Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 438 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Wednesday, August 20, 2014

The Chairless Chair, an invisible chair that you can wear


Several prototypes have been constructed: the latest weighs about two kilograms and can operate for 24 hours on battery power.



I could easily see this as being quite useful for stroke survivors. Is your doctor going to suggest this for your ambulatory and fatigue needs?
http://www.cnn.com/2014/08/20/tech/innovation/the-chairless-chair/index.html?hpt=hp_c4




Although the focus is on production lines, the device has other potential daily life applications.

















Video here:
https://www.youtube.com/watch?feature=player_embedded&v=8KSUJ9Xtw9E

Dr. Edward Tobinick - of etanercept (Enbrel) fame suing a blogger

Dr. Tobinick could easily solve all these problems of his by writing up proof of his clinical research but he goes down the dubious route of suing critics. In my opinion a sign of desperation when truth and facts are not on your side.
I never would have gone down this route anyway, there never was anything other than anecdotes for this as a stroke treatment.

Case docket here:
http://dockets.justia.com/docket/florida/flsdce/9:2014cv80781/443251
Dr. Gorski writing about it here;
http://www.sciencebasedmedicine.org/another-lawsuit-to-suppress-legitimate-criticism-this-time-sbm/

Can instant noodles lead to heart disease, diabetes and stroke?

Young women are going to have to stop eating ramen and taking birth control. A little alarmist maybe? If they were to study the underlying reason that eating ramen causes this, that would be much more useful than this secondary prevention tactic. Come on, rub a couple of neurons together once in a while. Somebody out there in the stroke medical world has to have a working brain. We may be past the four humors theory but just barely.
Illustration from the book, Minerva Britanna. At the top of the page is the word phlegma, and an illustration of a man sitting next to the fire of a hearth, with a turtle near his feet.

Phlegmatic

  • Humor: Phlegm
  • Element: Water
  • Season: Autumn
  • Age: Maturity
  • Qualities: Cold & Moist
  • Organ: Brain
  • Planet: Moon

http://www.mdlinx.com/internal-medicine/newsl-article.cfm/5477508/ZZF307965849E94474BB34FC062CEC0F93/?
Recent Baylor research shows that significant consumption of the convenient food product – ramen included – may increase a person's risk for cardiometabolic syndrome, especially in women. The findings, recently published in The Journal of Nutrition, could shed new light on the risks of a worldwide dietary habit. Dr. Shin, who led the study on behalf of the Baylor Heart and Vascular Hospital (BHVH), found that eating instant noodles two or more times a week was associated with cardiometabolic syndrome, which raises a person's likelihood of developing heart disease and other conditions, such as diabetes and stroke. Dr. Shin also found that those results were more prevalent in women. He said that can likely be attributed to biological differences (such as sex hormones and metabolism) between the sexes, as well as obesity and metabolic syndrome components. In addition, men and women's varied eating habits and differences in the accuracy of food reporting may play a role in the gender gap. Another potential factor in the gender difference is a chemical called bisphenol A (BPA), which is used for packaging the noodles in Styrofoam containers. Studies have shown that BPA interferes with the way hormones send messages through the body, specifically estrogen. Regardless of the gender–related findings or their causes, Dr. Shin said, the study represents the importance of understanding the foods we feed our bodies.

Global sodium consumption and death from cardiovascular causes

You're going to have to 'trust' your doctor on this one. There is so much conflicting information out there. I've only written 10 posts on it if you want to educate yourself for your doctors meeting.
This seems to be putting one hell of a lot of credence into correlation.  And a second level correlation at that, salt causes high blood pressure, high blood pressure causes cardiovascular disease.
http://www.mdlinx.com/internal-medicine/newsl-article.cfm/5481933/ZZF307965849E94474BB34FC062CEC0F93/?
High sodium intake increases blood pressure, a risk factor for cardiovascular disease, but the effects of sodium intake on global cardiovascular mortality are uncertain. In this modeling study, 1.65 million deaths from cardiovascular causes that occurred in 2010 were attributed to sodium consumption above a reference level of 2.0 g per day.
Methods
  • Authors collected data from surveys on sodium intake as determined by urinary excretion and diet in persons from 66 countries (accounting for 74.1% of adults throughout the world), and they used these data to quantify the global consumption of sodium according to age, sex, and country.
  • The effects of sodium on blood pressure, according to age, race, and the presence or absence of hypertension, were calculated from data in a new meta–analysis of 107 randomized interventions, and the effects of blood pressure on cardiovascular mortality, according to age, were calculated from a meta–analysis of cohorts.
  • Cause–specific mortality was derived from the Global Burden of Disease Study 2010
  • Using comparative risk assessment, they estimated the cardiovascular effects of current sodium intake, as compared with a reference intake of 2.0 g of sodium per day, according to age, sex, and country.
Results
  • In 2010, the estimated mean level of global sodium consumption was 3.95 g per day, and regional mean levels ranged from 2.18 to 5.51 g per day.
  • Globally, 1.65 million annual deaths from cardiovascular causes (95% uncertainty interval [confidence interval], 1.10 million to 2.22 million) were attributed to sodium intake above the reference level; 61.9% of these deaths occurred in men and 38.1% occurred in women.
  • These deaths accounted for nearly 1 of every 10 deaths from cardiovascular causes (9.5%).
  • Four of every 5 deaths (84.3%) occurred in low– and middle–income countries, and 2 of every 5 deaths (40.4%) were premature (before 70 years of age).
  • The rate of death from cardiovascular causes associated with sodium intake above the reference level was highest in the country of Georgia and lowest in Kenya.

Randomized controlled trial on hemifield eye patching and optokinetic stimulation in acute spatial neglect

I'm sure your doctor will be telling you shortly that this trial failed. But ask anyway about the protocol used to see if you want to try it anyway.
http://www.mdlinx.com/internal-medicine/newsl-article.cfm/5436311/ZZF307965849E94474BB34FC062CEC0F93/?
In a randomized controlled trial, the authors compared the combined treatment of hemifield eye patching and repetitive optokinetic stimulation in acute stroke patients with neglect to the spontaneous course. An early intervention of combined hemifield eye patching and optokinetic stimulation in acute stroke patients with spatial neglect has no additive effect to the spontaneous remitting course of the disorder.

Chronic stress, depressive symptoms, anger, hostility, and risk of stroke and transient ischemic attack in the multi-ethnic study of atherosclerosis

They could have just said, 'We know nothing about stroke and don't care. It's not our problem'.
http://www.mdlinx.com/internal-medicine/newsl-article.cfm/5436283/ZZF307965849E94474BB34FC062CEC0F93/?
This study investigated chronic stress, depressive symptoms, anger, and hostility in relation to incident stroke and transient ischemic attacks in middle–aged and older adults. Higher levels of stress, hostility, and depressive symptoms are associated with significantly increased risk of incident stroke or transient ischemic attacks in middle–aged and older adults. Associations are not explained by known stroke risk factors.
(Then do some f*cking work and figure out what the risk factor is. God are people lazy. My guess is that these all cause inflammation and inflammation is a known risk factor.)
Methods
  • Data were from the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based cohort study of 6749 adults, aged 45 to 84 years and free of clinical cardiovascular disease at baseline, conducted at 6 US sites.
  • Chronic stress, depressive symptoms, trait anger, and hostility were assessed with standard questionnaires.
  • The primary outcome was clinically adjudicated incident stroke or transient ischemic attacks during a median follow-up of 8.5 years.
Results
  • One hundred ninety-five incident events (147 strokes; 48 transient ischemic attacks) occurred during follow-up.
  • A gradient of increasing risk was observed for depressive symptoms, chronic stress, and hostility (all P for trend ≤0.02) but not for trait anger (P>0.10).
  • Hazard ratios (HRs) and 95% confidence intervals indicated significantly elevated risk for the highest-scoring relative to the lowest-scoring group for depressive symptoms (HR, 1.86; 95% confidence interval, 1.16–2.96), chronic stress (HR, 1.59; 95% confidence interval, 1.11–2.27), and hostility (HR, 2.22; 95% confidence interval, 1.29–3.81) adjusting for age, demographics, and site.
  • HRs were attenuated but remained significant in risk factor–adjusted models.
  • Associations were similar in models limited to stroke and in secondary analyses using time-varying variables.

Tuesday, August 19, 2014

Regularly practicing hatha yoga may improve brain function for older adults

Amy, you could contact  the editor with your ideas on meditation.
How to contact the editor
Please send tips or questions toMichelle Brandt. - See more at: http://scopeblog.stanford.edu/about-scope/#sthash.9wh7436M.dpuf
 Please send tips or questions to Michelle Brandt - mbrandt@stanford.edu
She didn't followup my idea of the state of stroke research.
http://scopeblog.stanford.edu/2014/08/19/regularly-practicing-hatha-yoga-may-improve-brain-function-for-older-adults/

How to contact the editor
Please send tips or questions toMichelle Brandt. - See more at: http://scopeblog.stanford.edu/about-scope/#sthash.9wh7436M.dpuf

Targeted stimulation of specific brain cells boosts stroke recovery in mice

So who is going to take charge of getting this into human clinical trials? We know it is not going to be the ASA, NSA or WSO because obviously their boards of directors have no intention of ever solving any stroke problem.
Only a GREAT STROKE ASSOCIATION will ever tackle all the hardest problems in stroke.
http://scopeblog.stanford.edu/2014/08/19/targeted-stimulation-of-specific-brain-cells-boosts-stroke-recovery-in-mice/ 

Physical Fitness Makes Kids' Brains Bigger

Whom is going to follow these for the next 70 years to see if they survive stroke better and end up with less disability?
 This is pretty much what John J. Ratey, MD, author of Spark: The Revolutionary New Science of Exercise and the Brain, wrote about neurogenesis in 2008.

http://www.biosciencetechnology.com/news/2014/08/physical-fitness-makes-kids-brains-bigger?
A new study of 9- and 10-year-olds finds that those who are more aerobically fit have more fibrous and compact white-matter tracts in the brain than their peers who are less fit. “White matter” describes the bundles of axons that carry nerve signals from one brain region to another. More compact white matter is associated with faster and more efficient nerve activity. 
 
The team reports its findings in the open-access journal Frontiers in Human Neuroscience
 
“Previous studies suggest that children with higher levels of aerobic fitness show greater brain volumes in gray-matter brain regions important for memory and learning,” said University of Illinois postdoctoral researcher Laura Chaddock-Heyman, who conducted the study with kinesiology and community health professor Charles Hillman and psychology professor and Beckman Institute director Arthur Kramer. “Now for the first time we explored how aerobic fitness relates to white matter in children’s brains.”
 
I was quite physically fit as a kid, walking and biking all over the place.
More at link.

Central pattern generators and the control of rhythmic movements

If these exist why does spasticity override them?
http://www.sciencedirect.com/science/article/pii/S0960982201005814
Under an Elsevier user license
  Open Archive

Abstract

Central pattern generators are neuronal circuits that when activated can produce rhythmic motor patterns such as walking, breathing, flying, and swimming in the absence of sensory or descending inputs that carry specific timing information. General principles of the organization of these circuits and their control by higher brain centers have come from the study of smaller circuits found in invertebrates. Recent work on vertebrates highlights the importance of neuro-modulatory control pathways in enabling spinal cord and brain stem circuits to generate meaningful motor patterns. Because rhythmic motor patterns are easily quantified and studied, central pattern generators will provide important testing grounds for understanding the effects of numerous genetic mutations on behavior. Moreover, further understanding of the modulation of spinal cord circuitry used in rhythmic behaviors should facilitate the development of new treatments to enhance recovery after spinal cord damage.

Introduction

Biologists often take for granted the rapidity at which new information is acquired. It is humbling, therefore, to reread the papers of the first systems neuroscientists, and to discover among them the first articulation of many of the basic concepts that we still struggle to elucidate today. Almost ninety years ago, Brown [1] suggested that the alternate flexion and extension of leg muscles in walking could be produced by rhythmic central circuits in which the antagonistic muscles were driven by neurons that inhibited each other. Nonetheless, the spinal reflex has dominated a century of textbooks, and many biologists labor under the misconception that rhythmic movements are produced by reflex activation, rather than by central circuits. This review is not intended to supplant or replace the many outstanding and detailed reviews of the organization of the neural control of rhythmic movements in both invertebrates and vertebrates 2., 3., 4., 5. and 6.. Rather, here our purpose is to provide a roadmap to the general principles underlying pattern generation. We hope that this review will be helpful to those looking for neural circuits with easily quantifiable outputs with which to evaluate the role of genes in neuronal function.

Fictive motor patterns show that rhythmic movements can be generated in the absence of sensory input

How does one show the existence of central circuits capable of the production of rhythmic movements? For many years early neuroscientists debated whether rhythmic movements were produced by chains of reflexes or central oscillators (Fig. 1a). The first direct experiments designed to address this question were attempts to cut all sensory feedback to the central nervous system. This is obviously a difficult task, and some of the earliest successful experiments of this kind were carried out by Wilson and colleagues 7., 8. and 9., who showed that a deafferented locust could generate rhythmic flight motor patterns in response to non-rhythmic stimulation of the nerve cord.

Cool images at  the link.

Re-learning Gait After a Stroke

A pretty complete description of gait retraining. My only quibble is the focus on early intensive and repetitive practice. This may have solved my post of Jan. 2013

When should rehabilitation begin after stroke?

But only your doctor can tell for sure, so ask.
http://physical-therapy.advanceweb.com/Student-and-New-Grad-Center/Student-Top-Story/Re-learning-Gait-After-a-Stroke.aspx

Blood pressure medication does not cause more falls

This then refutes this study; Are Blood Pressure Drugs Worth the Falls?
Ask your doctor for an analysis for which one is correct. This latest specifically studied diabetes patients. So have your doctor check that out.  
http://www.alphagalileo.org/ViewItem.aspx?ItemId=144566&CultureCode=en
Study on patients with type 2 diabetes examined fracture risk with antihypertensive treatment

It's time to question the common belief that patients receiving intensive blood pressure treatment are prone to falling and breaking bones. A comprehensive study in people ages 40 to 79 with diabetes, led by Karen Margolis, MD, of HealthPartners Institute for Education and Research in the US, found no evidence supporting this belief. The study¹ appears in the Journal of General Internal Medicine², published by Springer.
Evidence from various clinical trials shows that cardiovascular events such as strokes can be prevented by treating high blood pressure (hypertension).. However, physicians and patients still often express concern that its tight control may increase a person's risk of low blood pressure (hypotension) and subsequent falls and fractures.
Scientific data to support this notion are sparse. Therefore, Margolis and her associates compared the number of falls and fractures of type 2 diabetes patients receiving two types of blood pressure treatment. The intensive group (which included 1,534 participants) received treatment aimed at a systolic blood pressure of <120 mm Hg, while the target for the standard group (1,565 participants) was <140 mm Hg.

Participants were all part of ACCORD-BONE, an ancillary study of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) randomized trial, which tested how more intensive treatment of blood sugar, blood pressure and lipids affected cardiovascular disease outcomes in people with diabetes. Participants in the ACCORD-BONE study were, on average, about 62 years old; none were 80 or older.
The results show that patients who received intensive blood pressure treatment did not fall more than less intensively treated patients, nor did they incur more fractures over an average follow-up of about five years.

"Lowering blood pressure using intensive treatment compared with standard treatment did not result in an increased rate of falls or fractures and, in fact, showed possible trends towards fewer fractures in the intensively treated patients," explains Margolis. "Although intensive blood pressure treatment to the low levels in ACCORD did not lower cardiovascular events, our results and review of the literature suggest a need to carefully reconsider current thinking about whether antihypertensive treatment and blood pressure lowering increases risk for falls and fractures."

Results in older versus younger patients were not different. No evidence suggested that the risk of patients' falling varied over time, although there were not enough fractures to determine if the short-term risk might be higher at the beginning of intensive treatment. It is important to note that subjects in this study were more closely monitored than most patients in clinical practice; therefore, the results may not completely reflect what would happen in actual practice.

Hospitalizations, deaths from heart disease, stroke drop in last decade

Has your hospital followed the same trend? No statistics to support or refute that should be a fireable offense for the head of the stroke department. No available statistics from the ASA, NSA or WSO would be a fireable offense there also.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=144485&CultureCode=en
U.S. hospitalizations and deaths from heart disease and stroke dropped significantly in the last decade, according to new research in the American Heart Association journal Circulation.
“Interestingly, these improvements happened in a period when there were no real ‘miracle’ clinical advancements,” said Harlan Krumholz, M.D., S.M., lead author of the “most comprehensive report card to-date” on America’s progress in heart disease and stroke prevention and treatment. “Rather, we saw consistent improvements in the use of evidence-based treatments and medications and an increase in quality improvement initiatives using registries and other data to track performance and support improvement efforts — as well as a strong emphasis on heart-healthy lifestyles and behaviors.”
Researchers collected data on nearly 34 million Medicare Fee-For-Service recipients in 1999-2011. They analyzed trends in rates of hospitalization, dying within a month of being admitted, being admitted again within a month and dying during the following year. They considered patient factors including age, sex, race, other illnesses and geography.
By the end of 2011, hospitalization rates among all races and areas dropped:
  • 38 percent for heart attack;
  • 83.8 percent for unstable angina, sudden chest pain often leading to heart attack;
  • 30.5 percent for heart failure; and
  • 33.6 percent for ischemic stroke.
Furthermore, risks of dying for people who went to the hospital within a year decreased about 21 percent for unstable angina, 23 percent for heart attacks and 13 percent for heart failure and stroke.
“Huge strides in lifestyle, quality of care and prevention strategies for cardiovascular health have seemed to have a ripple effect on saving lives,” said Krumholz, director of the Center of Outcomes Research and Evaluation at Yale-New Haven Hospital in New Haven, Conn. “As a result, our country has undergone remarkable changes, which has reduced suffering and costs.”
Other significant contributions included improvements in identifying and treating high blood pressure, a rapid rise in the use of statins, marked declines in smoking and more timely and appropriate treatment for heart attack patients, he said.
“There is still more work to do as heart disease and stroke combined remain the leading cause of death and disability, but this study documents astonishing progress and national achievement,” Krumholz said.
http://newsroom.heart.org/news/hospitalizations-deaths-from-heart-disease-stroke-drop-in-last-decade?preview=c87ab8f95b372f13119c4a2c860374ab

Endogenous neurogenesis following ischaemic brain injury: Insights for therapeutic strategies

Ask your doctor to create a translational research project with other doctors to figure out what the standard stroke protocol should be for this. They will not do this on their own. YOU have to initiate this and create the expectation that they will follow thru.
If we had a great stroke association it could be handed off to them and the project would get done. But we have press release stroke associations. I don't know how the boards of directors can live with themselves for such pathetic efforts.
http://www.sciencedirect.com/science/article/pii/S1357272514002544
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Abstract

Ischaemic stroke is among the most common yet most intractable types of central nervous system (CNS) injury in the adult human population. In the acute stages of disease, neurons in the ischaemic lesion rapidly die and other neuronal populations in the ischaemic penumbra are vulnerable to secondary injury. Multiple parallel approaches are being investigated to develop neuroprotective, reparative and regenerative strategies for the treatment of stroke. Accumulating evidence indicates that cerebral ischaemia initiates an endogenous regenerative response within the adult brain that potentiates adult neurogenesis from populations of neural stem and progenitor cells. A major research focus has been to understand the cellular and molecular mechanisms that underlie the potentiation of adult neurogenesis and to appreciate how interventions designed to modulate these processes could enhance neural regeneration in the post-ischaemic brain. In this review, we highlight recent advances over the last 5 years that help unravel the cellular and molecular mechanisms that potentiate endogenous neurogenesis following cerebral ischaemia and are dissecting the functional importance of this regenerative mechanism following brain injury.
This article is part of a Directed Issue entitled: Regenerative Medicine: the challenge of translation.

Keywords

  • Stroke;
  • Neural stem cells;
  • Cell proliferation;
  • Brain repair;
  • Cell signalling
This article is part of a Directed Issue entitled: Regenerative Medicine: the challenge of translation.

Corresponding author at: Florey Institute of Neuroscience and Mental Health, Kenneth Myer Building, 30 Royal Parade, Parkville, VIC 3010, Australia. Tel.: +61 3 90356535; fax: +61 3 86779826.

Corresponding author. Tel.: +61 3 99029622; fax: +61 3 99052766.
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Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials

This makes it sound like tPA is 32.9% effective as compared to 12% from an earlier report. Your doctor should be able to compare their hospital statistics to see if they are least match this better result.  If your hospital doesn't even know how well tPA works then the head stroke doctor should be fired.
http://www.mdlinx.com/internal-medicine/newsl-article.cfm/5461158/ZZF307965849E94474BB34FC062CEC0F93/?
Alteplase is effective for treatment of acute ischaemic stroke but debate continues about its use after longer times since stroke onset, in older patients, and among patients who have had the least or most severe strokes. Authors assessed the role of these factors in affecting good stroke outcome in patients given alteplase. Irrespective of age or stroke severity, and despite an increased risk of fatal intracranial haemorrhage during the first few days after treatment, alteplase significantly improves the overall odds of a good stroke outcome when delivered within 4•5 h of stroke onset, with earlier treatment associated with bigger proportional benefits.
Methods
  • Authors did a pre–specified meta–analysis of individual patient data from 6756 patients in nine randomised trials comparing alteplase with placebo or open control.
  • They included all completed randomised phase 3 trials of intravenous alteplase for treatment of acute ischaemic stroke for which data were available.
  • Retrospective checks confirmed that no eligible trials had been omitted.
  • They defined a good stroke outcome as no significant disability at 3—6 months, defined by a modified Rankin Score of 0 or 1. (mine was obviously a failure)
  • Additional outcomes included symptomatic intracranial haemorrhage (defined by type 2 parenchymal haemorrhage within 7 days and, separately, by the SITS–MOST definition of parenchymal type 2 haemorrhage within 36 h), fatal intracranial haemorrhage within 7 days, and 90–day mortality.
Results
  • Alteplase increased the odds of a good stroke outcome, with earlier treatment associated with bigger proportional benefit.
  • Treatment within 3•0 h resulted in a good outcome for 259 (32•9%) of 787 patients who received alteplase versus 176 (23•1%) of 762 who received control (OR 1•75, 95% CI 1•35—2•27); delay of greater than 3•0 h, up to 4•5 h, resulted in good outcome for 485 (35•3%) of 1375 versus 432 (30•1%) of 1437 (OR 1•26, 95% CI 1•05—1•51); and delay of more than 4•5 h resulted in good outcome for 401 (32•6%) of 1229 versus 357 (30•6%) of 1166 (OR 1•15, 95% CI 0•95—1•40).
  • Proportional treatment benefits were similar irrespective of age or stroke severity.
  • Alteplase significantly increased the odds of symptomatic intracranial haemorrhage (type 2 parenchymal haemorrhage definition 231 [6•8%] of 3391 vs 44 [1•3%] of 3365, OR 5•55, 95% CI 4•01—7•70, p<0•0001; SITS–MOST definition 124 [3•7%] vs 19 [0•6%], OR 6•67, 95% CI 4•11—10•84, p<0•0001) and of fatal intracranial haemorrhage within 7 days (91 [2•7%] vs 13 [0•4%]; OR 7•14, 95% CI 3•98—12•79, p<0•0001).
  • The relative increase in fatal intracranial haemorrhage from alteplase was similar irrespective of treatment delay, age, or stroke severity, but the absolute excess risk attributable to alteplase was bigger among patients who had more severe strokes.
  • There was no excess in other early causes of death and no significant effect on later causes of death.
  • Consequently, mortality at 90 days was 608 (17•9%) in the alteplase group versus 556 (16•5%) in the control group (hazard ratio 1•11, 95% CI 0•99—1•25, p=0•07).
  • Taken together, therefore, despite an average absolute increased risk of early death from intracranial haemorrhage of about 2%, by 3—6 months this risk was offset by an average absolute increase in disability–free survival of about 10% for patients treated within 3•0 h and about 5% for patients treated after 3•0 h, up to 4•5 h.

Association of poor subjective sleep quality with risk for death by suicide during a 10-year period: a longitudinal, population-based study of late life

Is your doctor doing anything about your sleep problems other than having nurses hand out sleeping pills every night while in the hospital?
http://www.mdlinx.com/internal-medicine/newsl-article.cfm/5481324/ZZF307965849E94474BB34FC062CEC0F93/?
Older adults have high rates of sleep disturbance, die by suicide at disproportionately higher rates compared with other age groups, and tend to visit their physician in the weeks preceding suicide death. To authors' knowledge, to date, no study has examined disturbed sleep as an independent risk factor for late–life suicide. To examine the relative independent risk for suicide associated with poor subjective sleep quality in a population–based study of older adults during a 10–year observation period. The results indicate that poor subjective sleep quality is associated with increased risk for death by suicide 10 years later, even after adjustment for depressive symptoms. Disturbed sleep appears to confer considerable risk, independent of depressed mood, for the most severe suicidal behaviors and may warrant inclusion in suicide risk assessment frameworks to enhance detection of risk and intervention opportunity in late life.
Methods
  • A longitudinal case–control cohort study of late–life suicide among a multisite, population–based community sample of older adults participating in the Established Populations for Epidemiologic Studies of the Elderly.
  • Of 14 456 community older adults sampled, 400 control subjects were matched (on age, sex, and study site) to 20 suicide decedents.
  • Primary measures included the Sleep Quality Index, the Center for Epidemiologic Studies–Depression Scale, and vital statistics.
Results
  • Hierarchical logistic regressions revealed that poor sleep quality at baseline was significantly associated with increased risk for suicide (odds ratio [OR], 1.39; 95% CI, 1.14–1.69; P < .001) by 10 follow–up years.
  • In addition, 2 sleep items were individually associated with elevated risk for suicide at 10–year follow–up: difficulty falling asleep (OR, 2.24; 95% CI, 1.27–3.93; P < .01) and nonrestorative sleep (OR, 2.17; 95% CI, 1.28–3.67; P < .01).
  • Controlling for depressive symptoms, baseline self–reported sleep quality was associated with increased risk for death by suicide (OR, 1.30; 95% CI, 1.04–1.63; P < .05)

Triglycerides and cardiovascular disease

Once again I would argue that these people don't know cause and effect. Cholesterol doesn't cause cardiovascular disease. It is used to create plaque because of inflammation of the artery lining. The cause is whatever starts that inflammation. Solve that and all this crap about statins and cholesterol probably goes away. They aren't even looking at the right problem. Does nobody rub two brain cells together ever?
http://www.mdlinx.com/internal-medicine/newsl-article.cfm/5485946/ZZF307965849E94474BB34FC062CEC0F93/?
After the introduction of statins, clinical emphasis first focussed on LDL cholesterol–lowering, then on the potential for raising HDL cholesterol, with less focus on lowering triglycerides.
  • However, the understanding from genetic studies and negative results from randomised trials that low HDL cholesterol might not cause cardiovascular disease as originally thought has now generated renewed interest in raised concentrations of triglycerides.
  • This renewed interest has also been driven by epidemiological and genetic evidence supporting raised triglycerides, remnant cholesterol, or triglyceride–rich lipoproteins as an additional cause of cardiovascular disease and all–cause mortality.
  • Triglycerides can be measured in the non–fasting or fasting states, with concentrations of 2—10 mmol/L conferring increased risk of cardiovascular disease, and concentrations greater than 10 mmol/L conferring increased risk of acute pancreatitis and possibly cardiovascular disease.
  • Although randomised trials showing cardiovascular benefit of triglyceride reduction are scarce, new triglyceride–lowering drugs are being developed, and large–scale trials have been initiated that will hopefully provide conclusive evidence as to whether lowering triglycerides reduces the risk of cardiovascular disease.
Cool video of the problem here;
Inflammation In Atherosclerotic Plaque Formation

Extravirgin olive oil consumption reduces risk of atrial fibrillation

I haven't been following A-fib much so this one is up to you.
http://www.mdlinx.com/internal-medicine/newsl-article.cfm/5372608/ZZF307965849E94474BB34FC062CEC0F93/?
The authors assessed the effect of these diets on the incidence of atrial fibrillation in the PREDIMED trial. In the absence of proven interventions for the primary prevention of atrial fibrillation, this post hoc analysis of the PREDIMED trial suggests that extravirgin olive oil in the context of a Mediterranean dietary pattern may reduce the risk of atrial fibrillation.
Methods
  • Participants were randomly assigned to 1 of 3 diets: Mediterranean diet supplemented with extravirgin olive oil, Mediterranean diet supplemented with mixed nuts, or advice to follow a low-fat diet (control group).
  • Incident atrial fibrillation was adjudicated during follow-up by an events committee blinded to dietary group allocation.
Results
  • Among 6705 participants without prevalent atrial fibrillation at randomization, they observed 72 new cases of atrial fibrillation in the Mediterranean diet with extravirgin olive oil group, 82 in the Mediterranean diet with mixed nuts group, and 92 in the control group after median follow-up of 4.7 years.
  • The Mediterranean diet with extravirgin olive oil significantly reduced the risk of atrial fibrillation (hazard ratio, 0.62; 95% confidence interval, 0.45–0.85 compared with the control group).
  • No effect was found for the Mediterranean diet with nuts (hazard ratio, 0.89; 95% confidence interval, 0.65–1.20).

Monday, August 18, 2014

Stem cells for neonatal stroke- the future is here

When is the future for the rest of us survivors?
ASA - Dr. Mariell Jessup,  Whom are you going to assign to this task?

NSA - Mr. Baranski, Whom are you going to assign to this task?

WSO - Dr. Stephen Davis, Whom are you going to assign to this task?
http://journal.frontiersin.org/Journal/10.3389/fncel.2014.00207/full?

Stem Cells

In recent years stem cell therapy has emerged as a potential treatment for neonatal ischemic brain injury. The efficacy of cell- based therapies in restoring damaged brain tissue has been tested in a multitude of models for different CNS diseases. Several different stem and progenitor cell populations have been utilized as cell-based therapy, including neural stem cells, embryonic stem cells, human umbilical cord blood cells (HUBCs), hematopoietic stem and progenitor cells, and mesenchymal stem cells (MSCs). Most stem cell types appear to enhance recovery to some extent (Pimentel-Coelho and Mendez-Otero, 2010). However, because of their low immunogenicity, availability and positive results obtained from preclinical studies, MSCs are a particularly promising candidate to repair the devastating effects that are associated with neonatal stroke. MSCs were first isolated and identified in bone marrow, but can now be isolated from many tissues, including adipose tissue, muscle, skin and extraembryonic tissues like the placenta, umbilical cord and Wharton's jelly. The latter sources are of particular interest for neonates that experience an ischemic event around the time of birth, at which time cells can be harvested and transplanted from an autologous source. MSCs derived from different sources have slightly different characteristics, but as of yet it is unknown whether this influences their therapeutic potential.
Our group and others have shown that administration of MSCs reduces lesion volume, provides positive effects on the white matter and improves motor function (van Velthoven et al., 2012). Numerous studies have been done under the premise that transplanted stem cells contribute to brain repair by directly replacing damaged or lost tissue. While there is evidence that transplanted cells undergo differentiation toward neuronal lineages, improved outcomes have been observed even when survival of transplanted cells is low and engrafted cells are absent. This suggests that rather than replacing damaged cells, transplanted cells may improve outcome via indirect mechanisms. For example, MSCs have been shown to secrete many factors that can influence important processes like apoptosis, neurogenesis, angiogenesis and synaptogenesis.

More pages at link.

Sickest Reap Greatest Gain From BP Treatment

Have these doctors considered the overall health of these patients?  Don't listen to me I'm obviously stroke addled to even consider questioning the medical gods.
Are Blood Pressure Drugs Worth the Falls?

Low blood pressure and dementia in elderly people: the Kungsholmen project

Claudia Kawas: If you have high blood pressure, it looks like your risk of dementia is lower.

And for you stroke survivors, does your doctor know about any of these?
1. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset
 2. Early Intensive Blood-Pressure Lowering Improves Recovery in Patients With Acute Intracerebral Haemorrhage
 3.  Systolic Blood Pressure During Acute Stroke Is Associated With Functional Status and Long-term Mortality in the Elderly
 4. External Counterpulsation Augments Blood Pressure and Cerebral Flow Velocities in Ischemic Stroke Patients With Cerebral Intracranial Large Artery Occlusive Disease


 Sickest Reap Greatest Gain From BP Treatment

Education Level and Inequalities in Stroke Reperfusion Therapy Observations in the Swedish Stroke Register

This just proves that tPA should be considered a complete failure and something better found. Beating a dead horse is not going to make it race any faster. And yet I bet our stroke medical world will continue down the same failed path for years to come. Unless we overthrow them all.  Notice that they don't talk about results(how many fully recovered due to tPA?). They talk about reperfusion as if that is the important thing to measure. It's not. 
GAH!!! The Stupidity.
http://stroke.ahajournals.org/content/early/2014/07/29/STROKEAHA.114.005323.abstract?sid=f5ba2ff2-c68f-4a20-9420-a2bf07af24c0
  1. Marie Eriksson, PhD
+ Author Affiliations
  1. From the Departments of Public Health and Clinical Medicine (A.S., E.-L.G., K.A.) and Statistics (M.E.), Umeå University, Umeå, Sweden; and Department of Clinical Sciences, Section of Neurology, Lund University, Lund, Sweden (B.N.).
  1. Correspondence to Anna Stecksén, RPT, MSc, Department of Public Health and Clinical Medicine, Umeå University, S-901 87 Umeå, Sweden. E-mail anna.stecksen@medicin.umu.se

Abstract

Background and Purpose—Previous studies have revealed inequalities in stroke treatment based on demographics, hospital type, and region. We used the Swedish Stroke Register (Riksstroke) to test whether patient education level is associated with reperfusion (either or both of thrombolysis and thrombectomy) treatment.
Methods—We included 85 885 patients with ischemic stroke aged 18 to 80 years registered in Riksstroke between 2003 and 2009. Education level was retrieved from Statistics Sweden, and thrombolysis, thrombectomy, patient, and hospital data were obtained from Riksstroke. We used multivariable logistic regression to analyze the association between reperfusion therapy and patient education.
Results—A total of 3649 (4.2%) of the patients received reperfusion therapy. University-educated patients were more likely to be treated (5.5%) than patients with secondary (4.6%) or primary education (3.6%; P<0.001). The inequality associated with education was still present after adjustment for patient characteristics; university education odds ratio, 1.14; 95% confidence interval, 1.03 to 1.26 and secondary education odds ratio, 1.08; 95% confidence interval, 1.00 to 1.17 compared with primary education. Higher hospital specialization level was also associated with higher reperfusion levels (P<0.001). In stratified multivariable analyses by hospital type, significant treatment differences by education level existed only among large nonuniversity hospitals (university education odds ratio, 1.20; 95% confidence interval, 1.04–1.40; secondary education odds ratio, 1.14; 95% confidence interval, 1.01–1.29).
Conclusions—We demonstrated a social stratification in reperfusion, partly explained by patient characteristics and the local hospital specialization level. Further studies should address treatment delays, stroke knowledge, and means to improve reperfusion implementation in less specialized hospitals.

Abracadabra Robotics: Not-cute robots to help stroke patients

The movie 'Robot and Frank' pretty well described personal robots, but they do need a moral filter.
http://www.haaretz.com/business/start-up-of-the-week/1.610907

Can Hearing Loss Predict—or Lead to—Cognitive Decline?

Is your doctor assigning your cognitive decline post-stroke to the stroke because of  Occams' Razor  rather than really finding out the cause?
http://www.dana.org/News/Can_Hearing_Loss_Predict%E2%80%94or_Lead_to%E2%80%94Cognitive_Decline_/

The man with the missing brain

This sounds like the recovery that Pedro Bach-y-Rita made.
http://www.telegraph.co.uk/culture/books/11039266/The-man-with-the-missing-brain.html

Has your doctor contacted them to save the protocols for their severely damaged survivors?

Lamotrigine Treatment for Post-Stroke Pathological Laughing and Crying

Well at least this one is only 11 years old, still incompent but not mind-boggling.
http://journals.lww.com/clinicalneuropharm/Abstract/2003/09000/Lamotrigine_Treatment_for_Post_Stroke_Pathological.6.aspx

Ramasubbu, Rajamannar

Collapse Box

Abstract

Pathologic laughing and crying (PLC) is a common distressing and socially disabling condition in stroke patients. Antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), have been increasingly recognized as the treatment of choice for pathologic crying (PC). However, little is known about etiologies and other treatment options for various clinical manifestations of PLC. This case report illustrates the beneficial effect of lamotrigine, a novel antiepileptic drug with antidepressant and mood-stabilizing properties in post-stroke PLC. A 60-year-old woman developed PLC after an ischemic stroke affecting the left frontal and temporal lobes. She was treated with lamotrigine initially at the dose of 50 mg a day, which was gradually increased to 100 mg a day over a 4-week period. There was a significant and rapid recovery in both laughing and crying components of PCL with lamotrigine treatment. The symptoms of pathologic laughing have shown a better response to lamotrigine than PC. Controlled investigations are needed to evaluate the beneficial as well as the differential effects of lamotrigine on PLC.
The syndrome of pathologic laughing and crying (PLC) involves uncontrollable motor expression of emotion in the absence of corresponding feelings of sadness or happiness. PLC is often precipitated by nonspecific stimuli. 1 Emotional lability is a second type of pathologic affect that represents a rapid fluctuation in emotional expression that is out of proportion to an appropriate stimulus or situation and is accompanied by an alteration in mood states. 1 The validity of the existence of these two types has not been substantiated because of a great deal of overlap in the phenomenology between PLC and emotional lability. 2 In this context, a commonly used instrument, namely the pathologic laughing and crying scale (PLCS), has included items to measure both the intensity of pathologic laughing (PL) and pathological crying (PC) and also the severity of emotional lability. 3 The other terms used in the literature to describe the pathologic affect of laughing and crying include emotionalism, 4 emotional incontinence, 5 and pseudobulbar affect. 6
PLC is a common emotional consequence of stroke. Approximately 15% to 20% of patients may experience this condition during the first year after stroke. 7 Pathologic crying is the most common manifestation in stroke patients. However, some patients may have episodes of laughing without episodes of crying and some display both laughing and crying. Brain stem lesions and right frontal damage are frequently associated with PLC. 7 Double-blind placebo-controlled studies documented the efficacy of both tricyclics (nortriptyline, amitriptyline) and selective serotonin reuptake inhibitors (SSRIs) (citalopram, fluoxetine, sertraline) in PLC. 3,8–11 However, since the controlled treatment studies to date focused largely on patients with PC and only a few patients with PL were in the cohort, our understanding of the efficacy of antidepressants in PL is limited. Furthermore, anecdotal reports described a rapid transition of PC to PL during treatment with SSRIs 12 and a slow transformation of PC to PL as a natural course of PLC in some patients. 13,14
L-dopa was reported to be effective in patients with PL in an open trial. 15 However, taking into account the depressogenic side effect of l-dopa 16 and the frequent co-occurrence of depression with PLC in stroke patients, 7 l-dopa may not be a suitable agent for post-stroke patients with PLC and depression. This report describes a case of post-stroke PLC that markedly improved with lamotrigine, a novel antiepileptic drug with antidepressant and mood stabilizing properties.

Cerebroprotective Effect of Lamotrigine After Focal Ischemia in Rats

It has only been 19 f*cking years. Has anyone followed this up with human trials?
This just completely and totally proves that stroke has no strategic plan with the existing medical team. They all need to be fired and we need to start over with stroke-addled survivors. We can't do any worse than supposedly healthy brain normal people.
https://stroke.ahajournals.org/content/26/1/117.full
  1. Brian S. Meldrum, MB, BChir, PhD
+ Author Affiliations
  1. From the Department of Neurology, Institute of Psychiatry, De Crespigny Park, Denmark Hill, UK.
  1. Correspondence to B.S. Meldrum, Department of Neurology, Institute of Psychiatry, De Crespigny Park, Denmark Hill, SE5 8AF, UK.

Abstract

Background and Purpose Glutamate receptor antagonists are protective in animal models of focal cerebral ischemia. Lamotrigine (3,5-diamino-6-[2,3-dichlorophenyl]-1,2,4-triazine) is an anticonvulsant drug that blocks voltage-gated sodium channels and inhibits the ischemia-induced release of glutamate. We describe the cerebroprotective effect of lamotrigine (as the isethionate salt) after middle cerebral artery occlusion in rats.
Methods Neurological deficit and infarct volume (visualized by the lack of reduction of 2,3,5-triphenyltetrazolium chloride) 24 hours after permanent left middle cerebral artery occlusion were studied in Fischer rats (n=8 per group per dose).
Results Lamotrigine at 20 mg/kg IV over 10 minutes administered immediately after middle cerebral artery occlusion reduced total infarct volume by 31% and cortical infarct volume by 52%. Lamotrigine at 8 mg/kg IV over 10 minutes reduced cortical infarct volume by 38%. Lamotrigine at 50 mg/kg IV for 10 minutes was not cerebroprotective and induced a decrease of 29±15 mm Hg in mean arterial blood pressure (P<.05, n=8). The optimum dose of lamotrigine (20 mg/kg IV over 10 minutes) when administered with a 1-hour delay after middle cerebral artery occlusion reduced cortical infarct volume by 41%. Lamotrigine (20 mg/kg IV over 10 minutes) with a 2-hour delay after middle cerebral artery occlusion was ineffective. Neurological deficits after 24 hours were improved after immediate treatment with lamotrigine at 20 mg/kg IV over 10 minutes.
Conclusions The cerebroprotective effect of lamotrigine in rats is limited to a narrow dose range between 8 and 20 mg/kg. Lamotrigine or analogous compounds may be useful when given shortly after the onset of stroke.

Pathophysiology of traumatic brain injury

Will the secondary impacts of TBI correspond to strokes neuronal cascade of death?  And can any of their solutions be applied to stroke?
http://bja.oxfordjournals.org/content/99/1/4
  1. K. Engelhard
+ Author Affiliations
  1. Klinik für Anästhesiologie, der Johannes Gutenberg-Universität Mainz, Langenbeckstrasse 1, D-55131 Mainz, Germany
  1. *Corresponding author. E-mail: werner@anaesthesie.klinik.uni-mainz.de

Abstract

The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). It is influenced by changes in cerebral blood flow (hypo- and hyperperfusion), impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Understanding the multidimensional cascade of secondary brain injury offers differentiated therapeutic options.

The combination of rhythm and pitch can account for the beneficial effect of melodic intonation therapy on connected speech improvements in Broca’s aphasia

Have at it for your edification on aphasia solutions.
http://journal.frontiersin.org/Journal/10.3389/fnhum.2014.00592/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w34-2014
  • 1Faculty of Medicine, School of Speech Pathology and Audiology, Université de Montréal, Montreal, QC, Canada
  • 2CRBLM, Centre for Research on Brain, Language and Music, McGill University, Montreal, QC, Canada
  • 3BRAMS, International Laboratory for Research on Brain, Music, and Sound, Université de Montréal, Montreal, QC, Canada
  • 4Faculty of Arts and Science, Department of Psychology, Université de Montréal, Montreal, QC, Canada
Melodic intonation therapy (MIT) is a structured protocol for language rehabilitation in people with Broca’s aphasia. The main particularity of MIT is the use of intoned speech, a technique in which the clinician stylizes the prosody of short sentences using simple pitch and rhythm patterns. In the original MIT protocol, patients must repeat diverse sentences in order to espouse this way of speaking, with the goal of improving their natural, connected speech. MIT has long been regarded as a promising treatment but its mechanisms are still debated. Recent work showed that rhythm plays a key role in variations of MIT, leading to consider the use of pitch as relatively unnecessary in MIT. Our study primarily aimed to assess the relative contribution of rhythm and pitch in MIT’s generalization effect to non-trained stimuli and to connected speech. We compared a melodic therapy (with pitch and rhythm) to a rhythmic therapy (with rhythm only) and to a normally spoken therapy (without melodic elements). Three participants with chronic post-stroke Broca’s aphasia underwent the treatments in hourly sessions, 3 days per week for 6 weeks, in a cross-over design. The informativeness of connected speech, speech accuracy of trained and non-trained sentences, motor-speech agility, and mood was assessed before and after the treatments. The results show that the three treatments improved speech accuracy in trained sentences, but that the combination of rhythm and pitch elicited the strongest generalization effect both to non-trained stimuli and connected speech. No significant change was measured in motor-speech agility or mood measures with either treatment. The results emphasize the beneficial effect of both rhythm and pitch in the efficacy of original MIT on connected speech, an outcome of primary clinical importance in aphasia therapy.

More at link.

Gain control mechanisms in spinal motoneurons

Send your damned doctor off to study this to see if controlling this would solve the spasticity problem. You get spasticity solved and a large majority of movement problems could be solved. And that is in direct contradiction to Dr. William M. Landau and his blasted opinion;

Spasticity After Stroke: Why Bother?

http://journal.frontiersin.org/Journal/10.3389/fncir.2014.00081/full?
Motoneurons provide the only conduit for motor commands to reach muscles. For many years, motoneurons were in fact considered to be little more than passive “wires”. Systematic studies in the past 25 years however have clearly demonstrated that the intrinsic electrical properties of motoneurons are under strong neuromodulatory control via multiple sources. The discovery of potent neuromodulation from the brainstem and its ability to change the gain of motoneurons shows that the “passive” view of the motor output stage is no longer tenable. A mechanism for gain control at the motor output stage makes good functional sense considering our capability of generating an enormous range of forces, from very delicate (e.g., putting in a contact lens) to highly forceful (emergency reactions). Just as sensory systems need gain control to deal with a wide dynamic range of inputs, so to might motor output need gain control to deal with the wide dynamic range of the normal movement repertoire. Two problems emerge from the potential use of the brainstem monoaminergic projection to motoneurons for gain control. First, the projection is highly diffuse anatomically, so that independent control of the gains of different motor pools is not feasible. In fact, the system is so diffuse that gain for all the motor pools in a limb likely increases in concert. Second, if there is a system that increases gain, probably a system to reduce gain is also needed. In this review, we summarize recent studies that show local inhibitory circuits within the spinal cord, especially reciprocal and recurrent inhibition, have the potential to solve both of these problems as well as constitute another source of gain modulation.

More pages at link.

Sunday, August 17, 2014

How corpse brain scans help the living

I think this should be absolutely necessary for those suspected of dying from a stroke. Putting stroke on the death certificate is completely stupid. You didn't die from the stroke, you died from the damage to your brain. And if you never correlate damage to death you will never be able to tell if changes in interventions could have saved your life. It is the exact same reason that old age is not allowed on death certificates anymore.  With no factual basis of why you died you can never fix the problems.  A great stroke association would be able to change this custom. But we have jackshit for stroke associations right now. And for some reason their boards of directors are ok with that.
http://www.theguardian.com/science/2014/aug/17/how-corpses-help-the-living-brain-scans-mri-imaging

Contracture: understanding mechanisms and testing treatments

One more sequalae about stroke we know nothing about.  Damn, is there anything that our doctors know about treating stroke problems?
From NeuRA Blog is an initiative of Neuroscience Research Australia
NeuRA Blog is an initiative of Neuroscience Research Australia - See more at: http://blog.neura.edu.au/about/#sthash.XtTRZ8p5.dpuf
NeuRA Blog is an initiative of Neuroscience Research Australia - See more at: http://blog.neura.edu.au/about/#sthash.XtTRZ8p5.dpuf

http://blog.neura.edu.au/2014/08/18/contracture/?utm_source=rss&utm_medium=rss&utm_campaign=contracture
There has been surprisingly little research into the mechanisms of contracture. As a result, the mechanisms are poorly understood. - See more at: http://blog.neura.edu.au/2014/08/18/contracture/?utm_source=rss&utm_medium=rss&utm_campaign=contracture#sthash.eOop3nIO.dpuf
 There has been surprisingly little research into the mechanisms of contracture. As a result, the mechanisms are poorly understood. 

Who the hell is tasked with solving these problems? They've only been around since stroke was known about.
One more thing you as a survivor is going to have to solve or prevent on your own.

"Luke," a robotic prosthetic arm

Katie Couric Interviews Bionic Arm Inventor Dean Kamen.

This should be able to be repurposed to survivors who need help with hand/finger movement. That consumer base would make the size of the market feasible.

http://news.yahoo.com/katie-couric-interviews-bionic-arm-inventor-185134268.html 

 

Saturday, August 16, 2014

Adult neurogenesis: bridging the gap between mice and humans

See if your doctor can create a stroke protocol from this. Have them do some work for all the money you are paying them.
http://www.hifo.uzh.ch/research/jessberger/publications/JessbergerGage2014.pdf

Non-Invasive Brain Stimulation and its Supposed Site of Action in the Rehabilitation of Parkinson's Disease and Stroke

This is kind of getting into the magical recovery part.
http://omicsgroup.org/journals/non-invasive-brain-stimulation-and-its-supposed-site-of-action-in-the-rehabilitation-ijn-1000e103.pdf
Two non-invasive brain stimulations have spread all over the
world: repetitive transcranial magnetic stimulation (rTMS) and
transcranial direct current stimulation (tDCS). TMS is based on the
current induction with a changing electromagnetic field in the nervous
system [1] while tDCS changes the polarity of cell membranes.

4 more pages to go if you need to school your doctor on this. If you want this YOU are going to have to demand your hospital get this. Otherwise it will take 30-40 years to get to your hospital. Your choice; Now or never?

A pilot study of augmented reality-based postural control training in stroke rehabilitation

You will need to ask your doctor/therapist what augmented reality is and when this might be available in the therapy dept.
http://www.papersearch.net/view/detail.asp?detail_key=2a500043

Objective: The purpose of this study was to determine the effects of Augmented Reality-based Postural Control (ARPC) training on balance and gait function in patients with stroke. Design: Single-blind randomized controlled trial. Methods: Twenty participants who experienced a stroke were enrolled in the study and randomly assigned to the ARPC (n=10) or control group (n=10). Subjects in both groups received conventional physical therapy for 60 min per session, 5 days per week, for 4 weeks. In addition, subjects in the ARPC group received ARPC training for 30 min per day, 3 days per week, for 4 weeks. The participants watched established normal postural control patterns on a head-mounted display and repeated the movements in ARPC training. Outcome measurements were assessed using the Berg Balance Scale (BBS) and 10-Meter Walk Test (10MWT) before and after 4 weeks of training. Results: Of the 20 randomized participants, only 18 completed the 4-week training program. The ARPC group showed significant improvement in the BBS and 10MWT after training (p<0.05). Meanwhile, the control group did not exhibit improvement in either variable. In addition, the ARPC group showed significantly greater improvement than the control group in the 10MWT (p<0.05), whereas no significant difference was observed between the groups for the BBS.
Conclusions: The results of this study confirmed the benefits of ARPC training on dynamic balance and functional gait ability. and gait ability in patients after a chronic stroke.

A formative evaluation of the implementation of an upper limb stroke rehabilitation intervention in clinical practice: a qualitative interview study

The GRASP study. Has your hospital implemented this yet? Created a stroke protocol for it? Only 22 pages.
 http://scholar.google.com/scholar_url?hl=en&q=http://www.implementationscience.com/content/pdf/s13012-014-0090-3.pdf&sa=X&scisig=AAGBfm1wgC-_YJ4o3TJngRDPrjA6EgtPHg&oi=scholaralrt
Background 
The Graded Repetitive Arm Supplementary Program (GRASP) is a hand and
arm exercise programme designed to increase the intensity of exercise achieved in inpatient stroke rehabilitation
.  GRASP was shown to be effective in a randomised controlled trial in 2009 and has since experienced unusually rapid uptake into clinical practice. The aim of this study was to conduct a formative evaluation of the implementation of GRASP to inform the development and implementation of a similar intervention in the United Kingdom.

NOX2-mediated artery dysfunction in smokers: acute effect of dark chocolate

I assume post-stroke we do want artery dilatation.  So is this in your post-stroke hospital diet? Can your doctor use enough brains to see if this would work even in non-smokers? Do not do this without your doctors prescription. You know how damned dangerous dark chocolate is.
http://heart.bmj.com/content/early/2011/07/30/heartjnl-2011-300304
  1. Francesco Violi
+ Author Affiliations
  1. I Clinica Medica, Sapienza University, Rome, Italy
  1. Correspondence to Professor Francesco Violi, I Clinica Medica, Viale del Policlinico 155, Roma 00161, Italy; francesco.violi@uniroma1.it
  1. Contributors Conception and design: FV, LL. Analysis and interpretation of data: FV, LL, RC, PP. Flow-mediated dilation analysis: LL. Patient enrolment: LP, EC, TA, RC, FA. Laboratory analysis: RC, CN, CP. Drafting the article: FV, LL.
  • Accepted 30 June 2011
  • Published Online First 31 July 2011

Abstract

Background Cocoa seems to exert artery dilatation via oxidative stress inhibition but the mechanism is still unclear.
Objectives To investigate whether in smokers, dark chocolate elicits artery dilatation via down-regulation of NOX2, the catalytic core of NADPH oxidase.
Methods Flow-mediated dilatation (FMD), oxidative stress (as assessed by urinary isoprostanes excretion), nitric oxide generation (as assessed by serum levels of nitrite/nitrate (NOx)), NOX2 activity (as assessed by blood levels of soluble NOX2 derived peptide (sNOX2-dp)) and serum epicatechin were studied in 20 smokers and 20 healthy subjects (HS) in a crossover, single-blind study. Patients were randomly allocated to 40 g dark chocolate (>85% cocoa) or 40 g of milk chocolate (≤35% cocoa). FMD, urinary isoprostanes, NOx and sNOX2-dp were assessed at baseline and 2 h after chocolate ingestion.
Results Smokers had lower FMD and NOx and higher sNOX2-dp compared to HS. After dark chocolate intake, urinary isoprostanes and sNOX2-dp significantly decreased and FMD and NOx significantly increased in smokers but not in HS. No changes of the above variables were observed after milk chocolate intake. Multiple linear regression analysis showed that in smokers the only independent predictive variable associated with a change in FMD was a change in sNOX2-dp. Serum epicatechin increased in either group only after dark chocolate intake, reaching values higher than 0.1 μM. Platelets from smokers (n=5), but not from HS (n=5), showed lower p47phox translocation to platelet membrane and higher NOx when incubated with 0.1–10 μM epicatechin.
Conclusion Results suggest that in smokers, cocoa enhances artery dilatation by lowering of NOX2 activation.

Revealed: The Type of Music That Makes You Feel Most Powerful

Shouldn't your doctor know about and prescribe the right type of music for your power needs when doing therapy?
http://www.spring.org.uk/2014/08/revealed-the-type-of-music-that-makes-you-feel-most-powerful.php
After testing 31 clips they found that songs rated the most powerful were:
  • Queen’s “We Will Rock You”
  • 2 Unlimited’s “Get Ready for This”
First here’s 2 Unlimited’s “Get Ready for This”:
And now Queen’s “We Will Rock You”
Image credit: Thomas Hawk


 Does your doctor have any clue about the role of music in stroke recovery?  Has your doctor read any of the following research articles?

11 Problems Music Can Solve

How playing an instrument benefits your brain - Anita Collins

Why does music therapy work? The Science Behind the Music.

Musical Training Can Increase Blood Flow in Brain

Neurologic Music Therapy in Stroke Rehabilitation

Music helps stroke patients find their voice

Listening to classical music ameliorates unilateral neglect after stroke

Music brings memories back to the brain injured 

Plasticity in the sensorimotor cortex induced by Music-supported therapy in stroke patients: a TMS study

 Moderating variables of music training-induced neuroplasticity: a review and discussion

 

The reason for music listening is not to fight depression but to facilitate recovery.
http://brain.oxfordjournals.org/cgi/content/full/131/3/866
Music listening enhances cognitive recovery and mood after middle cerebral artery stroke
http://www.therapytimes.com/content=0402J84C48968A84406040441
Music Therapy Speeds Post-Stroke Recovery
music therapy
http://www.msnbc.msn.com/id/35502970/ns/technology_and_science-science/
http://www.epsychology.us/rhythm-of-life-music-shows-potential-in-stroke-rehabilitation/
http://hubpages.com/hub/Music-Therapy-Healing including Kenny Rogers, I couldn't have handled this. Ask your doctors if you can listen to music to make sure it doesn't have negative side effects.