.news.cornell.edu/stories/2016/06/indicator-chronic-fatigue-syndrome-found-gut-bacteria
Physicians have been mystified by chronic fatigue syndrome, a condition where normal exertion leads to debilitating fatigue that isn’t alleviated by rest. There are no known triggers, and diagnosis requires lengthy tests administered by an expert.
Due to this lack of information, some people have even suggested the disease may be psychosomatic.
Now, for the first time, Cornell researchers report they have identified biological markers of the disease in gut bacteria and inflammatory microbial agents in the blood.
In a study published June 23 in the journal Microbiome, the team describes how they correctly diagnosed myalgic encephalomyeletis/chronic fatigue syndrome (ME/CFS) in 83 percent of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.
“Our work demonstrates that the gut bacterial microbiome in ME/CFS patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” said Maureen Hanson, the Liberty Hyde Bailey Professor in the Department of Molecular Biology and Genetics and the paper’s senior author. “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”
Ruth Ley, associate professor in the Departments of Molecular Biology and Genetics and Microbiology, is a co-author.
“In the future, we could see this technique as a complement to other noninvasive diagnoses, but if we have a better idea of what is going on with these gut microbes and patients, maybe clinicians could consider changing diets, using prebiotics such as dietary fibers or probiotics to help treat the disease,” said Ludovic Giloteaux, a postdoctoral researcher in both Hanson’s and Ley’s labs and first author of the study.
Researchers have evidence that an overactive immune system plays a role in chronic fatigue. Symptoms include fatigue even after sleep, muscle and joint pain, migraines and gastrointestinal distress. One hallmark of the condition is post-exertional malaise, meaning patients may take weeks to recover from minor exertion. To test for ME/CFS, clinicians may give patients a cardio-pulmonary exercise test where they ride a bike until they become fatigued. If the test is repeated the following day,  ME/CFS patients usually cannot reproduce their performance from the first day.
“That’s very typical and specific of people with ME/CFS, because healthy people, or even people who have heart disease, can reproduce the exercise on the second day, but these people cannot,” Giloteaux said.
In the study, Ithaca campus researchers collaborated with Dr. Susan Levine, an ME/CFS specialist in New York City, who recruited 48 people diagnosed with ME/CFS and 39 healthy controls to provide stool and blood samples.
The researchers sequenced regions of microbial DNA from the stool samples to identify different types of bacteria. Overall, the diversity of types of bacteria was greatly reduced and there were fewer bacterial species known to be anti-inflammatory in ME/CFS patients compared with healthy people, an observation also seen in people with Crohn’s disease and ulcerative colitis.
At the same time, the researchers discovered specific markers of inflammation in the blood, likely due to a leaky gut from intestinal problems that allow bacteria to enter the blood, Giloteaux said.
Bacteria in the blood will trigger an immune response, which could worsen symptoms.
The researchers have no evidence to distinguish whether the altered gut microbiome is a cause or a whether it is a consequence of disease, Giloteaux added.
In the future, the research team will look for evidence of viruses and fungi in the gut, to see whether one of these or an association of these along with bacteria may be causing or contributing to the illness.
Co-authors include Julia Goodrich, a doctoral student, and William Walters, a postdoctoral researcher, both in Ley’s lab.
The study was funded by the National Institutes of Health.

Ischemic stroke therapy – does the gut microbiota hold the key? by Sara Adães

You can read all about it, but it is not going to do one but of good because we have NO stroke leadership to follow this up with more research. You are screwed along with your children and grandchildren. I'm sure your doctor can explain this all to you because I can't even figure out what to highlight,

Ischemic stroke therapy – does the gut microbiota hold the key? by Sara Adães

As the world’s population grows older, the burden of stroke continues to increase. Epidemiological data indicates that around 17 million people suffer a stroke each year, making it the second leading cause of death in the world and a major source of disability.
The incidence of ischemic stroke (occurring due to loss of blood supply to the brain) in young adults is also increasing, almost doubling since the 1990s; epidemiological projections estimate that the total worldwide number of ischemic stroke survivors may rise to 77 million people by 2030. Post-stroke complications are frequent and include motor deficits, dementia, depression, or fatigue, for example.
Despite major advances in knowledge of the pathophysiology of stroke, effective therapeutic options for ischemic stroke are still fairly limited. Research has shown that inflammation is a key component in the pathophysiological mechanisms of cerebral ischemia and that immune responses seem to play important roles in the primary and secondary progression of ischemic lesions, as well as in their repair and recovery, thus having a vital impact on the overall post-stroke outcome.

Proposed mechanism of protection from ischemic brain injury induced by intestinal microbial dysbiosis. Two weeks of AC treatment results in microbial dysbiosis. mLN DCs that originate in the small intestine induce Treg cells. After homing to the gut, IL-10–secreting Treg cells suppress IL-17+ γδ T cell differentiation. Effector T cells traffic from the intestine to the meninges, where a reduction in IL-17+ γδ T cells decreases post-ischemic chemokine (Cxcl1 and Cxcl2) expression and leukocyte infiltration, improving outcome after brain ischemia. (Benakis et al., 2016; Nature Medicine)

Immune and inflammatory mechanisms are now being explored as potential therapeutic targets, but there is still a lot to be understood about their roles in the pathophysiology of ischemic stroke until new and effective therapeutic strategies arise. Given its increasingly acknowledged role in the modulation of systemic immune and inflammatory responses, the gut microbiota has become a particularly engaging research subject.
The immune system, the gut microbiota, and the brain
The interaction with our commensal microbes is essential for the development, maintenance, and function of our immune system. But the gut microbiota may also be a key regulator of brain function through the gut-brain axis. As research on this field blooms, the gut microbiota is impressively gaining awareness as a central regulator of many neurophysiological functions due to its ability to influence the brain’s chemistry through the release of neuroactive molecules and through modulation of immunological and inflammatory responses.
Through their interaction with the immune system, intestinal microbes have emerged as key regulators of lymphocyte popu­lations, including regulatory T (T_reg) and effector γδ T cells, both known to be involved in cerebral ischemic injury. γδ T cells are known to be able to exacerbate ischemic brain injury by secreting IL-17 and generating chemotactic signals for other immune cells; T_reg cells, on the other hand, can contribute to neuroprotection by decreasing post-ischemic inflammation and increasing the secretion of the anti-inflammatory cytokine IL-10. T_reg cells may modulate the peripheral immune system rather than directly act on the brain, and can maintain an anti-inflammatory environment in the gut by suppressing the proliferation of γδ T cells.
With these premises in mind, a new study recently published in Nature Medicine aimed at determining the effects of an altered intestinal microbiota on the immune system and on the outcome of cerebral ischemia. The results were groundbreaking – the study describes a new microbiota-gut-brain axis pathway with a potential impact on the outcome of ischemic stroke.
The gut microbiota may dictate stroke outcome
Using two groups of mice – a group sensitive to antibiotic treatment with amoxicillin–clavulanic acid, and a group resistant to the same antibiotic treatment – it was shown that antibiotic-induced alterations in the intestinal microbiota (dysbiosis) can reduce ischemic brain injury in mice. Causing an intestinal microbial imbalance altered immune homeostasis in the small intestine, leading to an increase in neuroprotective T_reg cells and a reduction in detrimental IL-17-producing γδ T cells.
But the most impressive finding of this study was that there is trafficking of intestinal T cells to the meninges; intestinal T cells were known to traffic to extra-intestinal lymph nodes and to the spleen, but the new data presented in this study now shows that, after stroke, intestinal T cells can preferentially accumulate in the meninges as opposed to the cervical lymph nodes, suggesting a specific mechanism of gut-brain trafficking.
So, according to this study, in a normal gut microbial environment, after stroke there is a trafficking of IL-17+ γδ T cells from the gut to the leptomeninges, where they enhance ischemic neuroinflammation by secreting IL-17; this then leads to an increased production of chemokines in the brain and to the subsequent infiltration of cytotoxic immune cells.
T_reg cells can inhibit the differentiation and proliferation of IL-17+ γδ T cells by secreting the anti-inflammatory cytokine IL-10. However, this ability is more efficiently achieved in mice treated with antibiotics, indicating that antibiotic-induced alterations in the intestinal microbiota can potentiate the neuroprotective effect of T_reg cells.
Since the levels of T_reg cells were increased in the small intestine but not in the meninges (nor in the colon, peripheral blood, spleen or lymph nodes of antibiotic-treated mice), changes in the bacterial composition in the small intestine are most likely accountable for this effect.
T_reg cells may therefore affect stroke outcome through an intestinal mechanism involving IL-17+ γδ T cell suppression. Indeed, fewer IL-17+ γδ T cells were found in the meninges after stroke in mice with intestinal dysbio­sis, and this was associated with reduced IL-17–responsive chem­okine expression in the brain, indicating that antibiotic treatment suppressed the trafficking of effector IL-17+ γδ T cells from the gut to the leptomeninges after stroke.
Similarly to the effect observed on T_reg cells, antibiotic treatment rendered dendritic cells isolated from the mesenteric lymph nodes more efficient in inducing T_reg cells proliferation than those isolated from mice resistant to antibiotic treatment, whereas their inhibitory effect on IL-17+ γδ T cell proliferation was less marked. This suggested that dendritic cells induce the proliferation of T_reg cells, which in turn suppress the proliferation of IL-17+ γδ T cells through the action of IL-10.
Therefore, a suppression of effector IL-17+ γδ T cell function by T_reg cells can be achieved by modulating the activity of intestinal dendritic cells though the induction of dysbiosis with antibiotic treatment. However, the bacterial species respon­sible for these protective effects of dysbiosis remain to be identified.
These findings thus unraveled a previously unknown gut-brain axis pathway and once again highlight the impact of the gut microbiota on the brain, in this case, on the outcome of ischemic brain injury. Importantly, these findings fit those from studies on human stroke: infiltration of γδ T cells and secretion of IL-17 have also been reported in ischemic human brain tissue, as well as increased levels of circulating IL-17 in stroke patients.
This research may open a new avenue for potential therapies for ischemic stroke.

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References 

1. Al Omran Y, & Aziz Q (2014). The brain-gut axis in health and disease. Adv Exp Med Biol., 817, 135-53. doi: 10.1007/978-1-4939-0897-4_6
2. Béjot Y, et al (2016). Epidemiology of stroke and transient ischemic attacks: Current knowledge and perspectives. Rev Neurol (Paris), 172(1):59-68. doi: 10.1016/j.neurol.2015.07.013
3.  Benakis C, et al (2016). Commensal microbiota affects ischemic stroke outcome by regulating intestinal γδ T cells. Nat Med, 22(5):516-23. doi: 10.1038/nm.4068
4.  Erny D, et al (2015). Host microbiota constantly control maturation and function of microglia in the CNS. Nat Neurosci, 18 (7), 965-77. doi: 10.1038/nn.4030
5.  Gelderblom M, et al (2012). Neutralization of the IL-17 axis diminishes neutrophil invasion and protects from ischemic stroke. Blood, 120(18):3793-802. doi: 10.1182/blood-2012-02-412726
6.  Iadecola C & Anrather J (2011). The immunology of stroke: from mechanisms to translation. Nat Med, 7;17(7):796-808. doi: 10.1038/nm.2399
7.  Li GZ, et al (2012). Expression of interleukin-17 in ischemic brain tissue. Scand J Immunol, 62(5):481-6. doi: 10.1111/j.1365-3083.2005.01683.x
8.  Park SG, et al (2010). T regulatory cells maintain intestinal homeostasis by suppressing γδ T cells. Immunity, 33(5):791-803. doi: 10.1016/j.immuni.2010.10.014

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Any views expressed are those of the author, and do not necessarily reflect those of PLOS. This article is not meant to encourage excessive alcohol consumption.   

Sara Adães has been a researcher in neuroscience for over a decade. She is a Biochemist and received her PhD in Neuroscience from the Faculty of Medicine of the University of Porto, in Portugal, where she studied the neurobiology of pain. You can follow her on twitter @saradaes (https://twitter.com/saradaes ).

The Way We Learn Today Is Just Wrong

I'm sure the same can be said for how stroke survivors relearn their lost functions. But NOTHING will be done about this in stroke rehab because we have NO FUCKING STROKE LEADERSHIP to bring such sensible ideas to fruition.
https://www.linkedin.com/pulse/way-we-learn-today-just-wrong-peter-diamandis

10 ways to control high blood pressure without medication

Even the Mayo Clinic doesn't seem to have the ability to create a diet that could reduce your high blood pressure. Who the hell out there can do that? All it would take is some additional research proving amounts needed.
http://www.mayoclinic.org/diseases-conditions/high-blood-pressure/in-depth/high-blood-pressure/art-20046974/?
Go to the link to see the complete listing from Mayo.  My links were added in here because Mayo was totally incomplete.
Here are 10 lifestyle changes you can make to lower your blood pressure and keep it down.

1. Lose extra pounds and watch your waistline

2. Exercise regularly

3. Eat a healthy diet.

Nothing here is clinically proven, don't do it. These are my findings of research  in the literature.

Antihypertensive Effect of Fermented Milk Products Under the Microscope

Melatonin reduces blood pressure and tunes up disrupted circadian rhythms in the elderly

Study: Aged Cheese Lowers Blood Pressure

Must-Have Foods That Can Help Lower Blood Pressure Naturally

Dietary nitrate lowers blood pressure

8 Produce Picks For Better Blood Pressure

UEA research shows high protein foods boost cardiovascular health

The Acute Electrocortical and Blood Pressure Effects of Chocolate

Daily Consumption of Blueberries May Lower Blood Pressure

Reduce High Blood Pressure with Beet Juice

New research shows almonds reduce the risk of heart disease

Regular pomegranate juice administered to hypertensive patients causeda significant drop in blood pressure [26], a reduction in carotid plaque development [27] 

4. Reduce sodium in your diet

Low-Salt Diet Ineffective, Study Finds. Disagreement Abounds.

 

5. Limit the amount of alcohol you drink

1.  Red Wine: Heart-Healthy? 

2. Acute effects of beer on endothelial function and hemodynamics: A single-blind, crossover study in healthy volunteers 

3. Dark beer is good for you, in moderation

 

6. Quit smoking

7. Cut back on caffeine

This one has this statement in it:

They performed the most rigorous investigation to date, a randomized, double-blind, placebo-controlled cross-over study that found that caffeine significantly improved endothelial function.  I'm assuming that improved function would actually reduce blood pressure, but don't listen to me.

Effect of coffee on endothelial function in healthy subjects: the role of caffeine

 

But did they consider those studies that have identified a single nugget of our DNA that seems to determine whether we process caffeine quickly or slowly? That, in turn, appears to have a large effect on whether coffee is good for your health.  

 8. Reduce your stress

9. Monitor your blood pressure at home and see your doctor regularly

10. Get support

Sometimes I wonder if there is anyone in the world that understands what needs to be done to prevent and solve strokes. Mayo Clinic obviously does not.

Stroke survivor who fought against all odds to walk again nominated for second award this year

Awards like this should not have to exist because we have stopped a lot of the dead and damaged neurons by stopping the neuronal cascade of death by these 5 causes. If your doctor and hospital don't recognize the solution(more research needed) to this stroke disability problem you have fucking idiots in charge.
 http://www.burtonmail.co.uk/Stroke-survivor-fought-odds-walk-nominated-second/story-29366707-detail/story.html

A woman who has fought against all odds to regain her ability to speak and walk following a stroke has been nominated for yet another award for her determination.
Maz Wedgwood, 72, from Barton, has been nominated in the Against All Odds category in the Mail's Community Champions awards for tackling her life-changing condition with a smile on her face.
And this is the second time this year that the inspirational stroke survivor has been nominated for her bravery in her recovery, despite being told by her consultant that she would never walk again.
Just last month, Maz hit the headlines when she was nominated by her personal trainer, Leon Simpson, for the Stroke Association's Life After Stroke Courage Award.

Read more: http://www.burtonmail.co.uk/Stroke-survivor-fought-odds-walk-nominated-second/story-29366707-detail/story.html#ixzz4BYlRhHCS
Follow us: @BurtonMailNews on Twitter | BurtonNews on Facebook

Commentary: Evidence-based care best hope to eliminate medical errors

If you didn't get to 100% recovery that should be considered a medical error. What is your doctor and hospital doing to recognize all the points that need changing to get the next stroke survivor to 100% recovery? Any version of the statement 'All strokes are different, all stroke recoveries are different' is grounds for a screaming match against those people, because they know absolutely nothing about stroke recovery. The answers are out there but will take lots of research. YOU are going to have to get your stroke hospital to change for the better. Your hospital will not change otherwise.
http://www.modernhealthcare.com/article/20160611/MAGAZINE/306119978

By Bernadette Mazurek Melnyk  | June 11, 2016

For all of the discussions about cost, access and bureaucracy, it's becoming increasingly clear that one of the biggest problems we face in healthcare is inertia.

Ironically, in a field that is constantly evolving with new research and scientific knowledge, healthcare providers have a natural instinct to do things the same way they learned years ago and have always done them—and patients are paying the price.

A study by researchers at Johns Hopkins University, released in May, found that medical errors in hospitals and other healthcare facilities account for more than 250,000 deaths each year, a significant increase since an Institute of Medicine 1999 study, To Err Is Human, offered solutions for the healthcare system to achieve a better safety record. Suggestions included developing safety oversight programs, raising performance standards and instituting mandatory reporting for adverse medical events. Years later, though, it's clear that people are still dying more from their care than they are from diseases such as Alzheimer's or stroke.

This is unacceptable by any measure. But let's not jump to the conclusion that these dangerous errors are the result of carelessness or disregard for the patient's well-being. I can attest from years of teaching and working with nurses and other healthcare professionals that clinicians working in hospitals, clinics and primary-care offices are as dedicated as I have ever seen. The problem is that many have yet to develop the knowledge and skills to consistently deliver the best evidence-based care.

A follow-up IOM study in 2001, “Crossing the Quality Chasm,” offered six aims to improve the quality of care—among them, that effective care means “providing services based in scientific knowledge.” However, that gap in care between the growth of evidence-based practices and what is actually happening at the point of care still exists today. Evidence-based practice is an approach to healthcare that melds clinical expertise and patient preferences with data emanating from relevant, high-quality research. When we are able to support that a particular practice generates better health outcomes than traditional practice, clinicians should adapt and make that change. It's about prioritizing problem-solving and implementing best evidence over doing what's become comfortable.

I would guess that most patients already enter a hospital or healthcare system thinking they are going to be receiving evidence-based care. However, studies have shown that is not the standard of care in many facilities.

The implementation of best standards of patient care won't happen without a concerted, systemwide effort. We're trying to accelerate this movement by launching, in the fall of 2017, a national institute for evidence-based practice in nursing and healthcare that will be headquartered at Ohio State University. Our goal is to revolutionize the future of patient care by replacing practices that are steeped in tradition with the best evidence-based care. We're also going to be ramping up our advocacy for the kind of sensible steps that will integrate evidence-based practice into all care settings.

This begins with strengthening nursing curriculums at schools nationwide and educating nursing and other health sciences students on how to implement the steps of “EBP” and access the premier standards of care, so that they can implement them in their clinical practices. We need to create online hubs for healthcare providers to review best practices and have access to reliable resources. And, in the interest of dynamic learning, there must be a constant stream of webinars, conferences and summits to disseminate newly emerging research, evidence and knowledge.

The Johns Hopkins study only confirmed what we've known for years. Patients, regardless of where they are receiving care, deserve the benefits of breakthrough research and best practices. It may take many years to develop cures for cancer, heart disease and other life-threatening illnesses, but the quarter-million lives lost annually to medical errors is a problem we can begin fixing now.

BRAIN-DERIVED NEUROTROPHIC FACTOR DELIVERED TO THE BRAIN USING POLY (LACTIDE-CO-GLYCOLIDE) NANOPARTICLES IMPROVES NEUROLOGICAL AND COGNITIVE OUTCOME IN MICE WITH TRAUMATIC BRAIN INJURY

More research needed in humans which won't occur because we have NO stroke leadership following up promising research. Oh well, Who cares? Certainly not our fucking failures of stroke associations.
http://www.tandfonline.com/doi/abs/10.1080/10717544.2016.1199609

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DOI:

10.1080/10717544.2016.1199609

Igor Khalin^a*, Renad Alyautdin^b, Tin Wui Wong^c, Justin Gnanou^a, Ganna Kocherga^d & Jörg Kreuter^e

Publishing models and article dates explained

• Received: 15 May 2016
• Accepted: 7 Jun 2016
• Accepted author version posted online: 08 Jun 2016
  Published online: 08 Jun 2016

Alert me

Abstract

Currently, traumatic brain injury (TBI) is the leading cause of death or of disabilities in young individuals worldwide. The multi-complexity of its pathogenesis as well as impermeability of the blood-brain barrier (BBB) make the drug choice and delivery very challenging. The brain-derived neurotrophic factor (BDNF) regulates neuronal plasticity, neuronal cell growth, proliferation, cell survival, and long term memory. However, its short half-life and low BBB permeability are the main hurdles to be an effective therapeutic for TBI. Poly(lactic-co-glycolic acid) (PLGA) nanoparticles coated by surfactant can enable the delivery of a variety of molecules across the BBB by receptor-mediated transcytosis. This study examines the ability of PLGA nanoparticles coated with poloxamer 188 (PX) to deliver BDNF into the brain and neuroprotective effects of BNDF in mice with TBI. C57bl/6 mice were subjected to weight-drop closed head injuries under anesthesia. Using enzyme-linked immunosorbent assay, we demonstrated that the intravenous (IV) injection of nanoparticle-bound BDNF coated by PX (NP-BDNF-PX) significantly increased BDNF levels in the brain of sham-operated mice (p < 0.001) and in both ipsi- (p < 0.001) and contralateral (p < 0.001) parts of brain in TBI mice compared to controls. The present study also showed using the passive avoidance (PA) test, that IV injection of NP-BDNF-PX 3 hours post-injury prolonged the latent time in mice with TBI thereby reversing cognitive deficits caused by brain trauma. Finally, neurological severity score test demonstrated that our compound efficiently reduced the scores at day 7 after the injury indicating the improvement of neurological deficit in animals with TBI. This study shows that PLGA nanoparticles coated with PX effectively deliver BDNF into the brain, and improve neurological and cognitive deficits in TBI mice, thereby providing a neuroprotective effect.

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Study explores history of penumbra in untreated acute stroke patients

Where is the study that shows the penumbra history in treated patients? I.E., what the neuronal cascade of death causes.
http://www.news-medical.net/news/20160526/Study-explores-history-of-penumbra-in-untreated-acute-stroke-patients.aspx

Radiological imaging is being used more often to evaluate stroke diagnosis and outcomes, with penumbra, or tissue that is at risk of progressing to dead tissue but is still salvageable if blood flow is returned, as a potential target for therapy.
However, there have been few studies about what happens to the penumbra without treatment to restore blood flow through the blocked arteries, known as reperfusion treatment.
A study led by Achala Vagal, MD, associate professor at the University of Cincinnati (UC) College of Medicine and a UC Health radiologist, looked at a group of untreated acute stroke patients and found that there was no evidence of time dependence on damage outcomes for the penumbra but rather an association with collateral flow—or rerouting of blood through clear vessels.

These findings are being presented at the American Society of Neuroradiology's annual meeting May 25 in Washington, DC.
Vagal says their sample size was small—only 110 patients—so larger studies are needed to examine how treatment may differ in a stroke with a delayed or unknown onset time.
"Using a large, multicenter stroke registry, we analyzed all untreated acute stroke patients who received baseline CT angiogram, an X-ray that uses a dye and camera (fluoroscopy) to take pictures of the blood flow in an artery, and CT perfusion, to show which areas of the brain were getting blood, within 24 hours of the onset of stroke, and follow-up CT angiogram or MR angiogram within 48 hours," she says. "Baseline CT angiogram results were reviewed for artery blockages and rerouting of blood flow, and follow-up imaging was reviewed to determine if blood flow was restored."
Vagal adds that CT perfusion was used to determine baseline numbers for the penumbra and that dead tissue was measured on follow up CT and MR imaging.
Results showed that there was no significant correlation between salvaged penumbra and time; however, there was a correlation between salvaged penumbra and the amount of collateral blood flow, meaning the blood flow that was rerouted.
"Larger studies are needed to understand the natural history of penumbra that could lead to future trials and have treatment implications particularly in delayed or unknown onset time," she says.

Source:

University of Cincinnati (UC) Academic Health Center

CardioBrief: Women With Migraine Face Increased CV Risk

But no explanation why. More research needed that will not occur in any reasonable amount of time. We need strong stroke leadership and a strategy, but have neither.
http://www.medpagetoday.com/Cardiology/CardioBrief/58237?xid=nl_mpt_DHE_2016-06-01&eun=g424561d0r

Women who have migraine headaches have a significantly increased risk of cardiovascular disease, according to new results from a large observational study published in The BMJ.
Earlier studies have established a strong link between migraine and stroke, which the new study now extends to other types of cardiovascular disease. However, the clinical implications are uncertain since there is no definite mechanism to explain the association.
Researchers analyzed data from more than 115,000 women followed for more than 20 years in the Nurses' Health Study II. More than 17,000 participants reported a migraine diagnosis. Women who had migraines were more likely to have other risk factors for cardiovascular disease, including hypertension, hypercholesterolemia, family history, obesity, and history of smoking.
After adjusting for the known risk factors, women with migraine had a significantly elevated risk for developing major cardiovascular disease (hazard ratio 1.50, 95% CI 1.33-1.69). The greatest increase in risk was for stroke (HR 1.62) and for angina/coronary revascularizations (HR 1.73).
The findings were consistent and robust across multiple analyses. But the authors acknowledged that, as with any observational study, cause and effect could not be demonstrated and that residual confounding factors might offer "a potential alternative explanation."
The chief weakness in the link between migraine and cardiovascular disease is the lack of "clear mechanisms ... that could explain the increased risk of cardiovascular disease," write the authors. There is also no evidence looking at "whether prevention of migraine attacks reduces these risks."
In an accompanying editorial, Rebecca Burch, MD, of Harvard Medical School, and Melissa Rayhill, MD, of SUNY Buffalo, wrote that "it is time to add migraine to the list of early life medical conditions that are markers for later life cardiovascular risk." But, they warned, "the magnitude of the risk should not be over-emphasized," because the increased risk "is small at the level of the individual patient but still important at a population level because migraine is so prevalent."
Burch and Rayhill also warned against any attempt to use the association to influence treatment. Without better evidence, they wrote, "migraine is probably best thought of as a situation in which the medical urge to 'do something' (beyond currently recommended assessments for cardiac risk and advocating a healthy lifestyle) should be resisted."
Burch affirmed her position in an email interview. "There is currently no evidence to recommend any changes in how physicians manage cardiovascular risk in patients with a history of migraine. If a patient has a history of migraine, it might remind the physician of the importance of assessing cardiovascular risk in that patient. Once the risk has been assessed, however, management would be the same: treatment of hypertension and hyperlipidemia, recommending regular exercise, etc."
The first author of the study, Tobias Kurth, MD, of the Harvard T.H. Chan School of Public Health, agreed with the editorialists and said that physicians "cannot really make any inference of treatment" based on the association in the study. "Physicians may want to discuss vascular risk with patients and reduce the risk by addressing known vascular risk factors (i.e., where we know that intervention helps)."

Interventions for improving community ambulation in individuals with stroke

Once again, more research needed that will never occur with NO stroke leadership or strategy. I don't see how this walking would not improve stroke recovery.
http://www.ncbi.nlm.nih.gov/pubmed/25767912

Barclay RE¹, Stevenson TJ, Poluha W, Ripat J, Nett C, Srikesavan CS.

Author information

Abstract

BACKGROUND:

Community ambulation refers to the ability of a person to walk in their own community, outside of their home and also indoors in private or public locations. Some people choose to walk for exercise or leisure and may walk with others as an important aspect of social functioning. Community ambulation is therefore an important skill for stroke survivors living in the community whose walking ability has been affected.

OBJECTIVES:

To determine: (1) whether interventions improve community ambulation for stroke survivors, and (2) if any specific intervention method improves community ambulation more than other interventions.

SEARCH METHODS:

We searched the Cochrane Stroke Group Trials Register (September 2014), the Cochrane Central Register of Controlled Trials (CENTRAL) (November 2013), PubMed (1946 to November 2013), EMBASE (1980 to November 2013), CINAHL (1982 to November 2013), PsycINFO (1887 to November 2013), Scopus (1960 to November 2013), Web of Science (1900 to November 2013), SPORTDiscus (1975 to November 2013), and PEDro, CIRRIE and REHABDATA (November 2013). We also searched ongoing trials registers (November 2013) and reference lists, and performed a cited reference search.

SELECTION CRITERIA:

Selection criteria included parallel-group randomised controlled trials (RCTs) and cross-over RCTs, studies in which participants are adult (aged 18 years or more) stroke survivors, and interventions that were aimed at improving community ambulation. We defined the primary outcome as participation; secondary outcomes included activity level outcomes related to gait and self-efficacy.

DATA COLLECTION AND ANALYSIS:

One review author independently screened titles. Two review authors screened abstracts and full text articles, with a third review author was available to resolve any disagreements. Two review authors extracted data and assessed risk of bias. All outcomes were continuous. The analysis for the primary outcome used the generic inverse variance methods for meta-analysis, using the standardised mean difference (SMD) and standard error (SE) from the participation outcomes. Analyses for secondary outcomes all used SMD or mean difference (MD). We completed analyses for each outcome with all studies, and by type of community ambulation intervention (community or outdoor ambulation practice, virtual practice, and imagery practice). We considered trials for each outcome to be of low quality due to some trial design considerations, such as who knew what group the participants were in, and the number of people who dropped out of the studies.

MAIN RESULTS:

We included five studies involving 266 participants (136 intervention; 130 control). All participants were adult stroke survivors, living in the community or a care home. Programmes to improve community ambulation consisted of walking practice in a variety of settings and environments in the community, or an indoor activity that mimicked community walking (including virtual reality or mental imagery). Three studies were funded by government agencies, and two had no funding.From two studies of 198 people there was low quality evidence for the effect of intervention on participation compared with control (SMD, 0.08, 95% confidence interval (CI) -0.20 to 0.35 (using inverse variance). The CI for the effect of the intervention on gait speed was wide and does not exclude no difference (MD 0.12, 95% CI -0.01 to 0.24; four studies, 98 participants, low quality evidence). We considered the quality of the evidence to be low for all the remaining outcomes in our review: Community Walk Test (MD -6.35, 95% CI -21.59 to 8.88); Walking Ability Questionnaire (MD 0.53, 95% CI -5.59 to 6.66); Six-Minute Walk Test (MD 39.62 metres, 95% CI -8.26 to 87.51) and self-efficacy (SMD 0.32, 95% CI -0.09 to 0.72). We downgraded the quality of the evidence because of a high risk of bias and imprecision.

AUTHORS' CONCLUSIONS:

There is currently insufficient evidence to establish the effect of community ambulation interventions or to support a change in clinical practice. More research is needed to determine if practicing outdoor or community walking will improve participation and community ambulation skills for stroke survivors living in the community.

The Novel Oral Syk Inhibitor, Bl1002494, Protects Mice From Arterial Thrombosis and Thromboinflammatory Brain Infarction

More research needed. Don't know who to tell you to call to accomplish more human research because stroke has NO leadership or strategy.
http://atvb.ahajournals.org/content/36/6/1247.abstract?etoc

1. Judith M.M. van Eeuwijk*,
2. David Stegner*,
3. David J. Lamb,
4. Peter Kraft,
5. Sarah Beck,
6. Ina Thielmann,
7. Friedemann Kiefer,
8. Barbara Walzog,
9. Guido Stoll,
10. Bernhard Nieswandt

+ Author Affiliations

1. From the Department of Experimental Biomedicine (J.M.M.v.E., D.S., S.B., I.T., B.N.) and Department of Neurology (P.K., G.S.), University Hospital Würzburg and Rudolf Virchow Center for Experimental Biomedicine (J.M.M.v.E., D.S., S.B., I.T., B.N.), University of Würzburg, Würzburg, Germany; Respiratory Diseases Research, Boehringer Ingelheim Pharma GmbH & Co KG, Biberach an der Riß, Germany (D.J.L.); Mammalian Cell Signaling Laboratory, Department of Vascular Cell Biology, Max Planck Institute for Molecular Biomedicine, Münster, Germany (F.K.); and Walter Brendel Centre of Experimental Medicine, Department of Cardiovascular Physiology and Pathophysiology, Ludwig Maximilian University of Munich, Munich, Germany (B.W.).

1. Correspondence to Bernhard Nieswandt, PhD, Department of Experimental Biomedicine, University Hospital, University of Würzburg, Josef-Schneider-Str. 2/D15, Würzburg 97078, Germany. E-mail bernhard.nieswandt@virchow.uni-wuerzburg.de

1. ↵* These authors contributed equally to this article.

Abstract

Objective—Ischemic stroke, which is mainly caused by thromboembolic occlusion of brain arteries, is the second leading cause of death and disability worldwide with limited treatment options. The platelet collagen receptor glycoprotein VI (GPVI) is a key player in arterial thrombosis and a critical determinant of stroke outcome, making its signaling pathway an attractive target for pharmacological intervention. The spleen tyrosine kinase (Syk) is an essential signaling mediator downstream of not only GPVI but also other platelet and immune cell receptors. We sought to assess whether Syk might be an effective antithrombotic target.

Approach and Results—We demonstrate that mice lacking Syk in platelets specifically are protected from arterial thrombus formation and ischemic stroke but display unaltered hemostasis. Furthermore, we show that mice treated with the novel, selective, and orally bioavailable Syk inhibitor BI1002494 were protected in a model of arterial thrombosis and had smaller infarct sizes and a significantly better neurological outcome 24 hours after transient middle cerebral artery occlusion, also when BI1002494 was administered therapeutically, that is, after ischemia.

Conclusions—These results provide direct evidence that pharmacological Syk inhibition might provide a safe therapeutic strategy to prevent arterial thrombosis and to limit infarct progression in acute stroke.

FTY720 Preserves Blood-Brain Barrier Integrity Following Subarachnoid Hemorrhage in Rats

Would this be a possible solution to  Inflammatory action leaking through the blood brain barrier. in the neuronal cascade of death? More research needed that will never occur.

1. Abdullah Muhammad₂,₃,
2. Jennifer Harris₁,
3. Benjarat Changyaleket₂,₃,
4. Dale Pelligrino₂,₃,
5. Hao-liang Xu₂,₃ and
6. Fernando Testai₂,₃

+Show Affiliations

1. Published online before print April 8, 2015, Neurology April 5, 2016 vol. 86 no. 16 Supplement P5.230

• Abstract

Abstract

Objective: In this study we investigated the effect of FTY720 in BBB function in the rat model of SAH.  

Background: In a recent study we showed that the sphingosine-1-phosphate agonist FTY720 reduces neuroinflammation, preserves pial arteriolar reactivity, and improves neurological outcome in rats subjected to subarachnoid hemorrhage (SAH). The immune response triggered by SAH leads to blood-brain barrier (BBB) disruption and brain edema formation which are important determinants of outcome.  

Methods: SAH was induced in rats via endovascular perforation of the anterior cerebral artery. Animals were divided into three groups: (1) sham control; (2) SAH-vehicle; (3) SAH-FTY720 treated. FTY720 (0.5 mg/kg) was applied intraperitoneally 3h post SAH. Brain tissue was collected 48h post SAH. BBB integrity was evaluated based on parenchymal extravasation of Evan’s blue (EB) and the expression of endothelial barrier antigen (EBA) and tight junction proteins (ZO-1 and occludin). Brain edema was assessed by measuring the brain water content using the weight/dry method.  

Results: The parenchymal extravasation of EB in the SAH-vehicle group was significantly higher than in the sham group (12.96±3.14 µg/g tissue, vs. 3.20±2.12 µg/g tissue in the sham surgical group; p<0.01). The treatment with FTY720 reduced the extravasation of EB by almost 50[percnt] (6.96±2.83 µg/g tissue). Immunohistochemistry staining demonstrated that ZO-1 and occludin, along with cerebral microvessels (EBA), held a strong perivascular expression pattern in the sham-control group. At 48h post SAH, the expression of these markers was reduced in the SAH-vehicle group but largely preserved in the SAH rats treated with FTY720. Also, the brain water content was significantly increased after SAH (SAH: 82.50±0.94[percnt], vs. sham: 79.38±0.37[percnt]; p<0.01), but this was normalized by the treatment with FTY720 (79.63±0.72 [percnt]). Conclusions: These results suggest that the neuroprotective role of FTY720 extends to the preservation of BBB integrity and attenuation of cerebral edema following SAH.

Anaemia Negatively Affects Recovery From Traumatic Brain Injuries

The same study should occur in stroke survivors but won't because we have NO stroke leadership or strategy to answer these simple questions. You're screwed and obviously no one cares enough to even attempt to solve all the problems in stroke.  It is pretty much; 'Fuck off and die'.
http://dgnews.docguide.com/anaemia-negatively-affects-recovery-traumatic-brain-injuries?
 Anaemia can negatively influence the outcomes of patients with traumatic brain injuries, according to a study presented at the recent 84th Annual Meeting of the American Association of Neurological Surgeons (AANS) and published in the journal World Neurosurgery.
“More research is needed to develop treatment protocols for anaemic patients with traumatic brain injuries,” said lead author N. Scott Litofsky, MD, Division of Neurological Surgery, University of Missouri School of Medicine, Columbia, Missouri. “Anaemia occurs when there is a shortage of red blood cells, which causes reduced oxygen flow to vital organs throughout the body. There has been a lack of consensus among physicians regarding the relationship of anaemia and traumatic brain injuries on a patient’s health. Because of this uncertainty, treatment protocols are unclear and inconsistent.”
“Our observational study found that a patient's outcome is worse when he or she is anaemic,” he said.
For the study, the researchers studied the outcomes of 939 patients with traumatic brain injuries with anaemia who were admitted to the Frank L. Mitchell Jr., MD Trauma Center -- a Level I trauma centre that is part of University of Missouri Health Care system. The researchers compared haemoglobin levels of these patients and their outcomes within 1 year of surgery.
Despite also having more severe head and systemic injuries, patients with lower levels of haemoglobin had poorer outcomes. For each increase in haemoglobin of 1 gram above 7 grams per decilitre of blood, the likelihood of a good outcome increased by 33%.
To restore a patient’s haemoglobin level, a patient can receive a blood transfusion, but stored blood may not perform as well as a patient's own blood, and patients may experience allergic reactions or viral infections as a result of the transfusion.
“The purpose of this study is not to propose transfusion guidelines, but rather to show that anaemia can be harmful to patients with traumatic brain injuries,” said Dr. Litofsky. “Now that we have shown that anaemia affects a patient’s recovery, further studies are needed to determine the best way to correct it. The ultimate goal of this research is to help patients recover more quickly from traumatic brain injuries.”
SOURCE: University of Missouri-Columbia

Traditional Chinese Medicines in the management of cardiovascular diseases: a comprehensive systematic review

Notice this says more research needed, do not start taking TCM because one anecdote from a friend suggests it works. With no idea of the active ingredients one ingredient could be useful, another could be dangerous.
http://www.ncbi.nlm.nih.gov/pubmed/27195823

Layne K¹, Ferro A¹.

Author information

Abstract

AIMS:

The aim was to perform a systematic review of the efficacy of Traditional Chinese Medicines (TCM) in cardiovascular disease.

METHODS:

Electronic databases were searched up to 11^th November 2015 for all randomised-controlled trials evaluating the effect of TCM in hypertension, ischaemic stroke, heart failure, coronary heart disease and type 2 diabetes mellitus. Pooled odds ratios (ORs) were calculated using a fixed-effects model.

RESULTS:

Four hypertension studies were eligible for statistical analysis and included 133 patients receiving TCM and 130 control patients. There were significant reductions in systolic blood pressure in patients receiving TCM, comparable to results achieved with pharmaceutical medicines. An OR of 3.781 (95% confidence interval 2.392, 5.977; p = 0.000) was observed for the anti-hypertensive effect of TCM. Significant heterogeneity was present (p = 0.011), with a tendency towards publication bias that did not reach significance (p = 0.05275). Outcome measures for other cardiovascular diseases were inconsistent.

CONCLUSIONS:

Certain TCM compounds appear to have significant anti-hypertensive effects, and although some are associated in some studies with improved outcomes in coronary heart disease, heart failure and type 2 diabetes mellitus the data are inconsistent and will require large-scale randomised-controlled trials to allow full evaluation of any potential therapeutic benefit in these areas.
This article is protected by copyright. All rights reserved.

PMID:

27195823

[PubMed - as supplied by publisher]

The Use of Doublecortin to Quantify the Effects of Pharmacological Treatment on Neurogenesis and Functional Recovery after Stroke

A thesis but your doctor needs to get this updated to the stroke strategy.  Only 71 pages. I know there is no strategy anyplace but if your stroke department head is not communicating with other heads to create one then you have an incompetent stroke department head. And stroke survivors are negatively affected by that incompetence. Without a change your children and grandchildren will be screwed.

The Use of Doublecortin to Quantify the Effects of Pharmacological Treatment on Neurogenesis and Functional Recovery after Stroke

Ischemic strokes account for 87% of all strokes and

can have debilitating effects on language, sensory, and motor skills. Currently, tPA is the only medication approved by the FDA for the treatment of ischemic stroke, but the window of time to administer the drug is very small. In this thesis, we investigate the use of a simvastatin and fluoxetine

drug combination (FS) as a possible alternative treatment for ischemic stroke victims. To analyze the effects of FS on neurogenesis and functional recovery, we utilize the Montoya Staircase and quantify the amount of neurogenesis using doublecortin. Although the results of this study show that the drug treatment did not produce the significant increase in neurogenesis when comparing the control with the drug-treated animals as we had hoped for, nor did it translate to an increase in functional recovery, there was significantly more neurogenesis in the right hemisphere in the anterior and middle region

of the subventricular zone (SVZ) of the FS rats than the left. This tells us that the drug treatment did produce a significant amount of neurogenesis in the SVZ, but further work needs to be done to better understand how the FS

drug treatment effects neurogenesis and functional recovery. There may be an optimal window of time and dosage that will lead to a greater significance in recovery and higher levels of neurogenesis. This could open the door for a better treatment option to increase the quality of life for ischemic stroke patients.