Cranberry flavonoids, atherosclerosis and cardiovascular health

So we have cranberry research from 2002, blueberries from 2013 and beets from 2010. Which food is in your dietary protocol? Or is your doctor, hospital and stroke association so fucking incompetent that they have done nothing about this for 13 years? And you are paying them money?

Cranberry flavonoids, atherosclerosis and cardiovascular health - 2002

High Anthocyanin Intake Is Associated With a Reduced Risk of Myocardial Infarction in Young and Middle-Aged Women - blueberries 2013

BEETS TO BEAT HEART DISEASE - 2010

Better detection of concussion in young football players

This should be transferable to detection of TBI and stroke if we had any strategy for stroke or stroke leadership at all. But we don't, so just fuck off and die is the message we are getting from our stroke associations.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=158773&CultureCode=en
Researcher Christian Duval, PhD, and his team have developed a new, simple and non-invasive approach to create a biomechanical and cognitive profile of football players and more quickly and accurately detect concussions in these individuals. Christian Duval and his post-doctoral student Hung Nguyen, PhD, work at the Research Centre of the Institut universitaire de gériatrie de Montréal, which is affiliated with the University of Montreal. They presented their preliminary research findings at the International Congress on Sport Sciences Research and Technology Support, which was held in Lisbon from November 15 to 17.
For their study, Christian Duval's team performed a dual-task assessment using simultaneous biomechanical and cognitive tests to evaluate the players every week. Thanks to a markerless motion capture system, this approach let them establish a unique profile for each person in just seven minutes and detect signs of concussion in a player before the medical team could. Developing such a fast and effective test is critical, as repeated impact on the young brain over time leaves damage similar to that caused by dementia.
“We had the players walk while avoiding obstacles and while executing cognitive tasks. The combination of these two results established each individual's personal signature. Our measurements let us quickly detect concussion symptoms that could go unnoticed by health care professionals or by the young athletes themselves. The test we developed also simulates game situations, because in football, players are stimulated both physically and intellectually,” explained Christian Duval.
In a sport in which many concussions go undetected, this approach could help health care professionals to not only better detect these brain injuries but also systematically monitor all players during the season to detect or monitor those who sustain a concussion to determine when they are ready to get back out on the field.

• Full bibliographic informationLongitudinal Study on the Detection and Evaluation of Onset Mild Traumatic Brain Injury During Dual Motor and Cognitive Tasks, 3rd International Congress on Sport Sciences Research and Technology Support, At Lisbon Portugal, Duval, Christian et al. Nov 19, 2015.

Researchers urge caution in prescribing commonly used drug to treat ADHD - Methylphenidate(Ritalin)

Research from 1998 suggests that this might be helpful in stroke rehab. Not that I think any doctor in the world is using it but for us stroke survivors this could have been important if we had a strategy that followed up promising research. But we have crap for stroke leadership.

Methylphenidate(Ritalin) and stroke rehab - 1998

 Researchers urge caution in prescribing commonly used drug to treat ADHD - Methylphenidate(Ritalin)

Authors of new Cochrane Review remain uncertain about effect of widely used medicine on ADHD symptoms, despite large amount of research. Some evidence of increased sleeplessness and loss of appetite leads researchers to encourage more caution in use of methylphenidate.

The Cochrane Library publishes one of the most comprehensive assessments to date on the benefits and harms of a widely prescribed drug used to treat Attention Deficit Hyperactivity Disorder (ADHD).

ADHD is one of the most commonly diagnosed childhood disorders and can continue through adolescence into adulthood. Symptoms include difficulty focusing attention and remaining “on task”, excessively impulsive behaviour, and extreme hyperactivity. It is estimated to affect about 5% of children, and diagnosis is based on clinical judgement rather than objective diagnostic markers.

Methylphenidate, more commonly known by its brand names - Ritalin®, Concerta®, Medikinet®, and Equasym®, amongst others - has been used to treat ADHD for more than 50 years. A team of Cochrane researchers has carefully evaluated and summarized the findings from all of the available randomized trials of this widely used drug.

This new Cochrane Review includes data from 185 randomized controlled trials involving more than 12,000 children or adolescents. The studies were conducted mainly in the US, Canada, and Europe, included males and females from ages 3-18, and all compared methylphenidate with either a dummy pill or no intervention.

When researchers combined data from identified trials, they found that methylphenidate led to modest improvements in ADHD symptoms, general behaviour, and quality of life. Analysis of adverse effects showed that children were more likely to experience sleep problems and loss of appetite while taking methylphenidate. However, the researchers’ confidence in all results was very low: it was apparent from assessing the included trials that it would have been possible for people involved in the trials to have been aware of which treatment the children were taking. In addition, the reporting of results was not complete in many of the trials, and for some analyses there was variation among trial results.

Based upon this information, the researchers urge clinicians to be cautious in prescribing methylphenidate, and to weigh up the benefits and risks more carefully.

The team of 18 researchers was led by Professor Ole Jakob Storebø, Clinical Psychologist from the Psychiatric Research Unit in Region Zealand, Denmark. He says, “This review highlights the need for long-term, large, better-quality randomized trials so that we can determine the average effect of this drug more reliably.”

Co-author Camilla Groth MD added, “This review shows very limited quality evidence for the effects of methylphenidate on children and adolescents with ADHD. Some might benefit, but we still don’t know which patients will do so. Clinicians prescribing methylphenidate must take account of the poor quality of the evidence, monitor treatment carefully, and weigh up the benefits and adverse effects."

Another co-author, Dr Morris Zwi, Consultant Child & Adolescent Psychiatrist added, “This evidence is important for health professionals and parents of children with ADHD. Our expectations of this treatment are probably greater than they should be, and whilst our review shows some evidence of benefit, we should bear in mind that this finding was based on very low-quality evidence. What we still need are large, well-conducted trials in order to clarify the risks versus the benefits for this widely used treatment.”

The researchers have also urged that clinicians and families should not rush to discontinue using methylphenidate. Dr Zwi added, “If a child or young person has experienced benefits without experiencing adverse effects, then there may be good clinical grounds to continue using it. Patients and their parents should discuss any decision to stop treatment with their health professional before doing so.”

An abridged version of the Cochrane Review will appear in the BMJ later this week.
http://doi.wiley.com/10.1002/14651858.CD009885.pub2

• Full bibliographic informationFull citation:"Methylphenidate for children and adolescents with attention deficit hyperactivity disorder (ADHD)." Storebø OJ, Ramstad E, Krogh HB, Nilausen TD, Skoog M, Holmskov M, Rosendal S, Groth C, Magnusson FL, Moreira-Maia CR, Gillies D, Buch Rasmussen K, Gauci D, Zwi M, Kirubakaran R, Forsbøl B, Simonsen E, Gluud C. CRG: Developmental, Psychosocial and Learning Problems Group. Cochrane Database of Systematic Reviews 2015, Intervention review. DOI: 10.1002/14651858.CD009885.pub2
  URL Upon publication: http://doi.wiley.com/10.1002/14651858.CD009885.pub2

‘Connector Hubs’ Help Brain Network Coordination

Does your doctor even know if these connector hubs were damaged in your stroke? What is the stroke protocol to recover from such damage? Recover not compensate. Does your doctor know ANYTHING AT ALL? Will your doctor be talking to these researchers to see what knowledge can be gained for stroke rehab? Or will your doctor DO NOTHING like usual? I know our stroke associations will do nothing with this, so we are once again screwed like we always are. So much that can be done if only there was a working brain somewhere in stroke leadership.
http://neurosciencenews.com/neural-network-connector-hubs-3159/
Swinging a bat at a 90-mph fastball requires keen visual, cognitive and motor skills. But how do diverse brain networks coordinate well enough to hit the ball?
A new UC Berkeley study suggests the human brain’s aptitude and versatility can be credited in large part to “connector hubs,” which filter and route information. They coordinate and integrate the flow of data so that brain networks dedicated to specific roles, such as vision and movement, can focus on their jobs.
“Our findings show that connector hubs allow for distinct networks to each do their own thing, yet still interact with each other effectively,“ said study lead author Maxwell Bertolero, a Ph.D. student in neuroscience at UC Berkeley.
Moreover, the brain’s two dozen or so connector hubs play a key role in complex cognitive tasks, and are vulnerable to brain damage and dysfunction. Thus, the findings could “help neuroscientists shed more light on the neural bases of disorders such as schizophrenia and Alzheimer’s, ” which are marked by malfunctions in the brain’s wiring, Bertolero said.
The findings are the result of a meta-analysis conducted in January by Bertolero and fellow researchers at UC Berkeley and the National University of Singapore of more than 9,000 brain imaging studies in the BrainMap database that cover more than 75 cognitive tasks.
The study, just published in the Proceedings of the National Academy of Sciences, found heightened neural activity in the brain’s connector hubs during complex tasks, such as puzzles and video games, while networks dedicated to specific functions did not need to put in extra work.
The more complex the task, in that more networks are required for the job, the greater the activity in the connector hubs, keeping the burden off individual networks, the study found.
Like an airline hub, the brain’s main connector hubs link to multiple brain networks like transfer stations. These hubs have been found in the brains of many mammals, including mice and macaque monkeys.
Previous studies have linked connector hubs to the coordination and integration of information between multiple brain networks, but this latest study measured exactly how much of the work was being done by the hubs vis–à–vis networks dedicated to specific tasks.
The experiments used functional magnetic resonance imaging to measure increased blood flow throughout the brain, a marker of increased neural activity, during a wide range of activities, including finger-tapping, whistling, chewing, drawing, writing, reading, watching a movie and playing video games and memory games.
Researchers mapped the brain’s connections as one would analyze a large-scale network such as the U.S electrical grid, global flight patterns or Linkedin professional connections, creating a model of the brain’s “connectome.“
Using “graph theory,” which is used in many scientific fields to study networks, they identified 14 distinct networks of tightly interconnected regions and roughly 25 connector hubs.
They then compared neural activity in the connector hubs to activity in each of the brain’s dedicated networks during all the tasks recorded in the BrainMap database.They found that activity increased only at connector hubs as more networks were required for a task, indicating that connector hubs, but not individual networks, must process more information during these more complex tasks.
Next, Bertolero said, he and his co-authors plan to look into why evolution built a brain with distinct networks and connector hubs, precisely how connector hubs integrate and coordinate, and what happens when they are damaged by a stroke, for example.

Cool picture at link.

Microsleep: How Your Brain Can Fall Asleep for Seconds Without You Noticing

I'm sure this occurs a lot in stroke survivors.  What is your doctor doing to combat this?
http://abcnews.go.com/Health/microsleep-brain-fall-asleep-seconds-noticing/story?id=35304495

If you're exhausted and in the need to zone out, you might actually be grabbing bits of down time called "microsleep."

The phenomenon can occur most readily when a person is sleep-deprived, when their brain is primed to switch into sleep mode at any second. While a person can appear awake and even have their eyes open, their brain may have slipped into sleep mode, maybe reaching the first or second level of sleep. 

Dr. Ilene Rosen, a sleep expert and associate professor of clinical medicine at the University of Pennsylvania, explained if a person appears "zoned out" they might actually be catching some Z's.

"They might have been thinking about nothing," Rosen explained. "Something brings them back to focus attention."

Dan Childs, managing editor of ABC News' Medical Unit, stayed up for 50 hours straight this week -- 40 hours of it on the "Good Morning America" livestream, which was part of a slate of events to commemorate the 40th anniversary of "GMA."

During that period, Dr. Steven Feinsilver at Mount Sinai Hospital in New York, found evidence that Childs' was slipping in an out of consciousness after just a few minutes of sitting quietly. That becomes evident when a person is hooked up to an EEG scan to look at their brainwaves.

Certain brain waves called theta waves showed how quickly a person could be "asleep," Feinsilver said.

Microsleep episodes usually last a few seconds and the person often isn't even aware that the microsleep occurred. It can be dangerous especially if a person is driving, a few seconds of microsleep and a person can miss a red light or not notice a curve in the road, according to the National Institutes of Health.

Effects of golden hour thrombolysis: a Prehospital Acute Neurological Treatment and Optimization of Medical Care in Stroke (PHANTOM-S) substudy

I couldn't really tell from this if the reason better outcomes were observed was because the intervention was delivered fast enough not to trigger the neuronal cascade of death.  If we don't know what that time cutoff is then we don't know what the goal should be. And all these problems could be eliminated if we followed up on research to have a fast, easy and objective diagnosis with no neurologist involvement.
Test out these 17 diagnosis possibilities to find out which one is the best?  Or maybe the Qualcomm Xprize for the tricorder? 

Effects of golden hour thrombolysis: a Prehospital Acute Neurological Treatment and Optimization of Medical Care in Stroke (PHANTOM-S) substudy

Ebinger M¹, Kunz A¹, Wendt M², Rozanski M¹, Winter B², Waldschmidt C², Weber J², Villringer K¹, Fiebach JB¹, Audebert HJ¹.

Author information

Abstract

IMPORTANCE:

The effectiveness of intravenous thrombolysis in acute ischemic stroke is time dependent. The effects are likely to be highest if the time from symptom onset to treatment is within 60 minutes, termed the golden hour.

OBJECTIVE:

To determine the achievable rate of golden hour thrombolysis in prehospital care and its effect on outcome. (Wrong objective; should be better recovery results)

DESIGN, SETTING, AND PARTICIPANTS:

The prospective controlled Prehospital Acute Neurological Treatment and Optimization of Medical Care in Stroke study was conducted in Berlin, Germany, within an established infrastructure for stroke care. Weeks were randomized according to the availability of a specialized ambulance (stroke emergency mobile unit (STEMO) from May 1, 2011, through January 31, 2013. We included 6182 consecutive adult patients for whom a stroke dispatch (44.1% male; mean [SD] age, 73.9 [15.0] years) or regular care (45.0% male; mean [SD] age, 74.2 [14.9] years) were included.

INTERVENTIONS:

The STEMO was deployed when the dispatchers suspected an acute stroke during emergency calls. If STEMO was not available (during control weeks, when the unit was already in operation, or during maintenance), patients received conventional care. The STEMO is equipped with a computed tomographic scanner plus a point-of-care laboratory and telemedicine connection. The unit is staffed with a neurologist trained in emergency medicine, a paramedic, and a technician. Thrombolysis was started in STEMO if a stroke was confirmed and no contraindication was found.

MAIN OUTCOMES AND MEASURES:

Rates of golden hour thrombolysis, 7- and 90-day mortality, secondary intracerebral hemorrhage, and discharge home.

RESULTS:

Thrombolysis rates in ischemic stroke were 200 of 614 patients (32.6%) when STEMO was deployed and 330 of 1497 patients (22.0%) when conventional care was administered (P < .001). Among all patients who received thrombolysis, the proportion of golden hour thrombolysis was 6-fold higher after STEMO deployment (62 of 200 patients [31.0%] vs 16 of 330 [4.9%]; P < .01). Compared with patients with a longer time from symptom onset to treatment, patients who received golden hour thrombolysis had no higher risks for 7- or 90-day mortality (adjusted odds ratios, 0.38 [95% CI, 0.09-1.70]; P = .21 and 0.69 [95% CI, 0.32-1.53]; P = .36) and were more likely to be discharged home (adjusted odds ratio, 1.93 [95% CI, 1.09-3.41]; P = .02).

CONCLUSIONS AND RELEVANCE:

The use of STEMO increases the percentage of patients receiving thrombolysis within the golden hour. Golden hour thrombolysis entails no risk to the patients' safety and is associated with better short-term outcomes. (Tell us what those better results were)

TRIAL REGISTRATION:

clinicaltrials.gov Identifier: NCT01382862.

Four key studies that link coffee to heart attacks and hypertension

This seems to follow the same course as alcohol consumption. Only those with the proper genetic marker benefit. But your doctor will unlikely ever do gene testing prior to telling you coffee is bad for you because it raises your blood pressure. I most assuredly will not get gene testing to see if I'm in the right category. 

Four key studies that link coffee to heart attacks and hypertension

Is drinking coffee good for you? Some research indicates that that simple question cannot be answered without knowing something about your DNA.
Maybe the clearest evidence that genetics determines caffeine metabolism arises from a study of twins, published in 2002, that indicates that the speed with which a person processes caffeine is largely heritable.
At the same time, other studies 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.
For those who process caffeine slowly, this line of research indicates, drinking coffee raises the risks of heart attacks and high blood pressure. For those who process it quickly, drinking coffee seems to be safe - it may even protect against a heart attack or high blood pressure.
While researchers caution that more work needs to be done, they suggest that giving the public a general guideline regarding coffee doesn’t make sense. People are too different.
Here are some of the highlights in this line of research.
For the key studies in favor of coffee, try this.
“The interindividual differences in the 3-demethylation of caffeine alias CYP1A2 is determined by both genetic and environmental factors.”
Pharmacogenetics, August 2002.
http://www.ncbi.nlm.nih.gov/pubmed/12172216
Finding: Forty-nine identical twins and 34 fraternal twins were given 200 milligrams of caffeine; six hours later, a urine sample was taken. Those sample were then analyzed to see how quickly each person had broken down, or metabolized, the caffeine. In identical twins, the rates of metabolism were about twice as correlated as they were in fraternal twins. The scientists concluded that genetics largely determines the rate at which a person processes caffeine.
“CYP1A2 phenotype and genotype in a population from the Carboniferous Region of Coahuila, Mexico.”
Toxicology Letters, April 2005
http://www.ncbi.nlm.nih.gov/pubmed/15763632
Finding: Scientists in Mexico gave 46 volunteers a cup of instant coffee containing 140 milligrams of caffeine. Eight hours later, urine samples were collected. Those subjects who had one variant of the CYP1A2 gene processed caffeine more than twice as quickly as those who had the other, researchers found. Other similar efforts in China and Germany found a link between the gene and caffeine metabolism, predominantly in smokers.
“Coffee, CYP1A2 Genotype, and Risk of Myocardial Infarction”
JAMA, March 2006
http://www.ncbi.nlm.nih.gov/pubmed/16522833
Finding: Researchers compared about 2,000 people in Costa Rica who had a heart attack with 2,000 others who had not, examining both how much coffee they drank, as well as their DNA. In those subjects with the genetic marker indicating slow caffeine metabolism, the chance of heart attack appeared to rise with each cup of coffee. By contrast, those subjects with the genetic marker for rapid caffeine metabolism had a lower chance of heart attack with each cup.
The authors concluded: “Intake of coffee was associated with an increased risk of nonfatal [heart attack] only among individuals with slow caffeine metabolism, suggesting that caffeine plays a role in this association.”
“CYP1A2 genotype modifies the association between coffee intake and the risk of hypertension”
Journal of Hypertension, August 2009.
http://www.ncbi.nlm.nih.gov/pubmed/19451835
Finding: Researchers looked at the genetics, blood pressure and coffee habits of 553 young Italian over more than eight years. As with heart attacks (see above), the effects of coffee diverged depending on a person’s genetics.
For those with the gene for slow caffeine metabolism, the risks of high blood pressure rose dramatically with coffee intake. For those with the gene for rapid caffeine metabolism, the risk of high blood pressure dropped with coffee intake.
The authors concluded: People with the slower caffeine metabolism “are at increased risk and should thus abstain from coffee.” On the other hand, people with the genetics for the rapid caffeine metabolism “can safely drink coffee.”

Modafinil May Alleviate Poststroke Fatigue

The primary results do not correspond to the title. Whomever wrote the title is lying.
Maybe you want modafinil for this use:

Systematic review shows ‘smart drug’ modafinil does enhance cognition

or this:

Effects of modafinil on non-verbal cognition, task enjoyment and creative thinking in healthy volunteers

 

Modafinil May Alleviate Poststroke Fatigue

A Randomized, Placebo-Controlled, Double-Blinded Trial

1. Mai Bang Poulsen, MD;
2. Bodil Damgaard, MD;
3. Bo Zerahn, MD;
4. Karsten Overgaard, MD;
5. Rune Skovgaard Rasmussen, MA, PhD

+ Author Affiliations

1. Departments of Neurology (M.B.P., K.O., R.S.R.), Radiology (B.D.), and Clinical Physiology (B.Z.), Herlev University Hospital, Herlev, Denmark; and Department of Radiology, Hilleroed University Hospital, Hilleroed, Denmark (B.D.).

1. Correspondence to Mai Bang Poulsen, MD, Department of Neurology, Herlev Hospital, Herlev Ringvej 75, 2730 Herlev, Denmark. E-mail maibang@gmail.com

Abstract

Background and Purpose—Poststroke fatigue is common and reduces quality of life. Current evidence for intervention is limited, and this is the first placebo-controlled trial to investigate treatment of poststroke fatigue with the wakefulness promoting drug modafinil.

Methods—The trial was randomized, double-blinded, and placebo-controlled. Patients were treated with 400-mg modafinil or placebo for 90 days. Assessments were done at inclusion, 30, 90, and 180 days. The primary end point was fatigue at 90 days measured by the Multidimensional Fatigue Inventory-20 general fatigue domain. Secondary end points included the Fatigue Severity Scale, the Montreal Cognitive Assessment, the modified Rankin Scale and the Stroke-specific quality of Life questionnaire. Adult patients with a recent stroke achieving a score of ≥12 on the Multidimensional Fatigue Inventory-20 general fatigue domain were consecutively included. Exclusion criteria were severe cognitive disabilities and contraindications for modafinil treatment.

Results—One thousand one hundred twenty-one patients with stroke were screened and 41 patients included, 21 received modafinil. The primary end point, the Multidimensional Fatigue Inventory-20 general fatigue score, did not differ between groups. Patients in the modafinil group obtained better scores on the Fatigue Severity Scale (P=0.02) and in some subscales of the stroke-specific quality of life questionnaire (0.001<P<0.05), which were secondary outcomes. No serious adverse reactions were observed and there was no difference in blood pressure between groups.

Conclusions—There were no significant differences between the 2 groups with regard to the primary end point. There were secondary significant outcomes that should be explored in future trials.

Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT01800097.

Does stroke location predict walk speed response to gait rehabilitation?

Well shit, Is water wet?
http://onlinelibrary.wiley.com/doi/10.1002/hbm.23059/abstract

1. P. Simon Jones¹,
2. Valerie M. Pomeroy²,
3. Jasmine Wang³,
4. Gottfried Schlaug³,
5. S. Tulasi Marrapu¹,
6. Sharon Geva¹,
7. Philip J. Rowe⁴,
8. Elizabeth Chandler²,
9. Andrew Kerr⁴,
10. Jean-Claude Baron^1,5,* and
11. for the SWIFT-Cast investigators

Article first published online: 19 NOV 2015

DOI: 10.1002/hbm.23059

© 2015 The Authors Human Brain Mapping Published by Wiley Periodicals, Inc.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Human Brain Mapping

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Additional Information(Show All)

How to CiteAuthor InformationPublication HistoryFunding Information

1. Conflicts of Interest: None.

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Keywords:

• MRI;
• voxel-based lesion–symptom mapping;
• cortico-spinal tract;
• ambulation;
• recovery

Abstract

Objectives

Recovery of independent ambulation after stroke is a major goal. However, which rehabilitation regimen best benefits each individual is unknown and decisions are currently made on a subjective basis.(Everything in stroke should be objective) Predictors of response to specific therapies would guide the type of therapy most appropriate for each patient. Although lesion topography is a strong predictor of upper limb response, walking involves more distributed functions. Earlier studies that assessed the cortico-spinal tract (CST) were negative, suggesting other structures may be important.

Experimental Design: The relationship between lesion topography and response of walking speed to standard rehabilitation was assessed in 50 adult-onset patients using both volumetric measurement of CST lesion load and voxel-based lesion–symptom mapping (VLSM) to assess non-CST structures. Two functional mobility scales, the functional ambulation category (FAC) and the modified rivermead mobility index (MRMI) were also administered. Performance measures were obtained both at entry into the study (3–42 days post-stroke) and at the end of a 6-week course of therapy. Baseline score, age, time since stroke onset and white matter hyperintensities score were included as nuisance covariates in regression models.

Principal Observations: CST damage independently predicted response to therapy for FAC and MRMI, but not for walk speed. However, using VLSM the latter was predicted by damage to the putamen, insula, external capsule and neighbouring white matter.

Conclusions

Walk speed response to rehabilitation was affected by damage involving the putamen and neighbouring structures but not the CST, while the latter had modest but significant impact on everyday functions of general mobility and gait. Hum Brain Mapp, 2015.

Problem-Solving Therapy During Outpatient Stroke Rehabilitation Improves Coping and Health-Related Quality of Life

So rather than finding recovery solutions for survivors we have persons researching coping skills. You wouldn't need so many fucking coping skills if you solved the goddamned problems in stroke. God I hate stupid people. 

Problem-Solving Therapy During Outpatient Stroke Rehabilitation Improves Coping and Health-Related Quality of Life

Randomized Controlled Trial

1. Marieke M. Visser, MSc,
2. Majanka H. Heijenbrok-Kal, PhD,
3. Adriaan van‘t Spijker, PhD,
4. Engelien Lannoo, PhD,
5. Jan J.V. Busschbach, PhD and
6. Gerard M. Ribbers, MD, PhD

+ Author Affiliations

1. From the Department of Rehabilitation Medicine (M.M.V., M.H.H.-K., G.M.R.) and Department of Psychiatry, Section Medical Psychology and Psychotherapy (A.v.S., J.J.V.B.), Erasmus University Medical Center, Rotterdam, The Netherlands; Rotterdam Neurorehabilitation Research Department (RoNeRes), Rijndam Rehabilitation Center, Rotterdam, The Netherlands (M.M.V., M.H.H.-K., G.M.R.); and Department of Physical and Rehabilitation Medicine, Ghent University Hospital, Ghent, Belgium (E.L.).

1. Correspondence to Majanka H. Heijenbrok-Kal, PhD, Rotterdam Neurorehabilitation Research (RoNeRes), Rijndam Rehabilitation Center, PO Box 23181, 3001 KD, Rotterdam, The Netherlands. E-mail mheijenbrok@rijndam.nl

Abstract

Background and Purpose—This study investigated whether problem-solving therapy (PST) is an effective group intervention for improving coping strategy and health-related quality of life (HRQoL) in patients with stroke .

Methods—In this multicenter randomized controlled trial, the intervention group received PST as add-on to standard outpatient rehabilitation, the control group received outpatient rehabilitation only. Measurements were performed at baseline, directly after the intervention, and 6 and 12 months later. Data were analyzed using linear-mixed models. Primary outcomes were task-oriented coping as measured by the Coping Inventory for Stressful Situations and psychosocial HRQoL as measured by the Stroke-Specific Quality of Life Scale. Secondary outcomes were the EuroQol EQ-5D-5L utility score, emotion-oriented and avoidant coping as measured by the Coping Inventory for Stressful Situations, problem-solving skills as measured by the Social Problem Solving Inventory-Revised, and depression as measured by the Center for Epidemiological Studies Depression Scale.

Results—Included were 166 patients with stroke, mean age 53.06 years (SD, 10.19), 53% men, median time poststroke 7.29 months (interquartile range, 4.90–10.61 months). Six months post intervention, the PST group showed significant improvement when compared with the control group in task-oriented coping (P=0.008), but not stroke-specific psychosocial HRQoL. Furthermore, avoidant coping (P=0.039) and the utility value for general HRQoL (P=0.034) improved more in the PST group than in the control after 6 months.

Conclusions—PST seems to improve task-oriented coping but not disease-specific psychosocial HRQoL after stroke >6-month follow-up. Furthermore, we found indications that PST may improve generic HRQoL recovery and avoidant coping.

Clinical Trial Registration—URL: http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=2509. Unique identifier: CNTR2509.

Mechanisms and Functional Significance of Stroke-induced Neurogenesis

If I had a 'good' stroke doctor I would expect that person to have read this and updated stroke protocols within a week. Then contacting every single stroke patient of theirs to inform them of the good news. But I bet there isn't one single 'good' stroke doctor in the world. Not even great, just 'good'.  Doing that is the minimum I would expect from my doctor,. anything else should be a fireable offense. 

Mechanisms and Functional Significance of Stroke-induced Neurogenesis 

Quentin Marlier¹, Sébastien Verteneuil¹, Renaud Vandenbosch¹ and Brigitte Malgrange^1*

• ¹GIGA-Neurosciences, University of liège, Belgium

Stroke affects one in every six people worldwide, and is the leading cause of adult disability. After stroke, some limited spontaneous recovery occurs, the mechanisms of which remain largely unknown. Multiple, parallel approaches are being investigated to develop neuroprotective, reparative and regenerative strategies for the treatment of stroke. For years, clinical studies have tried to use exogenous cell therapy as a means of brain repair, with varying success. Since the rediscovery of adult neurogenesis and the identification of adult neural stem cells in the late nineties, one promising field of investigation is focused upon triggering and stimulating this self-repair system to replace the neurons lost following brain injury. For instance, it is has been demonstrated that the adult brain has the capacity to produce large numbers of new neurons in response to stroke. The purpose of this review is to provide an updated overview of stroke-induced adult neurogenesis, from a cellular and molecular perspective, to its impact on brain repair and functional recovery.

Feeling grateful for you today - National Stroke Association email

I'm not grateful for the NSA. Reasoning below in red. And Matt Lopez is even a stroke survivor and should know better.
http://support.stroke.org/site/R?i=-dRLK_3QIKAU0JYeLg_AWA

Dear dean,

As 2015 comes to a close, I am excited about the lives that have been saved and impacted by the work of National Stroke Association. This year, we launched Stroke Recover Navigator—a game-changer for anyone who has experienced the life-altering effects of a stroke. This impactful program helps stroke survivors in those confusing and frightening first few months when they have left the hospital and are trying to make sense of their new life. Then, this summer, Come Back Strong was unveiled. With the launch of the Come Back Strong movement, our goal is to provide stroke survivors with hope after stroke so they can begin their journey to recovery and Come Back Strong. Have you gotten involved with the Come Back Strong movement yet? This Come Back Strong initiative wouldn't be  necessary if you would create protocols that get survivors back to 100% recovery. More important if you solved and prevented the neuronal cascade of death. You aren't even solving the problems out there. You're trying to ameliorate the aftereffects. Damn it all, use some of your fucking neurons and understand cause and effect.

This year, I am so grateful for your support.

I am giving thanks this year to you. We have a passion for increasing awareness of life-saving stroke information, improving quality of life for stroke survivors and caregivers, and impacting survivor empowerment. Because of you, this important work will continue.

The next year is going to be exciting. We look forward to sharing with you more new resources and programs that continue to reduce the incidence of stroke and improve your quality of life. You have told us what your greatest needs are(Really, I haven't been contacted) and we look forward to continuing to meet those needs.

Thank you for trusting us to be the voice of the stroke community. I don't trust you because you have no outreach to survivors. Look at what a great stroke association would be doing for outreach.

With thanks,

Matt Lopez
CEO, Stroke Survivor
National Stroke Association

If you haven't done the reading, why expect to be treated as a stroke professional?

This is what I happen to think is our stroke professions major failing. They haven't kept up with the research. Without this there can never be a strategy. There are probably thousands of research possibilities that I have written about and I'm sure I've missed thousands more. Everyone seems to be sitting on their university knowledge and hoping that will get them through their career. CMEs are not the answer because they only are for the major topics. True stroke professionals would be all over me and pointing out exactly where I'm wrong. Yet no professional seems to have ever commented on my blog.
Seth Godin again;
http://sethgodin.typepad.com/seths_blog/2015/11/did-you-do-the-reading.html

Did you do the reading?

It's absurd to think of going to a book group meeting and opining about a book you didn't even read.
More rude: Going to a PhD seminar and participating in the discussion without reading the book first.
And of course, no one wants a surgeon operating on them if she hasn't read the latest journal article on this particular procedure.
It makes no sense to me to vote for a candidate who doesn't care enough to have read (and understood) the history of those that came before.
A first hurdle: Are you aware of what the reading (your reading) must include? What's on the list? The more professional your field, the more likely it is that people know what's on the list.
The reading isn't merely a book, of course. The reading is what we call it when you do the difficult work of learning to think with the best, to stay caught up, to understand.
The reading exposes you to the state of the art. The reading helps you follow a thought-through line of reasoning and agree, or even better, challenge it. The reading takes effort.
If you haven't done the reading, why expect to be treated as a professional?

Objective real-time motion analysis using wearable devices for post stroke rehabilitation

It takes a graduate student to think up these innovative ideas.

Objective real-time motion analysis using wearable devices for post stroke rehabilitation

Brandon J. Allen, University of Tennessee at ChattanoogaFollow

Committee Chair

Sartipi, Mina

Committee Member

Yang, Li; Liang, Yu; Ward, Mike

College

College of Engineering and Computer Science

Publisher

University of Tennessee at Chattanooga

Place of Publication

Chattanooga (Tenn.)

Abstract

With the growing population of the elderly, there is an increasing need for reliable, inexpensive, and quantifiable clinical measures. This thesis proposes mStroke, a practical, accurate, and mobile health system that remotely measures a stroke patient's proficiency in standard post-stroke therapy activities. The proposed system is delivered as an application (App) running on a hardware system consisting of two bluetooth low energy (BLE) modular sensor devices and an iPad. The system uses accelerometers, gyroscopes, and magnetometers to measure movement during three single-tasked clinical activities: the functional reach test, the NIHSS motor arm test, and the NIHSS motor leg test. The proposed system has been extensively tested using emulated and real data from physical therapy students. Key Words: Motion Analysis, Stroke, Functional Reach, NIHSS.

Degree

M. S.; A thesis submitted to the faculty of the University of Tennessee at Chattanooga in partial fulfillment of the requirements of the degree of Master of Science.

Date

12-2015

Subject

Motor ability -- Testing; Cerebrovascular disease -- Patients -- Rehabilitation; Human-computer interaction

Keyword

Motion Analysis; Stroke; Functional Reach; NIHSS

Discipline

Computer Sciences

Document Type

Masters theses

Extent

x, 46 leaves

Language

English

Rights

Under copyright.

License

http://creativecommons.org/licenses/by-nc-nd/3.0/

Recommended Citation

Allen, Brandon J., "Objective real-time motion analysis using wearable devices for post stroke rehabilitation" (2015). Masters Theses and Doctoral Dissertations.
http://scholar.utc.edu/theses/437

Intraventricular Infusion of a Low Fraction of Serum Enhances Neurogenesis and Improves Recovery in a Rodent Stroke Model

Is this interesting enough to be proposed for human clinical trials? I want to know whom in the world can answer that question and then follow thru with the research to prove it one way or another. But that won't occur because we have no stroke strategy or stroke leaders at all. 

Intraventricular Infusion of a Low Fraction of Serum Enhances Neurogenesis and Improves Recovery in a Rodent Stroke Model

• Yi-Chen Li^a,
• Li-Kai Tsai^{b, ,} ,
• Tai-Horng Young^{a, ,}

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doi:10.1016/j.neulet.2015.11.020

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Highlights

•

A serum fraction (100K) was easily derived from serum.

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100K/bFGF enhanced cell proliferation at SVZ area and infarcted brain.

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100K/bFGF increased the number of MAP-2 cells at infarcted brain in MCAO rat.

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100K/bFGF improved animals' motor coordination of MCAO rat.

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Abstract

Enhancing endogenous neurogenesis is a potential therapeutic strategy in stroke treatment. We have previously domonstrated that treatment with a fraction of serum with molecular weight of less than 100kDa (100K) combined with bFGF promoted neurogenesis of cultured stem and progenitor cells (NSPCs). In this study, we further evaluated the efficacy of intraventricular administration of 100K with bFGF (100K/bFGF) in a rat model of transient middle cerebral artery occlusion (MCAO). Rats administered 100K/bFGF on post-stroke day 1 exhibited a higher number of Ki67 and Nestin immunoreactive cells at the subventricular zone (SVZ) area and in the infarcted brain, indicating promotion of NSPCs proliferation. The 100K/bFGF treatment also predominantly increased the number of MAP-2 immunoreactive cells rather than GFAP immunoreactive cells at the SVZ area and in the infarcted regions, implying that 100K/bFGF dominated NSPCs differentiating into neurons rather than astrocytes. Importantly, treatment with 100K/bFGF significantly improved the animals' motor coordination. These findings demonstrated that treatment with a low serum fraction and bFGF benefited ischemic stroke likely through promotion of the proliferation and neuronal differentiation of endogenous NSPCs.

Systemic Proteasome Inhibition Induces Sustained Post-stroke Neurological Recovery and Neuroprotection via Mechanisms Involving Reversal of Peripheral Immunosuppression and Preservation of Blood–Brain–Barrier Integrity

This sounds like something that needs further research into translating into a hyperacute stroke protocol. But it won't occur because we have no strategy and no person in charge of executing that strategy. So we will be screwed for another 50 years at least. 

Systemic Proteasome Inhibition Induces Sustained Post-stroke Neurological Recovery and Neuroprotection via Mechanisms Involving Reversal of Peripheral Immunosuppression and Preservation of Blood–Brain–Barrier Integrity

• Thorsten R. Doeppner 
• , Britta Kaltwasser
• , Ulrike Kuckelkorn
• , Petra Henkelein
• , Eva Bretschneider
• , Ertugrul Kilic
• , Dirk M. Hermann

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Abstract

In view of its profound effect on cell survival and function, the modulation of the ubiquitin-proteasome-system has recently been shown to promote neurological recovery and brain remodeling after focal cerebral ischemia. Hitherto, local intracerebral delivery strategies were used, which can hardly be translated to human patients. We herein analyzed effects of systemic intraperitoneal delivery of the proteasome inhibitor BSc2118 on neurological recovery, brain injury, peripheral and cerebral immune responses, neurovascular integrity, as well as cerebral neurogenesis and angiogenesis in a mouse model of transient intraluminal middle cerebral artery occlusion. Systemic delivery of BSc2118 induced acute neuroprotection reflected by reduced infarct volume when delivered up to 9 h post-stroke. The latter was associated with reduced brain edema and stabilization of blood–brain–barrier integrity, albeit cerebral proteasome activity was only mildly reduced. Neuronal survival persisted in the post-acute stroke phase up to 28 days post-stroke and was associated with improved neurological recovery when the proteasome inhibitor was continuously delivered over 7 days. Systemic proteasome inhibition prevented stroke-induced acute leukocytosis in peripheral blood and reversed the subsequent immunosuppression, namely, the reduction of blood lymphocyte and granulocyte counts. On the contrary, post-ischemic brain inflammation, cerebral HIF-1α abundance, cell proliferation, neurogenesis, and angiogenesis were not influenced by the proteasome inhibitor. The modulation of peripheral immune responses might thus represent an attractive target for the clinical translation of proteasome inhibitors.

A reason persuasion is surprisingly difficult - stroke leaders?

Knowing how to do this in stroke is imperative. We have to somehow convince everyone in stroke leadership positions that they have no clue in how to solve anything in stroke.
Another great Seth Godin blog post.
http://sethgodin.typepad.com/seths_blog/2015/11/a-reason-persuasion-is-surprisingly-difficult.html
Each of us understands that different people are swayed by different sorts of arguments, based on different ways of viewing the world. That seems sort of obvious. A toddler might want an orange juice because it's sweet, not because she's trying to avoid scurvy, which might be the argument that moves an intellectual but vitamin-starved sailor to take action.
So far, so good.
The difficult part is this: Even when people making an argument know this, they don't like making an argument that appeals to the other person's alternative worldview.
This is key. What is the worldview of stroke leaders that they don't see all the problems in stroke and just focus on press releases, prevention tidbits and F.A.S.T.?
Worth a full stop here. Even when people have an argument about a political action they want someone else to adopt, or a product they want them to buy, they hesitate to make that argument with empathy. Instead, they default to talking about why they believe it.

Impact of High-Fat Diet on Red Blood Cells May Cause Cardiovascular Disease

Which way is your doctor and hospital leaning for fat in diets? Do they have any dietary protocol at all?
Maybe you want to read this article which suggests that sugar is the problem;

The evidence for saturated fat and for sugar related to coronary heart disease

Impact of High-Fat Diet on Red Blood Cells May Cause Cardiovascular Disease 

University of Cincinnati researchers have discovered the negative impact a high fat diet has on red blood cells and how these cells, in turn, promote the development of cardiovascular disease. 

This is one of the first studies to demonstrate the effect of red blood cells on the disease and could also affect the way patients with other health conditions, like cancer, who are prone to developing cardiovascular issues, are diagnosed and treated. It will be published in the Nov. 17 edition of the journal Circulation with an accompanying editorial. 

"Obesity caused by chronic consumption of a high-calorie, high-fat diet is a worldwide epidemic, representing one of the greatest threats to global health,” says principal investigator Vladimir Bogdanov, PhD, associate professor and director of the Hemostasis Research Program within the Division of Hematology Oncology at the UC College of Medicine and member of the Cincinnati Cancer Center and UC Cancer Institute. "White blood cells play a key role in fueling adipose tissue (fat) inflammation and insulin resistance in obesity and also promote the clogging of arteries, or atherosclerosis, setting the stage for heart attack and stroke. While these outcomes linked with a high fat diet and fat in the blood on white blood cells have been shown in animal models and humans, the impact of high fat diets on other bone marrow-derived cells, like red blood cells, is not well defined.

"Evidence is emerging that red blood cells play an important regulatory role in the development of atherosclerosis, binding pro-inflammatory proteins that cause dysfunction in the inner lining of the blood vessel wall—the endothelium. We explored how a high fat-diet causes red blood cell dysfunction in this study.”

Bogdanov and his team fed a 60 percent high-fat diet to a group of animal models for 12 weeks and saw an increased amount of key proteins that stimulate white blood cells bound to red blood cells. These white blood cells, also known as macrophages, are a type of white blood cell that "eats” cellular debris, foreign substances, microbes, cancer cells and anything else that does not have the types of proteins specific to the surface of healthy body cells on its surface. They also play a crucial role in atherosclerosis.

"In red blood cells from animal models fed a high-fat diet, there was an increase in cholesterol found in the cell membrane and phosphatidylserine levels, promoting inflammatory reactions. Phosphatidylserine is a phospholipid membrane component which plays a key role in the cycle of cells,” Bogdanov says. "When red blood cells from the animals being fed the high-fat diet were injected into a control group, eating a normal diet, there was a three-fold increase in their spleens’ uptake of red blood cells. The spleen is involved in the removal of blood cells, as well as systemic inflammation.

"All of these findings show that the dysfunction of red blood cells, corresponding with dysfunction of the lining of blood vessels, occurs very early in diet-induced obesity and may play a part in the formation of atherosclerosis. Diets high in saturated fat have long been associated with endothelial dysfunction, the precursor to atherosclerosis, but to our knowledge, the effects of high-fat diet on red blood cells have not been rigorously examined.”

He adds that in humans, high cholesterol is associated with alterations in red blood cells which are improved by treatment with statins, but the majority of obese humans do not have severe high cholesterol as was the case with the animal models in the study. 

Bogdanov stresses that this project would have never been successful were it not for a close collaboration between his lab and that of Professor Neal Weintraub, MD, from the Vascular Biology Center at the Medical College of Georgia, Georgia Regents University (GRU). Weintraub, who is a co-principal investigator and a former UC faculty member, is working on expanding the team’s findings in animal models to human disease. His team has recently conducted a study which demonstrated that a single high-fat meal produces harmful effects on red blood cells in humans. Bogdanov adds that these findings may also help patients with cancer who are frequently prone to thrombosis (blood clots).

"This study was funded using start-up funds I received from the university when I came here, which also helped me collaborate with other labs, like that of Dr. Weintraub’s, Dr. (Xiaoyang) Qi’s in my own division, throughout the medical campus and elsewhere in the country and abroad, to create an academically balanced study touching on aspects of both cardiovascular disease and cancer. These types of packages are vital for making progress on innovative research that may not otherwise be feasible.”

Scientists look to heart disease and strokes for clues to treating Alzheimer's

So what is the link between stroke and dementia/Alzheimers? Does your doctor know anything? Have a protocol to prevent your descent into dementia? Doing ANYTHING AT ALL?
Your 33% dementia chance post-stroke from an Australian study?
Then this study came out and seems to have a range from 17-66%.
A 20% chance in this research. 
http://medicalxpress.com/news/2015-01-scientists-heart-disease-clues-alzheimer.html

A growing body of research suggests that the most common cause of dementia in older people is a mix of vascular and Alzheimer's-related brain abnormalities, and that approximately half of people who die with Alzheimer's also have evidence of strokes in their brains. Furthermore, when strokes and hallmark Alzheimer's plaques and tangles are combined, it increases a person's likelihood of experiencing dementia. Stroke, or as it is known more generally as cerebrovascular disease, occurs with aging and is made worse by conditions like smoking, hypertension or diabetes.

Recommendations by a group of scientists to bolster research on how Alzheimer's and vascular conditions progress together and influence each other are available online today, in advance of publication, by Alzheimer's & Dementia: The Journal of the Alzheimer's Association. The authors hope this research agenda, if executed, will uncover new clues for effectively treating or preventing dementia.
"We are encouraged by the potential for new treatment strategies for dementia to arise from studying the crossover of vascular factors with the progression of Alzheimer's," says Heather M. Snyder, Ph.D., director of medical and scientific operations for the Alzheimer's Association, and first author of the new article. "In terms of next steps, we need to develop the research tools and collaborations necessary to further scientific investigation in this promising area of study."
Cerebrovascular disease can be prevented with a variety of drug and lifestyle interventions; however, this has not yet been established for dementia. Snyder says, "Whether improved control of vascular risk factors can be translated to decreased dementia risk is not known, but results from a number of studies suggest that it is possible, and this untapped potential definitely deserves greater research attention."
In December 2013, the Alzheimer's Association, with scientific input from the National Institutes of Health's National Institute of Neurological Disorders and Stroke (NINDS) and National Heart, Lung and Blood Institute (NHLBI), convened a group of scientific experts to discuss the scientific findings to date and gaps in research on vascular contributions in Alzheimer's and related forms of dementia. The newly-published article summarizes the meeting and discussions, including an outline of next steps.
"Blood vessels that deliver nutrients to the brain and carry away waste are vital for normal cognitive function," says co-author Roderick Corriveau, Ph.D., the NINDS program director who oversees dementia research. "Understanding vascular contributions to cognitive impairment and dementia, including changes due to stroke, heart disease and diabetes, are critically important to guide the development of preventions and treatments for dementia."
"Inadequate blood flow can damage and eventually kill cells anywhere in the body," says Donna M. Wilcock, Ph.D., a neurovascular researcher who is an assistant professor in the Department of Physiology at the University of Kentucky College of Medicine in Lexington and a co-author of the paper. "Since the brain has one of the body's richest networks of blood vessels, it is especially vulnerable. Considering this and demonstrated success in reducing risk for heart disease, stroke and other vascular-related diseases through healthy lifestyle modifications and use of medications, it only makes sense to increase our understanding of the role vascular factors play in Alzheimer's and dementia."
The authors of the article recommend filling gaps in several key areas of research, including:

• The relationship between diabetes and insulin resistance and risk of vascular disease, Alzheimer's and related dementia.
• Genetic factors that may influence vascular processes and other changes in the brain.
• Impact of immune system response on blood flow in the brain in the progression of Alzheimer's disease.
• The role of fat breakdown in the brain in the removal of amyloid build-up that leads to the hallmark brain plaques in Alzheimer's disease.
• Controlling the impact of vascular risk factors on memory and thinking abilities.

The authors also conclude that biological markers, which are used to detect and measure disease progression, of key vascular processes related to impairment of brain function, memory and thinking abilities are needed to move this research further and faster.
"Having the methods to detect early signs of vascular-related brain injury or disease with the greatest impact on Alzheimer's and dementia would greatly enhance our efforts to develop effective therapies," says David Knopman, M.D., professor of neurology at the Mayo Clinic College of Medicine in Rochester, MN, and a co-author of the paper. "Especially needed are tools that are highly accurate and do not require invasive procedures to collect and measure." Dr. Knopman is vice chair of the Alzheimer's Association Medical and Scientific Advisory Council.
Among the biological markers the authors say are necessary are:

• Ability to detect amyloid in blood vessels in the brain.
• Imaging technology that can detect changes from dying brain tissue.
• Indicators of risk for Alzheimer's in pre-diabetic individuals.
• Improved methods for measuring the impact of blood flow in the brain on memory and thinking abilities.

"Future investment for these areas of scientific discovery will be essential to galvanize the scientific community and provide forums of communication between the dementia and vascular fields," the authors state in the paper.
As a further next step, research sessions and scientific presentations focusing on the relationship between vascular factors, Alzheimer's disease and related dementias are being planned for upcoming major scientific and medical conferences—including meetings hosted or sponsored by the Alzheimer's Association, the American Heart Association, and the National Institutes of Health.