Effects of Statins on Energy and Fatigue With Exertion: Results From a Randomized Controlled Trial

So ask your doctor.
 http://archinte.jamanetwork.com/article.aspx?doi=10.1001/archinternmed.2012.2171

No drug is without adverse effect potential, and fatigue and exertional intolerance are adverse effects reported by patients receiving statins.^{1 - 2} Little direct information is available regarding the typical or average impact of statins on energy or exertional fatigue.

Although many observational reports have cited fatigue and exertional fatigue with statin use, to our knowledge, no randomized trials have addressed this issue to date. Energy and exertional fatigue were measured as tertiary and/or exploratory outcomes in the University of California, San Diego (UCSD) Statin Study, which aimed to examine a range of noncardiac outcomes.³ We capitalized on these data to evaluate whether moderate-dose statins affected energy and exertional fatigue in a broadly sampled primary prevention population.

METHODS

Methods

A total of 1016 subjects (692 men 20 years or older and 324 nonprocreative women, with screening low-density lipoprotein cholesterol levels 115-190 mg/dL [to convert to millimoles per liter, multiply by 0.0259] and no cardiovascular disease or diabetes) were randomized equally to 20-mg simvastatin (lipophilic statin), 40-mg pravastatin (hydrophilic statin), or microcrystalline-cellulose placebo, to be taken at bedtime in identical blinding capsules for 6 months.

Methods

The off-site study pharmacist matched sequentially numbered bottles to sequential computer-generated randomization assignment stratified by sex (block size, 20; designed by statistician [H.L.W.]). Bottles were transferred to the study site and given to successive eligible subjects by staff blinded to the randomization schedule.⁴

Methods

The protocol was approved by the UCSD Human Subjects Protection Program. All subjects (seen exclusively at UCSD) gave written informed consent. The data and safety monitoring board provided independent study oversight.

Methods

Outcome

Single-item self-ratings of change from baseline in “energy” and “fatigue with exertion” were used, assessed on 6-month follow-up, and rated (5-point scale) from “much less”(−2) to “much more”(+2) vs baseline.

Outcome

Energy and fatigue with exertion were rated at baseline from 0 (none) to 10 (maximum possible). All subjects rated energy; the final 397 subjects (a randomized subset) rated baseline fatigue with exertion (omitted initially to limit subject burden, restored for the final 40% of subjects). Missing values of baseline and change score were imputed using the Stata “impute” command (StataCorp). “EnergyFatigEx” values were generated by summing ratings for the energy and fatigue with exertion measures, aligning signs with lower values worse (ie, recoding such that for both variables lower values signified worse status), for baseline and on-treatment, yielding a single outcome (on-treatment score range, −4 to +4).

Methods

Statistical Analysis

We assessed the correlation of EnergyFatigEx with actual exercise (baseline assessment: episodes per week of vigorous exercise >20minutes). The unpaired t test was used to examine the difference in mean on-treatment EnergyFatigEx in all subjects and women separately. Ordinal logistic regression with robust (“White”) standard errors⁵ adjusted for baseline values of the combined variable, addressing baseline disparities and regression to the mean (a source of power-eroding variance). The χ² test was used to examine whether statins shifted, relative to placebo, the proportion reporting changes of subjectively large magnitude (“much worse” or “much better” vs placebo on both outcomes; the same principle that guides sign tests). Analyses used Stata statistical software versions 8.0 and 11.0 (StataCorp). A 2-sided α level of .05 designated significance.

RESULTS

Results

For CONSORT (Consolidated Standards for Reporting of Trials) and study baseline characteristics, see eFigure and eTable. Energy and predictors of exertional fatigue were comparable at baseline; however, in the subsample with measured baseline exertional fatigue, pravastatin values differed from other arms and influenced imputed baseline values (Table). There was a significant relation between measured baseline EnergyFatigEx and actual exercise (r = 0.20; P < .001). The drop in low-density lipoprotein cholesterol level with 20-mg simvastatin (49 mg/dL) exceeded that with 40-mg pravastatin (40 mg/dL) (P < .001).

Results

Results of t tests of difference in mean on-treatment change in EnergyFatigEx were significant for combined statins vs placebo. Each statin contributed (effects separately significant for simvastatin) (Table). Women were disproportionately affected. The 0.4 mean difference observed for women receiving simvastatin vs placebo would arise if 4 in 10 treated women cited worsening in either energy or exertional fatigue; 2 in 10 characterized both as “worse” or either as “much worse”; 1 in 10 characterized both components as “much worse”; or combinations of these conditions, with the fractions of subjects for which each statement holds, summing to 1. Adjusted for baseline EnergyFatigEx (via ordinal logit), effects on EnergyFatigEx were significantly unfavorable for combined statins and each statin separately.

Results

The balance of those reporting maximal worsening vs maximal improvement (“much worse” vs baseline on each component vs “much better” on each) was adversely shifted for statins vs placebo (P = .002) and for each statin separately (simvastatin, P = .03; pravastatin, P = .01). These are based on small numbers, and findings are provisional.

COMMENT

Comment

To our knowledge, this is the first randomized evidence affirming unfavorable statin effects on energy and exertional fatigue. Effects were seen in a generally healthy sample given modest statin doses, and both simvastatin and pravastatin contributed to the significant adverse effect of statins on energy and fatigue with exertion. Particularly for women, these unfavorable effects were not uncommon. Findings support case reports citing adverse effects to these outcomes and are buttressed by literature rationale.^{1 ,6} These findings are important, given the central relevance of energy and functional status to well-being.

Comment

These effects, germane to quality of life, merit consideration when prescribing or contemplating use of statins, particularly in groups without expected net morbidity/mortality benefit, extending to “high-risk” primary prevention and women and elderly persons (including those with coronary artery disease).^{7 - 9} There was a significant relation between EnergyFatigEx and actual activity: reduced activity and exertional tolerance (irrespective of activity) in turn predict hard adverse outcomes. Effects may take time to manifest, as may benefits of statin use. Thus, long-term trials are important, if statin use is to be recommended in younger individuals. Meanwhile, physicians should be alert to patients' reports of exertional fatigue or diminished energy during statin use.

A news report on it.
http://www.msnbc.msn.com/id/47772793/ns/health/#.T9bdzsVPGxM

A blogger writing about it.
 http://www.medrants.com/archives/6864

A different drummer: Stanford engineers discover neural rhythms drive physical movement

So who's going to take this and make a hypothesis about how to use this information to help stroke patients recover?
http://engineering.stanford.edu/news/different-drummer-stanford-engineers-discover-neural-rhythms-drive-physical-movement
The neurons that control movement are not a predictable bunch. Scientists working to decode how such neurons convey information to muscles have been stymied when trying to establish a one-to-one relationship between a neuron’s behavior and factors such as muscle activity or movement velocity.
In an article published online June 3rd by the journal Nature, a team of electrical engineers and neuroscientists working at Stanford University propose a new theory of the brain activity behind arm movements. Their theory is a significant departure from existing understanding and helps to explain, in relatively simple and elegant terms, some of the more perplexing aspects of the activity of neurons in the motor cortex.
In their paper, electrical engineering Associate Professor Krishna Shenoy and post-doctoral researchers Mark Churchland, now a professor at Columbia, and John Cunningham of Cambridge University, now a professor at Washington University in Saint Louis, have shown that the brain activity controlling arm movement does not encode external spatial information – such as direction, distance, and speed – but is instead rhythmic in nature.

Understanding the brain

Neuroscientists have long known that the neurons responsible for vision encode specific, external-world information – the parameters of sight. It had been theorized and widely suggested that motor cortex neurons function similarly, conveying specifics of movement such as direction, distance and speed, in the same way the visual cortex records color, intensity and form.
“Visual neurons encode things in the world. They are a map, a representation,” said Churchland, who is first author of the paper. “It’s not a leap to imagine that neurons in the motor cortex should behave like neurons in the visual cortex, relating in a faithful way to external parameters, but things aren’t so concrete for movement.”
Scientists have disagreed about which movement parameters are being represented by individual neurons. They could not look at a particular neuron firing in the motor cortex and determine with confidence what information it was encoding.
“Many experiments have sought such lawfulness and yet none have found it. Our findings indicate an alternative principle is at play,” said co-first author Cunningham.
“Our main finding is that the motor cortex is a flexible pattern generator, and sends rhythmic signals down the spinal cord,” said Churchland.


19th century mathematician Joseph Fourier showed that two rhythms could be summed to produce a third rhythm. Researchers at Stanford have shown that such mathematics are at play in the brain activity that produces arm movements.

Engine of movement

To employ an automotive analogy, the motor cortex is not the steering wheel, odometer or speedometer representing external-world information. It is more like an engine, comprised of parts whose activities appear complicated in isolation, but which cooperate in a lawful way as a whole to generate motion.
“If you saw a piston or a spark plug by itself, would you be able to explain how it makes a car move?” asked Cunningham rhetorically. “Motor-cortex neurons are like that, too, understandable only in the context of the whole.”
In monitoring electrical brain activity of motor-cortex neurons, researchers found that they typically exhibit a brief oscillatory response. These responses are not independent from neuron to neuron. Instead, the entire neural population oscillates as one in a beautiful and lawfully coordinated way.
The electrical signal that drives a given movement is therefore an amalgam – a summation – of the rhythms of all the motor neurons firing at a given moment.
“Under this new way of looking at things, the inscrutable becomes predictable,” said Churchland. “Each neuron behaves like a player in a band. When the rhythms of all the players are summed over the whole band, a cascade of fluid and accurate motion results.”

In a series of striking graphs, the Stanford team plotted the signals from individual neurons in the motor cortex as monkeys completed a series of reaches. The reaching motions are shown by the starburst patterns at the top left of each graph. The neuronal patterns are then plotted atop one another for the entire series of reaches, clearly establishing the rhythmic nature of the brain activity.

Precedents in nature

In the new model, a few relatively simple rhythms explain neural features that had confounded science earlier.
“Many of the most-baffling aspects of motor-cortex neurons seem natural and straightforward in light of this model,” said Cunnigham.
The team studied non-rhythmic reaching movements, which made the presence of rhythmic neural activity a surprise even though, the team notes, rhythmic neural activity has a long precedence in nature. Such rhythms are present in the swimming motion of leeches and the gait of a walking monkey, for instance.
“The brain has had an evolutionary goal to drive movements that help us survive. The primary motor cortex is key to these functions. The patterns of activity it displays presumably derive from evolutionarily older rhythmic motions such as swimming and walking. Rhythm is a basic building block of movement,” explained Churchland.

Reaching for the grail

To test their hypothesis, the engineers studied the brain activity of monkeys reaching to touch a target. According to the researchers, experiments show this ‘underlying rhythm’ strategy works very well to explain both brain and muscle activity. In their reaching studies, the pattern of shoulder-muscle behavior could always be described by the sum of two underlying rhythms.
“Say you’re throwing a ball. Beneath it all is a pattern. Maybe your shoulder muscle contracts, relaxes slightly, contracts again, and then relaxes completely, all in short order,” explained Churchland.
The researchers say that although the activity may not be exactly rhythmic, it can be created by adding together two or three other rhythms. The team asserts that this may be how the brain solves the problem of creating patterns of movement.
"This surprised us a bit. In decidedly arrhythmic movements, there were these unmistakable patterns,” said Churchland.
"This research builds on a strong theoretical framework and adds to growing evidence that rhythmic activity is important for many fundamental brain functions," said Yuan Liu of the National Institute of Neurological Disorders and Stroke, NIH.  "Further research in this area may help us devise more effective technology for controlling prosthetic limbs." Liu is the co-lead of the NIH-NSF Collaborative Research in Computational Neuroscience program.
"In trying to find the basic response properties of the motor cortex, Dr. Shenoy and his colleagues are searching for the holy grail of neuroscience," said Dr. Daofen Chen, Program Director, Systems and Cognitive Neuroscience at the National Institute of Neurological Disorders and Stroke at the National Institutes of Health. "They consistently tackle important but tough questions in thought-provoking ways and in ambitious proposals. NIH is proud to support this kind of pioneering and transformative research."
Accordingly, the seemingly complex system that is the motor cortex can now be at least partially understood in more straightforward terms.
"The motor cortex is an engine of movement that obeys lawful dynamics,” said Shenoy.
Stanford post-doctoral fellow Matthew Kaufman, bioengineering PhD student and medical science training program student Paul Nuyujukian, electrical engineering graduate student Justin Foster, and electrical engineering consulting assistant professor and Palo Alto Medical Foundation neurosurgeon Stephen Ryu were also authors on this paper.
The work of the various co-authors was supported in part by the National Institutes of Health, the Burroughs Wellcome Fund Career Awards in the Biomedical Sciences (BWF-CABS) and an Engineering and Physical Sciences Research Council grant. The work of Krishna Shenoy was supported in part by: NIH Director’s Pioneer Award (1DP1OD006409), NIH NINDS EUREKA Award (R01-NS066311), NIH NINDS BRP (R01-NS064318), NIH NINDS CRCNS (R01-NS054283), DARPA REPAIR, and BWF-CABS.

Hepatocyte growth factor mediates mesenchymal stem cell-induced recovery in multiple sclerosis models

Two versions. But first we need to determine if demyelination occurs as an aftermath of stroke.
 Who's going to take question that on?
The abstract here;

Hepatocyte growth factor mediates mesenchymal stem cell-induced recovery in multiple sclerosis models

The understandable blogger on it here:
http://blog.uberbrain.net/2012/06/stem-cells-to-cure-multiple-sclerosis.html

NeuroApps: MRI Atlas of Human White Matter By Elsevier, Inc

Ask your doctor to show you this and compare it to where your white matter is damaged. Don't take, 'I don't know' for an answer. They can afford the $99.95 especially since they need it for all their patients.

http://itunes.apple.com/us/app/neuroapps-mri-atlas-human/id508105278

Description

Find, visualize major fiber tracts from 3 orientations and in both MRI and DTI, and learn to identify the major pathways through the brain and their proximity to key neuroanatomical structures. Scroll through the brain in sequence to follow a tract from beginning to end. View one, two, or all three orientations at the same time between coronal, axial, and sagittal sections. This app is the next generation in brain visualization!

An EEG-based study of discrete isometric and isotonic human lower limb muscle contractions

I'll just repeat a line from the abstract.
This type of functional neuroimaging could be a powerful tool for neurological rehabilitation. It could enable clinicians to monitor changes in motor control related cortical dynamics associated with a therapeutic intervention.
Until we get to this level of specificity all the therapy interventions are just a shot in the dark - we could just as well be using bloodletting.
http://www.jneuroengrehab.com/content/9/1/35/abstract

Abstract (provisional)

Background

Electroencephalography (EEG) combined with independent component analysis enables functional neuroimaging in dynamic environments including during human locomotion. This type of functional neuroimaging could be a powerful tool for neurological rehabilitation. It could enable clinicians to monitor changes in motor control related cortical dynamics associated with a therapeutic intervention, and it could facilitate noninvasive electrocortical control of devices for assisting limb movement to stimulate activity dependent plasticity. Understanding the relationship between electrocortical dynamics and muscle activity will be helpful for incorporating EEG-based functional neuroimaging into clinical practice. The goal of this study was to use independent component analysis of high-density EEG to test whether we could relate electrocortical dynamics to lower limb muscle activation in a constrained motor task. A secondary goal was to assess the trial-by-trial consistency of the electrocortical dynamics by decoding the type of muscle action.

Methods

We recorded 264-channel EEG while 8 neurologically intact subjects performed isometric and isotonic, knee and ankle exercises at two different effort levels. Adaptive mixture independent component analysis (AMICA) parsed EEG into models of underlying source signals. We generated spectrograms for all electrocortical source signals and used a naive Bayesian classifier to decode exercise type from trial-by-trial time-frequency data.

Results

AMICA captured different electrocortical source distributions for ankle and knee tasks. The fit of single-trial EEG to these models distinguished knee from ankle tasks with 80% accuracy. Electrocortical spectral modulations in the ankle/knee region of the contralateral sensorimotor cortex were significantly different for isometric and isotonic tasks (p<0.05). Isometric contractions elicited an event related desynchronization (ERD) in the alpha-band (8-12 Hz) and beta-band (12-30 Hz) at joint torque onset and offset. Isotonic contractions elicited a sustained alpha- and beta-band ERD throughout the trial. Classifiers based on contralateral sensorimotor cortex sources achieved a 4-way classification accuracy of 69% while classifiers based on electrocortical sources in multiple brain regions achieved a 4-way classification accuracy of 87%.

Conclusions

Independent component analysis of EEG reveals unique spatial and spectro-temporal electrocortical properties for different lower limb motor tasks. Using a broad distribution of electrocortical signals may improve classification of human lower limb movements from single-trial EEG.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Positive effects of robotic exoskeleton training of upper limb reaching movements after stroke

This is for chronic so thats great, I think I'd prefer the Japanese one
 http://www.jneuroengrehab.com/content/pdf/1743-0003-9-36.pdf
Background
Impairment of upper limb function is one of the most common sequelae following stroke; in
particular arm function is found to be altered in 73% to 88% of first time stroke survivors
(infarctions only), and 55% to 75% still experience problems that impair their activities of
daily living for up to 3 to 6 months or more [1,2].
Impairments limit the patient’s autonomy in daily living and may lead to permanent disability
[3]. The deficits are typically characterized by weakness of specific muscles [4], lack of
mobility between structures at the shoulder girdle [5], incorrect timing of components within
a movement pattern [6,7] and loss of interjoint coordination [8]. Consequently goal directed
movements in hemiplegic patients are characterized by lower movement amplitude,
prolonged movement time, segmented trajectories and abnormal pattern of muscle activation.
Compensatory motor strategies, characterized by adaptations to muscle imbalance [9], are
commonly adopted by stroke patients in attempt to overcome these impairments.
Various rehabilitation interventions to improve skill reacquisition have shown promising
results in overcoming motor impairment after stroke [10].
High intensity and task specific upper limb treatment consisting of active, highly repetitive
movement is one of the most effective approaches to arm function post-stroke restoration
[11-13]. Recent studies moreover suggest that given appropriate training, motor
improvements of the upper limb can continue well into the chronic stage of stroke [14-16].
The use of robot devices in rehabilitation can provide high intensity, repetitive, task specific
and interactive treatment of the impaired upper limb and an objective, reliable mean of
monitoring patients progress. Systematic review confirms the potential for robotic assisted
devices to elicit improvements in upper limb function [17,18]. Moreover virtual reality
provided a unique medium where therapy can be provided within a functional, purposeful and
motivating context and can be readily graded and documented [19]. The cortical
reorganization and associated functional motor recovery after virtual reality in patient with
chronic stroke are documented also by fMRI [20].
 While several studies have already investigated the effects of robot assisted training in planar
movements performed in the horizontal plane [21], the effect of training on the control and
production of multi-joint and spatial functional arm movements, including movements
against gravity, in hemiparetic subjects has received less attention.
It has been already shown that stereotyped movement patterns [8] due to abnormal muscle
co-activation result in a reduced active range of motion against gravity. In particular
providing antigravity limb support, leads to a reduction of the abnormal coupling between
shoulder abduction/elbow flexion [22] and promising results have been found in the robotic
training of patients with antigravity vertical movements that involve shoulder elevation [23].
Moreover orthoses providing only passive gravity assistance to the arm in reaching
movements can induce comparable clinical improvements to those obtained with robotic
training [24].
In this study we have investigated the effects of robot aided training on the recovery of spatial
reaching movements, with a focus on point-to-point reaching movements performed in
different directions, analysing how muscle imbalance in stroke influences the process of
motor recovery in terms of regain of smooth movement, interjoint coordination and
agonistic/antagonistic muscle recruitment.
A robotic treatment was administered through the L-EXOS [25,26], a robotic exoskeleton for
the upper limb, in a group of nine patients with chronic hemiparetic stroke. Exoskeleton
robotic systems allow to execute full spatial multi-joint functional arm movements, including
elevation movements with shoulder abduction, providing either variable gravity support or
active assistance to the impaired arm [27].
To assess the carry-over of the observed improvements in movement during training into
improved function, changes in movement execution and smoothness of motion were analysed
through a kinesiologic assessment, consisting in the motion and dynamic electromyographic
analysis of reaching movements performed before and after training.
The kinesiologic performance (movement time, smoothness of motion) was then analysed in
relation to the changes in the EMG pattern of agonist–antagonist muscle co-activation and
shoulder-elbow interjoint coordination.

Juxtaluminal Black Area in Carotid Artery Plaques May Predict Strokes

I wish they would put a picture in here with pointer arrows.

Juxtaluminal Black Area in Carotid Artery Plaques May Predict Strokes

  Researchers from the Imperial College Faculty of Medicine in London in the United Kingdom (S Kakkos, M Griffin, A Nicolaides, E Kyriacou, M Sabetai, T Tegos, G Geroulakos) revealed that the presence and size of a juxtaluminal black (hypoechoic) area (JBA) on carotid ultrasound of asymptomatic carotid artery plaques can predict the occurrence of ipsilateral ischemic stroke. Their findings were explained today at the 66th Vascular Annual Meeting presented by the Society for Vascular Surgery®.


Co-author Stavros K. Kakkos, MD, MSc, PhD, RVT, who also is in the Department of Vascular Surgery at the University Hospital of Patras in Patras, Greece, said that the JBA is associated with a lipid core close to the lumen or a thrombus on the plaque surface and is defined as an area of carotid plaque pixels with gray scale median (GSM) value less than 25 which is adjacent to the vessel lumen and lacks a visible echogenic cap, after image normalization of the ultrasound plaque images.

This is the best I can find of images; unreadably pathetic.



The size of a JBA was measured in the carotid plaque images of 1,121 patients with asymptomatic carotid stenosis that was 50-99 percent in relation to the bulb which was followed for up to eight years. “We confirmed that JBA had a linear association with future stroke rate,” said Dr. Kakkos. “The area under the ROC curve was 0.816. Using Kaplan Meier curves, the mean annual stroke rate was 0.4 percent in 706 patients with a JBA size <4 mm2, 1.4 percent in 171 patients with JBA size 4-8 mm2, 3.2 percent in 46 patients with JBA size 8-10 mm2, and 5 percent in 198 patients with JBA size >10 mm2 with a highly significant statistical significance (P<.001).”


In multivariate analysis using a Cox model with ipsilateral ischemic events (amaurosis fugax, transient ischemic attack [TIA] or stroke) as the dependent variable, JBA (<4, 4-8, >8, in mm2) was still significant after adjusting for other plaque features known to be associated with increased risk. These include stenosis, GSM, presence of discrete white areas without acoustic shadowing (DWA) indicating neovascularization, plaque area and history of contralateral TIA or stroke. However, plaque area and GSM were not significant.


Using the significant variables (stenosis, DWA, JBA and history of contralateral TIA or stroke), this model predicted the annual risk of stroke (range 0.5-10.0 percent). The average annual stroke risk was <1 percent in 734 patients; 1-1.9 percent in 94; 2-3.9 percent in 134; 4-5.9 percent in 125; and 6-10 percent in 34.


“The size of JBA is linearly related to the risk of stroke and can be used in risk stratification models,” said Dr. Kakkos. “These findings need to be confirmed in future prospective studies or in the medical arm of randomized controlled studies in the presence of optimal medical therapy.”

Games for Stroke rehabilitation

While this is a worthwhile study this person should have realized that therapy after the fact needs to be avoided at all costs. The therapy works poorly and needs to be avoided. One of the main ways to do that is to prevent the neuronal cascade of death. Then the focus could be on neurogenesis and stem cells to replace the dead area.
Doesn't anyone think through what needs to completely change for stroke rehab?
 http://www.cs.auckland.ac.nz/compsci705s1c/exams/SeminarReports/Final%20Report%20epen234.pdf
Full 4 pages at the link.
ABSTRACT
Strokes are a leading cause of death and disability and have been described as a “worldwide epidemic” [5]. Strokes cause disability, partial paralysis and leave up to 85% of their victims with some form of motor impairment. Stroke rehabilitation starts as soon as possible and involves repetitive movement which people find repetitive and boring. A study [1] has found that as few as 31% of people complete their exercises as recommended. Adding to this the high cost of one on one therapy and transport to see specialists, stroke rehabilitation is a major problem. Games have been trialed for stroke rehabilitation to increase patient motivation and reduce costs. This literature review aims to find out to what extent games have therapeutic value and further, what characteristics make a good game for stroke rehabilitation. We find that in order for a game to be successful it must be based on solid therapeutic principles as well as game design principles including “challenge” and “meaningful feedback”. Different hardware and software can be used as long as it follows game design principles to encourage patients to perform therapeutic exercises. Games must also take into account the low morale of recent stroke victims and avoid discouraging beginners.

Models of CNS injury in the nonhuman primate: A new era for treatment strategies

This stuff needs more visibility, with 1000 failed human therapies that worked in rats or mice this shouldn't be behind a 34.95 paywall. Ask your doctor to get this for you.
http://www.springerlink.com/content/t2h3u213231k5622/

Abstract

Central nervous system (CNS) injuries affect all levels of society indiscriminately, resulting in functional and behavioral deficits with devastating impacts on life expectancies, physical and emotional wellbeing. Considerable literature exists describing the pathophysiology of CNS injuries as well as the cellular and molecular factors that inhibit regrowth and regeneration of damaged connections. Based on these data, numerous therapeutic strategies targeting the various factors of repair inhibition have been proposed and on-going assessment has demonstrated some promising results in the laboratory environ. However, several of these treatment strategies have subsequently been taken into clinical trials but demonstrated little to no improvement in patient outcomes. As a result, options for clinical interventions following CNS injuries remain limited and effective restorative treatment strategies do not as yet exist. This review discusses some of the current animal models, with focus on nonhuman primates, which are currently being modeled in the laboratory for the study of CNS injuries. Last, we review the current understanding of the mechanisms underlying repair/regrowth inhibition and the current trends in experimental treatment strategies that are being assessed for potential translation to clinical applications.

Who Needs Professionals? A new book says scientific innovation will come from the minds of "amateurs."

Medically we do need professionals because we can't practice medicine without a license. However we can point out the incompetence(naked emperor and all) of the stroke research and rehab practitioners.
I believe in throwing bombs, someday someone will contradict everything I have to say. I look forward to that day.
http://www.genomeweb.com//node/1082801
Author and New York Times Magazine contributing editor Jack Hitt has written a book called Bunch of Amateurs: A Search for the American Character, in which he talks about how important garage tinkerers and weekend innovators are in America, and how much they contributed to all facets of society. In an excerpt of the book published in Popular Science, Hitt says the next breakthrough in synthetic biology may come from an amateur scientist tinkering around in a garage. "Ever since Ben Franklin left Boston for Philadelphia, and continuing right up through when Mark Zuckerberg abandoned Harvard Square for Palo Alto, there has been this sense that a certain kind of creativity happens on the fly, often on the lam, after beginning in one of those proving grounds of American ingenuity: the dorm room, the weekend hobby club, the garage," Hitt writes. He describes San Francisco resident and DIY biologist Meredith Patterson, who shows Hitt her equipment made up of common household devices, takes him to a Trader Joe's where she gets some of her supplies, and gives him a demonstration of her work with green fluorescent protein.
"Ask most people about the amateur spirit, and they'll say, well, that was then. It's almost common wisdom that the golden age of the self-invented upstart ended sometime about a generation ago," Hitt writes. "But the fact is, we've been hearing this line for at least a century, and it's always wrong. The time of outsiders and amateurs and cranks is not a bygone era, but rather a cycle that comes around just when you think it's over. This cycle is an essential part of America's history — arguably the country's genesis story."

Drinking Coffee May Delay Alzheimer’s Disease

So is this enough to reduce our risk to normal levels? Where are our researchers on this question?

Link of Alzheimers to stroke here:

Drinking Coffee May Delay Alzheimer’s Disease

 http://www.webmd.com/alzheimers/news/20120607/coffee-may-help-turn-tide-on-alzheimers-disease

Drinking three cups of coffee per day may help turn the tide against Alzheimer's disease among older adults who are already showing signs of memory problems, a new study shows.

According to the findings, people older than 65 who had higher blood levels of caffeine developed Alzheimer's disease two to four years later than their counterparts with lower caffeine levels. The findings will appear in the Journal of Alzheimer's Disease.

Full article at the link.

I have to do this right now in order to combat my continuous fatigue.

Letting a chiropractor 'crack' your neck to ease pain could trigger stroke

Most of the commentators on this story refuse to believe in anything scientific.
Don't do it. No one even discusses whether chiropractic has any basis in science, subluxations anyone?
The chiropractic version of subluxation;
 http://www.chiro.org/LINKS/subluxation.shtml
The  reformed chiropractor version here;
http://quackfiles.blogspot.com/2004/09/elusive-chiropractic-subluxation.html
The health article here;
http://www.dailymail.co.uk/health/article-2156179/Letting-chiropractor-crack-neck-ease-pain-trigger-stroke.html?ito=feeds-newsxml
In a medical debate on bmj.com, experts argue the technique is ‘unnecessary and inadvisable’. 
Researchers, writing in the British Medical Journal, say the representatives of chiropractors and osteopaths should advise their members the risks outweigh the benefits by too much to justify the use of manipulation.

wheelchair like segway

The WHILL turns any wheelchair into an electric vehicle.

Just think, no more one armed or one-legged driving your wheelchair.

 http://www.gizmag.com/whill-powered-wheelchair/20784/

Wheelchair users with full use of their arms generally don't need electric wheelchairs ... but sometimes, especially if those users have long distances to cover, it sure would be nice to have one. Instead of going out and buying themselves a full electric wheelchair, however, those people may soon have the option of using a WHILL. Recently spotted by Gizmag staff at the Tokyo Motor Show, the prototype device clamps onto the wheels of an existing manual wheelchair, temporarily providing it with electric drive.

 

37 second video here:
http://www.youtube.com/watch?feature=player_embedded&v=tCa_7n4e5eQ

Job search

After being forced out last October I went on the search for a new job. I decided that I wanted to get back into mainframe programming, something I had done with great skill for 25+ years. I created 2 resumes, one chronological which went back 32 years and one functional which summarized my skills and listed months of experience. Resume coaches suggest after you get past a certain age you just use a functional one because it doesn't directly say how old you are. My experience was that recruiters hated that one because they couldn't determine how old your experience was. So I created a composite and just blasted all my experience into one long time period. You hear from the unemployment agency that 85% of all jobs are found by word-of-mouth. In my profession internet job boards are the only way to apply for jobs and you hope that the search firm thinks well enough of your resume to pass it onto the hiring company. I also heard that employers won't hire men with beards. My resume seemed to do the job, I got lots of calls on it but lots fewer references to the hiring managers. I think this was because I only had 8 out of the 10 requirements needed. I didn't get to use  the response I used 32 years ago when I was asked why they should hire me, ' Because I'm the smartest person they will hire'. God I'm arrogant. In February I had a contingent offer from Lockheed-Martin in West Virginia if they got a contract from the government, they didn't get it. Went through three interviews for a MN state colleges job, I think I blew the answer to the question,'Why do you want to work for us?' I had initial interviews for contracts in Bloomington IL, Madison, Omaha and Eveleth,MN. Three phone interviews for an IBM job in East Lansing MI, received and accepted an offer from them. I start there June 20, getting a furnished apt. I get to work on really old school programming language of Assembler, which I actually love doing and am very good at it.


The hiring world has changed. Gone are the days when you walked into a business and applied for a job in person.

"Email your resume," they say. "Go to our website." "Apply online."

Is it easy? Maybe. Is it frustrating? YES.
The internet makes it too easy for employers to hide. Too easy for them to brush off a simple response. And too hard for you to take that next critical step and follow up with the decision-makers after applying for a job.

Contact me if  you would like to get together in Lansing.
Some coding;
PRODPAGE NOP continue
MVI PRODPAGE+1,x'f0'
Continue DS 0h
  Who can tell me what that set of instructions does? I may not have remembered it quite correctly.

I'll leave you with an old programming joke.
There are 10 types of people in the world, those that understand binary and those that don't. Think about it. This statement is completely true, you are making an incorrect assumption of what 10 stands for.
And a cartoon that hung on my wall for years.

Function electrical stimulation mediated by iterative learning control and 3D robotics reduces motor impairment in chronic stroke

All these words  expended and my explanation for the results given is quite simple - They de-weighted the arm. All the rest is just superfluous. I can do the same with my cane.
http://www.jneuroengrehab.com/content/9/1/32/abstract

Abstract (provisional)

Background

Novel stroke rehabilitation techniques that employ electrical stimulation (ES) and robotic technologies are effective in reducing upper limb impairments. ES is most effective when it is applied to support the patients' voluntary effort; however, current systems fail to fully exploit this connection. This study builds on previous work using advanced ES controllers, and aims to investigate the feasibility of Stimulation Assistance through Iterative Learning (SAIL), a novel upper limb stroke rehabilitation system which utilises robotic support, ES, and voluntary effort.

Methods

Five hemiparetic, chronic stroke participants with impaired upper limb function attended 18, 1 hour intervention sessions. Participants completed virtual reality tracking tasks whereby they moved their impaired arm to follow a slowly moving sphere along a specified trajectory. To do this, the participants' arm was supported by a robot. ES, mediated by advanced iterative learning control (ILC) algorithms, was applied to the triceps and anterior deltoid muscles. Each movement was repeated 6 times and ILC adjusted the amount of stimulation applied on each trial to improve accuracy and maximise voluntary effort. Participants completed clinical assessments (Fugl-Meyer, Action Research Arm Test) at baseline and post-intervention, as well as unassisted tracking tasks at the beginning and end of each intervention session. Data were analysed using t-tests and linear regression.

Results

From baseline to post-intervention, Fugl-Meyer scores improved, assisted and unassisted tracking performance improved, and the amount of ES required to assist tracking reduced.

Conclusions

The concept of minimising support from ES using ILC algorithms was demonstrated. The positive results are promising with respect to reducing upper limb impairments following stroke, however, a larger study is required to confirm this.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

High-tech sports tool helping stroke, brain-injury patients at Edmonton rehab hospital

Demand your stroke clinic have something similar.
http://metronews.ca/news/edmonton/254747/high-tech-sports-tool-helping-stroke-brain-injury-patients-at-edmonton-rehab-hospital/
Mell Snyder knows he is well on the road to recovery thanks to work at the Glenrose Rehabilitation Hospital – because he got his driver’s licence back.
The 62-year-old Lamont man had a stroke in March, leaving him with blurred vision and right-side weakness.
He wraps up rehab in Edmonton next week – and credits recently acquired technology for helping him get to this point.
“It’s improved my reaction, it’s improved my feeling,” said Snyder. “So it will get me back in the workforce.”
Dynavision D2 is a computerized light board with tiny buttons that light up. Numerous drills can be run on the board, all with the idea of hitting whichever buttons are lit.
The technology was first developed for professional athletes to improve hand-eye co-ordination, reaction time, peripheral vision, visual awareness and concentration skills.
“It’s nice to have a piece of equipment that has summarized actual data,” said Quentin Ranson, rehabilitation technology leader. “The patients can see their improvements.”
The equipment arrived about a year ago, and between 10 and 15 patients train twice weekly on it every month.
“It’s being used more and more,” said Ranson. “The trend has bumped up since the new year.”
The equipment resides in the Building Trades of Alberta Courage Centre and was donated by the Glenrose Rehabilitation Hospital Foundation.

Picture at the link.

Information, at the point where it’s needed, can save a life

For all us patients, Dave has some good points to make.
http://epatientdave.com/2012/06/03/information-at-the-point-where-its-needed-can-save-a-life-new-speech/
The Kanter Family Foundation “was born of the frustrations [Joseph Kanter] faced as a prostate cancer patient unable to obtain scientific evidence about ‘what works best’ in health care, based on the collective real-world experiences of other patients – evidence that would have helped me, and others like me, make better informed, life-or-death health decisions.”
This sounds exactly like what is wrong with stroke care. With only a 10% success rate for full recovery, we need Dr. Algorithm.

Feeling Depressed? Get...Botox? - Bodily Feedback and the implications of Embodied Cognition for Psychiatry

This is not botox for spasticity.
http://mancpsychsoc.blogspot.com/2012/05/feeling-depressed-get-botox-bodily.html
The cartoon here is pretty good.

Some antibiotic, antifungal drugs don’t mix with warfarin

Read this from Harvard Health publications
 http://www.health.harvard.edu/blog/some-antibiotic-antifungal-drugs-dont-mix-with-warfarin-201206074857
Millions of people depend on the blood thinner warfarin to prevent clots from forming in their blood. It’s an important drug, but tricky to use. One problem with warfarin (Coumadin, Jantoven, generic) is that it interacts in potentially harmful ways with other medications. Two problematic types are antibiotics and antifungal agents. As we write in the June issue of the Harvard Heart Letter, this isn’t just a problem with pills, but can also happen with ointments, creams, and suppositories.
Rest at link.

Safe, simple eye test may help save lives by preventing stroke

So we would need to know the difference between optometrists and ophthalmologists and what the large eye chains use.
http://www.sciencecodex.com/safe_simple_eye_test_may_help_save_lives_by_preventing_stroke-92935
A simple eye test may someday offer an effective way to identify patients who are at high risk for stroke, say researchers at the University of Zurich. They showed that a test called ocular pulse amplitude (OPA) can reliably detect carotid artery stenosis (CAS), a condition that clogs or blocks the arteries that feed the front part of the brain. It's a known risk factor for stroke. The OPA test could be performed by ophthalmologists – physicians who treat eye diseases – during routine exams. The study, which is published in the June issue of Ophthalmology, the journal of the American Academy of Ophthalmology, confirmed that patients who had the lowest OPA scores also had the most seriously blocked arteries.
Each year, approximately 795,000 Americans suffer a new or recurrent stroke, and more than 137,000 of these people die as a result. People with severe CAS are much more likely to suffer stroke. Physicians would like to catch and treat CAS before that can happen, but because CAS has no symptoms and an efficient test is not currently available, the disease often goes undetected.
The Swiss research team used a device called the dynamic contour tonometer to check the OPA of 67 patients who were assumed to have CAS. The OPA score is calculated by finding the difference between the two pressure levels that occur inside the eye during the two phases of the heartbeat − the systolic and diastolic. The tonometer measures the two pressure levels, then instantly computes the patient's OPA score. When blood flow to the eye is blocked by CAS, there is not much difference between the two pressure levels, so the OPA score is low. The study confirmed that patients with the lowest OPA scores also had the most seriously blocked arteries. The researchers used ultrasound exams to corroborate that each study participant had CAS and to detail the severity of his or her blockage.
"Our results show that ocular pulse amplitude is a reliable, safe screening test for carotid artery stenosis," said lead researcher Pascal Bruno Knecht, M.D. "We recommend further study to confirm the value of using OPA to detect and assess the severity of CAS and to define its use in stroke prevention."
A research review performed for the U.S Preventive Services Task Force indicated that if an efficient screening test for CAS were available, the incidence of stroke and fatalities due to stroke could be substantially reduced. The review stated that the test should be able to detect clinically significant CAS, defined as 60 percent to 99 percent blockage of the carotid arteries. Some high-tech tests, such as magnetic resonance angiography and color duplex ultrasound, already meet this standard, but they are expensive and not widely available. Their primary use is in diagnosing patients who already have symptoms of stroke.
It could be efficient to perform the OPA test during a standard eye exam, if the ophthalmologist is already using the dynamic contour tonometer to screen for glaucoma. This type of tonometer is not widely used in the United States, although it is in Europe.
The researchers say that other than CAS, very few diseases could cause low OPA scores, and that an ophthalmologist could easily rule out these other diseases during an eye exam.

Stem Cells Behind Clogged Arteries, Mouse Study Reveals

The article itself here:
http://www.nature.com/ncomms/journal/v3/n6/full/ncomms1867.html

Abstract

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It is generally accepted that the de-differentiation of smooth muscle cells, from the contractile to the proliferative/synthetic phenotype, has an important role during vascular remodelling and diseases. Here we provide evidence that challenges this theory. We identify a new type of stem cell in the blood vessel wall, named multipotent vascular stem cells. Multipotent vascular stem cells express markers, including Sox17, Sox10 and S100β, are cloneable, have telomerase activity, and can differentiate into neural cells and mesenchymal stem cell-like cells that subsequently differentiate into smooth muscle cells. On the other hand, we perform lineage tracing with smooth muscle myosin heavy chain as a marker and find that multipotent vascular stem cells and proliferative or synthetic smooth muscle cells do not arise from the de-differentiation of mature smooth muscle cells. In response to vascular injuries, multipotent vascular stem cells, instead of smooth muscle cells, become proliferative, and differentiate into smooth muscle cells and chondrogenic cells, thus contributing to vascular remodelling and neointimal hyperplasia. These findings support a new hypothesis that the differentiation of multipotent vascular stem cells, rather than the de-differentiation of smooth muscle cells, contributes to vascular remodelling and diseases.

Ask your doctor what this means.
Popular   articles here:
http://news.health.com/2012/06/06/stem-cells-behind-clogged-arteries-mouse-study-reveals/
and here:

Newly discovered blood vessel stem cells point to new therapies for vascular disease

Report: Pradaxa tops FDA’s list for serious adverse events

Make sure you get from your doctor what to look for adverse events from Pradaxa or warfarin or statins.
http://www.cardiovascularbusiness.com/index.php?option=com_articles&view=article&id=34247:report-pradaxa-tops-fdas-list-for-serious-adverse-events
Dabigatran topped the list of direct reports to the FDA of serious adverse drug events in 2011, according to an analysis by the Institute for Safe Medication Practices. Dabigatran (Pradaxa, Boehringer Ingelheim) had the largest number of direct reports, at 817, followed by warfarin, at 490.

Reports from both the manufacturer and direct reports pointed to 3,781 serious adverse events associated with dabigatran in the U.S. in 2011, according to the analysis. Analysts identified 542 patient deaths, 2,367 cases of hemorrhage, 291 cases of acute renal failure, 644 cases of stroke and 15 cases of suspected liver failure. The FDA approved the use of dabigatran for the prevention of stroke and systemic embolism in non-valvular AF patients in 2010.

Warfarin had 1,106 cases overall in 2011, including 72 deaths. The authors noted that in past analyses, warfarin consistently ranked near the top for direct reports to the FDA.

“Two drugs that inhibit the formation of blood clots ranked first and second among all direct reports to the FDA in 2011, emphasizing that the combination of a vulnerable patient population and a powerful pharmacological action rank among the highest risks in prescription drug therapy,” the authors wrote in the report, QuarterWatch. “While a therapeutic goal of preventing strokes, pulmonary embolism, and other harm through unwanted blood clots is a worthy objective, these results demonstrate that treatment is accompanied by substantial risks.”

The European Medicines Agency (EMA) reported May 25 that its post-marketing data on dabigatran showed that the frequency of occurrence of fatal bleedings was significantly lower than what was observed in clinical trials. Nonetheless, the EMA called for an update of product information to give physicians clearer guidance on how to reduce and manage the risk of bleeding.

By QuarterWatch’s count, the FDA received 179,855 reports of serious, disabling and fatal adverse drug events in the U.S. in 2011, an increase of 9.4 percent from 2010. The majority, 88 percent, were submitted by drug manufacturers while the remaining 12 percent were submitted to the FDA by health professionals and patients.

In a section on suspect drugs linked to severe side effects in the U.S., the report listed simvastatin (Zocor, Merck) and rosuvastatin (Crestor, AstraZeneca) as first and second most frequently identified drugs linked to severe muscle damage in 2011. Simvastatin had 123 cases and rosuvastatin 73 cases. By contrast, atorvastatin (Lipitor, Pfizer) accounted for only 15 reported cases.

QuarterWatch is published by the Institute for Safe Medication Practices, a Horsham, Pa.-based nonprofit organization that monitors adverse drug events reported to the FDA. The QuarterWatch reports are funded through the institute and are based on analyses of computer excerpts that the agency releases for research use from its Adverse Event Reporting System.

A Phase 1/Phase 2 Study of Dalfampridine 10mg Extended Release Tablet in Subjects With Chronic Deficits After Ischemic Stroke

The actual trials I blogged about. Note the term chronic. If your doctor doesn't know about this, ask why.  Consult your doctor before joining.
Previous post;
http://oc1dean.blogspot.com/2012/05/acorda-therapeutics-presents.html

Recruitment here: Florida, Georgia, Virginia
http://www.clinicaltrials.gov/ct2/show/NCT01605825?term=Acorda&rank=4

Risk Score May Be Better ED Stroke Screen

Once again this is being looked at wrong, trying to make a subjective measure better, rather than figuring out an objective measurement like urine testing, blood testing, impedance spectroscopy.

The risk scoring here;
http://www.medpagetoday.com/Cardiology/Strokes/33106
Using a modified ABCD² risk score may be a better approach than the decades-old emergency department strategy of using subjective measures to assess dizzy patients for stroke, researchers suggested.
The modified ABCD² score -- which includes Age, Blood pressure, Clinical features, Diabetes, and Duration of symptoms -- was significantly higher for those presenting with dizziness who had cerebrovascular events than for those who did not have such events, reported Anthony S. Kim, MD, from the University of California in San Francisco, and colleagues.
Specifically, age over 60, blood pressure above 140/90 mmHg, and clinical features such as unilateral weakness or speech disturbance without weakness, but not diabetes were found significantly more often in those with cerebrovascular events, according to the study published in the June issue of Stroke: Journal of the American Heart Association.
The assessment of dizziness in the emergency department is currently based on a "symptom quality" approach that looks at vertigo, presyncope, disequilibrium, or nonspecific dizziness, a strategy which has "limited clinical utility in the ED setting," the researchers noted in their introduction.
The ABCD² score is well validated to predict stroke after transient ischemic attack (TIA), but it is unknown whether the application of this tool would work with those presenting with dizziness in the emergency department.
Dizziness is a common patient symptom, accounting for 3.3% of emergency department visits in the U.S. each year, and although it is usually attributable to benign etiologies such as peripheral vertigo, up to 5% of acute dizziness cases may be from cerebrovascular disease, they noted.
The modified ABCD² risk predictor, with a possible range of 0-7 points, is scored as follows:

• 1 point for age over 60
• 1 point for blood pressure over 140/90 mmHg
• 2 points for unilateral weakness, and 1 point for speech disturbance without weakness
• 1 point for diabetes
• 1 point for symptom duration of 10 to 59 minutes, and 2 points for symptom duration ≥60 minutes

The duration of symptoms was not readily available to investigators for this study, so they categorized all patients as having symptoms greater than an hour (2 points), "which effectively removes the contribution of this item to the overall score."
For the study, Kim and colleagues retrospectively identified 907 patients presenting to the UCSF emergency department complaining of dizziness, vertigo, or imbalance from 2007 to 2009.
In total, 4.1% of these patients had a cerebrovascular cause of dizziness: of those, 65% were ischemic strokes, 22% were TIAs, and 14% were intracerebral hemorrhages.
The mean age of those with a cerebrovascular event was 73, compared with 58 for those without such an event. Most of those with an event were men (75%) and were white (59%). Those with a cerebrovascular event had more risk factors than those without, and hypertension was the most prevalent risk factor (86%).
In both adjusted and unadjusted analysis, the individual components of the ABCD² except diabetes were significantly more common in those with cerebrovascular events.
Kim and colleagues reported that the c-statistic for the ABCD² score for predicting cerebrovascular event as the cause of dizziness was 0.79 (95% CI 0.73 to 0.85).
The median modified ABCD² score was 3. Five of 512 patients with an ABCD² score of 3 or less had a cerebrovascular event. However, 25 of 369 patients with a score of 4 or 5, and seven of 26 patients with a score of 6 or 7, all had cerebrovascular events.
The investigators concluded that the modified ABCD² score is effective at identifying those at low risk of cerebrovascular events who present with dizziness.
Given that there is room for clinical judgment, researchers said that their results "suggest that it may be possible to develop a risk score for dizziness to help streamline evaluations and target costly testing, consultation, and observation to the most appropriate patients."
The results may not be generalizable to other emergency departments, especially those that do not have 24/7 access to neruoimaging, researchers said. Also, they did not always know the specific features of dizziness, and follow-up data were not always complete.
Another limitation was the incomplete availability of duration of symptoms, which could have changed the performance of the model, Kim and colleagues said. Finally, they said the modified ABCD² risk score should be tested prospectively.

Changes in Brain Network May Be Behind Post Stroke Depression

Or is it because 10 days in your medical staff has not told you anything concrete about how to recover or what the prospect of full recovery is.  By using the terms, 'All strokes are different, all stroke recoveries are different', the medical staff has basically told you that they know nothing. I would be depressed after hearing that.
http://www.medicaldaily.com/news/20120605/10168/post-stroke-depression-brain.htm

Post stroke depression is associated with changes in network of brain that involves emotional regulation, says a new study.
For the study, the researchers looked at brain scans of 24 patients between ages 18 and 80 who recently had a stroke. The brain scans were taken 10 days after stroke.

inShare

The participants were evaluated for signs of depression 10 days after the stroke and once again at 3 months after the stroke.
Ten people in the study group had mild depression while 14 people were found to be without depression.
The brain scans of the people who developed depression had modification in their DMN or default-mode network. According to the researchers, modifications in DMN have been seen in depressive patients.

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"A third of patients surviving a stroke experience post-stroke depression (PSD)," said Dr. Igor Sibon, professor of neurology at the University of Bordeaux in Bordeaux, France, and the lead researcher of the study.
"However, studies have failed to identify a link between lesions in the brain caused by ischemia during a stroke and subsequent depression," Dr. Sibon said.
The brain scans of the participants were taken while they rested. Instead of looking at a specific region of the brain, the researchers looked at the entire network of emotional regulation.
"The default-mode network is activated when the brain is at rest. When the brain is not actively involved in a task, this area of the brain is engaged in internal thoughts involving self-related memory retrieval and processing," Dr. Sibon said.
Post stroke depression or PSD is a common occurrence with approximately one third of stroke survivors experiencing depression either immediately or after a few days. But, PSD often remains under-treated due to ineffective diagnosis.
Previous studies say that antidepressants might be helpful in treating people with PSD.
"We found a strong association between early resting-state network modifications and the risk of post-stroke mood disorders. These results support the theory that functional brain impairment following a stroke may be more critical than structural lesions," Dr. Sibon said.

StrokePAD: Canadian students develop innovative technology for stroke rehabilitation

Why does it take students to develop new stuff?
http://www.canadianstrokenetwork.ca/csnblog/strokepad-canadian-students-develop-innovative-technology-for-stroke-rehabilitation/
Clinicians needed to test new iPAD app with stroke patients

Morgan Moe is a Kinesiology graduate from Calgary AB who has also been a long-time volunteer, practicum student, and employee at the Association for the Rehabilitation of the Brain Injured (arbi.ca). It was through her work there that an idea first sparked her interest: “I wanted to create an app that would empower patients with better resources to be more engaged in rehabilitation, even from the comfort of their own homes.” It was shortly thereafter that Morgan was accepted into a prestigious entrepreneurship program called The Next 36 (thenext36.ca). This program selects 36 top undergraduates from across Canada and provides seed funding, incredible mentorship and MBA-level education for an entrepreneurial venture.
Through The Next 36, Morgan was teamed up with Simon Jalbert, Commerce graduate from Saint-Mary’s University, Anne-Marie Paquette, Architecture graduate from McGill, and Ben Docksteader, a Computer Science student from PEI. Together the team has worked diligently to pursue their mission of empowering stroke patients and caregivers. Morgan explains, “Alone this would have never been possible. The Next 36 has provided us with a phenomenal opportunity to blend a variety of individual strengths to create a truly transformative piece of technology that can have a tremendous impact on people’s lives.“
StrokePAD is a tablet application designed for patient use, which provides support in navigating care options, individualized health reference materials to prevent a secondary stroke, and personalized rehabilitation programs. The application connects with a web portal through which professionals can design, deliver, remotely change, and monitor rehabilitation programs.
The StrokePAD team is currently looking for healthcare professionals to get involved, institutions to trial the app with their patients, and academic partners looking for research opportunities. All interested individuals are encouraged to contact Morgan at morgan@strokepad.ca

Neural population dynamics during reaching

Getting a better understanding of how motor neurons work. This sounds similar to what Sebastian Seung talks about in Connectome.
Abstract here;
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11129.html
More understandable news story here;
http://www.newswise.com/articles/rhythmic-firing-of-nerves-involved-in-body-s-movements

Stroke rehab while driving a car

Don't even think of doing this.  This is my thought process, I have 4 options  to choose from.  I'm left side affected and cognitively can handle this limited amount of multitasking.
Is it warmer than 55 degrees? Not raining? Rain provides lots of tiny points of pain on bare skin.
1. Yes. Roll down the window before you start driving, I have to use my right hand to control the buttons.  I then lift my left arm out the window with my right arm and shove the hand below the window ledge. This is trying to relax the spasticity of my pecs and biceps, also creates extra sensation of the wind blowing against it. If its sunny extra vitamin D and maybe even sunburn to continue the pain later.
2. Lift my right leg enough to get my left thumb under it, and try to relax the fingers enough to let them dangle. This I do a lot when driving in town.
3. Grab the steering wheel with the left hand at the 7 o'clock position and just let it relax there. This is only possible  when stopped and then traveling on a straight road.
4. Grab the steering wheel at the 11 o'clock position, locking the elbow in a straight position. This is only possible on an on ramp on the interstate. I never let up on the steering knob in my right hand.  This position means I can't use my right hand to reach over and turn on the turn signals.

My next purchase will be a kids steering wheel so I can practice safely. Nothing here  should be considered any kind of medical endorsement, you know me I'm extremely stupid.

Noninvasive brain stimulation shown to impact walking patterns

I wonder if this corrects the spastic leg muscles?
http://medicalxpress.com/news/2012-06-noninvasive-brain-shown-impact-patterns.html
Previous studies in the lab of Amy Bastian, PhD, PT, director of the Motion Analysis Laboratory at Kennedy Krieger Institute, have shown that the cerebellum, a part of the brain involved in movement coordination, is essential for walking adaptation. In this new study, Dr. Bastian and her colleagues explored the impact of stimulation over the cerebellum on adaptive learning of a new walking pattern. Specifically, her team tested how anode (positive), cathode (negative) or sham (none) stimulation affected this learning process.
"We've known that the cerebellum is essential to adaptive learning mechanisms like reaching, walking, balance and eye movements," says Dr. Bastian. "In this study, we wanted to examine the effects of direct stimulation of the cerebellum on locomotor learning utilizing a split-belt treadmill that separately controls the legs."
The study, published today in the Journal of Neurophysiology, found that by placing electrodes on the scalp over the cerebellum and applying very low levels of current, the rate of walking adaptation could be increased or decreased. Dr. Bastian's team studied 53 healthy adults in a series of split-belt treadmill walking tests. Rather than a single belt, a split-belt treadmill consists of two belts that can move at different speeds. During split-belt walking, one leg is set to move faster than the other. This initially disrupts coordination between the legs so the user is not walking symmetrically, however over time the user learns to adapt to the disturbance.
The main experiment consisted of a two-minute baseline period of walking with both belts at the same slow speed, followed by a 15-minute period with the belts at two separate speeds. While people were on the treadmill, researchers stimulated one side of the cerebellum to assess the impact on the rate of re-adjustment to a symmetric walking pattern.
Dr. Bastian's team found not only that cerebellar tDCS can change the rate of cerebellum-dependent locomotor learning, but specifically that the anode speeds up learning and the cathode slows it down. It was also surprising that the side of the cerebellum that was stimulated mattered; only stimulation of the side that controls the leg walking on the faster treadmill belt changed adaptation rate.
"It is important to demonstrate that we can make learning faster or slower, as it suggests that we are not merely interfering with brain function," says Dr. Bastian. "Our findings also suggest that tDCS can be selectively used to assess and understand motor learning."
The results from this study present an exciting opportunity to test cerebellar tDCS as a rehabilitation tool. Dr. Bastian says, "If anodal tDCS prompts faster learning, this may help reduce the amount of time needed for stroke patients to relearn to walk evenly. It may also be possible to use tDCS to help sustain gains made in therapy, so patients can retain and practice improved walking patterns for a longer period of time. We are currently testing these ideas in individuals who have had a stroke."

Motor memory: The long and short of it

Good info for us to understand as we recover. So maybe my continual switching from task to task is helpful. It needs to be compared to massed practice and see at what point the switching should occur.
http://medicalxpress.com/news/2011-09-motor-memory-short.html
The research — from a team led by Nicolas Schweighofer of the Division of Biokinesiology and Physical Therapy at USC — could potentially pave the way to more effective rehabilitation for stroke patients.
It turns out that the phenomenon of motor memory is actually the product of two processes: short-term and long-term memory.
If you focus on learning motor skills sequentially — for example, two overhand ball throws — you will acquire each fairly quickly, but are more likely to forget them later. However, if you split your time up between learning multiple motor skills — say, learning two different throws — you will learn them more slowly but be more likely to remember them both later.
This phenomenon, called the "contextual interference effect," is the result of a showdown between your short-term and long-term motor memory, Schweighofer said. Though scientists have long been aware of the effect's existence, Schweighofer's research is the first to explain the mechanism behind it.
"Continually wiping out motor short-term memory helps update long-term memory," he said.
In short, if your brain can rely on your short-term motor memory to handle memorizing a single motor task, then it will do so, failing to engage your long-term memory in the process. If you deny your brain that option by continually switching from learning one task to the other, your long-term memory will kick in instead. It will take longer to learn both, but you won't forget them later.
"It is much more difficult for people to learn two tasks," he said. "But in the random training there was no significant forgetting."
Schweighofer uncovered the mechanism while exploring the puzzling results of spatial working memory tests in individuals who had suffered a brain stroke.
Those individuals, whose short-term memory is damaged from the stroke, show better long-term retention because they are forced to rely on their long-term memories.
Schweighofer's paper appears in the August issue of Journal of Neurophysiology.
In the long term, he said he hopes this research could help lead to computer programs that optimize rehabilitation for stroke patients, determining what method of training will work best for each individual.

Dark Chocolate: Sweet Prevention for CV Events

Someday, someone will consolidate all the food and supplement preventions in one place. I expect a medical person should do that because we patients are too stupid to understand research.
http://www.medpagetoday.com/Cardiology/Prevention/33010
Dark chocolate may be an inexpensive way to help prevent cardiovascular events in patients at risk for heart disease, researchers found.
A modeling study predicts that patients with metabolic syndrome who eat dark chocolate every day could have 85 fewer events per 10,000 population over 10 years, Chris Reid, PhD, of Monash University in Melbourne, and colleagues reported online in BMJ.
At a cost of only $42 per year, treatment with dark chocolate falls into an acceptable category of cost-effectiveness, at an incremental cost-effectiveness ratio (ICER) of $50,000 per years of life saved.
"Chocolate benefits from being by and large a pleasant, and hence sustainable, treatment option," they wrote. "Evidence to date suggests that the chocolate would need to be dark and of at least 60% to 70% cocoa, or formulated to be enriched with polyphenols." This is not your regular Hersheys or chocolate kisses.
Several recent studies have suggested that eating dark chocolate has blood-pressure and lipid-lowering effects. To assess whether it could be an effective and cost-effective treatment option in patients potentially at risk for cardiovascular events, the researchers looked at data from patients in the Australian Diabetes, Obesity, and Lifestyle study.
They used a Markov model to assess health effects and associated costs of daily consumption of plain dark chocolate compared with no chocolate in a population with metabolic syndrome but without diabetes or cardiovascular disease.
The investigators also used risk-prediction algorithms and population life tables to determine the probability of patients developing or dying from heart disease or other noncardiovascular causes each year.
Data on the blood-pressure-lowering effects of dark chocolate were taken from a meta-analysis of 13 randomized controlled trials, and lipid-lowering effects from a meta-analysis of eight short-term trials.
Costs were taken from a review of the costs of cardiovascular complications in a healthy population, and included the direct costs of myocardial infarction and stroke.
They calculated the number of deaths prevented by determining the difference in the number of deaths between those consuming and not consuming dark chocolate.
The final model included a total of 2,013 patients with metabolic syndrome, mean age 53.6, mean systolic blood pressure 141.1 mmHg, mean total cholesterol 6.1 mmol/L, mean HbA1c 34.4 mmol/mol, and mean waist circumference 100.4 cm.
Reid and colleagues found that daily consumption of dark chocolate -- a polyphenol content equivalent to 100 grams of dark chocolate -- can reduce cardiovascular events by 85 per 10,000 population over 10 years.
Specifically, with 100% compliance, treatment would prevent 70 non-fatal and 15 fatal cardiovascular events per 10,000 population over that time. The authors noted that this was a "best case scenario" analysis.
When compliance was reduced to 90%, the number of preventable non-fatal and fatal events fell to 60 and 10, respectively, and at a compliance of 80%, was reduced to 55 and 10, respectively. Even at these levels, however, daily dark chocolate was still considered an effective and cost-effective intervention strategy, they wrote.
At a cost of $42 per person per year, dark chocolate prevention strategies came to an estimated ICER of $50,000 per years of life saved -- a figure well within typical cost-effectiveness thresholds, the researchers said.
That $42 could be spent on advertising, educational campaigns, or subsidization of dark chocolate in higher-risk populations, they wrote.
Reid and colleagues noted that the study was limited by its reliance on the Framingham algorithm, which may underestimate risk in a high-risk population, and by assumptions about the risk of death following a cardiovascular event.
The study was also limited by the assumption that the benefits of dark chocolate, which have only been observed in short-term trials, extend to 10 years. Still, they concluded that the findings suggest dark chocolate may be an effective and cost-effective strategy for preventing heart disease in patients with metabolic syndrome.

But they never say the dosage, you will have to have your doctor buy the paper.
Before you self-medicate talk to your doctor to even see if you have this syndrome