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 493 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:

Tuesday, January 31, 2012

Exciting Data from Remedy Pharmaceutical-Sponsored Stroke Drug Trial to Be Presented at the 2012 International Stroke Conference in New Orleans

A hyperacute option for a hemorrhage, most of my posts are for ischemic so this is wonderful.
On February 2 in New Orleans, Dr. Kevin Sheth of the University of Baltimore Medical Center will address an audience at the International Stroke Conference to present promising preliminary results from an ongoing drug trial in patients with severe stroke.
“GAMES (Glyburide Advantage in Malignant Edema and Stroke) Pilot: Initial Design and Enrollment”
Every 40 seconds of every day, someone in the United States suffers a stroke. Stroke is the third leading cause of death in this country, surpassed only by heart disease and cancer. One recent high profile case that received much media attention involved 52-year old freshman Illinois Senator Mark Kirk, who won Barrack Obama’s vacated seat after he was elected president.
According to media reports, on Saturday January 21 Kirk was feeling dizzy and headachy when he checked himself into Lake Forest Hospital just outside Chicago. As doctors would soon learn, he had suffered a stroke. When his medical condition deteriorated, he was transferred to Northwestern Memorial Hospital in Chicago where a decision was made to perform what is termed “decompressive surgery.” The delicate procedure involves removing a portion of the skull (later reattached) to relieve cranial pressure caused by brain swelling.
Just down the street from where Senator Kirk underwent his surgery, a clinical trial using a new stroke drug was being conducted. Rush Hospital in Chicago is part of a group of U.S. medical centers taking part in a clinical trial, referred to as the GAMES-PILOT study. GAMES-PILOT is designed to test Remedy Pharmaceuticals’ drug, RP-1127 in patients with severe stroke who are likely to develop significant brain swelling. Had the senator been sent to Rush Hospital in time, it is possible he could have been eligible for inclusion in this study.
“Despite best available medical management, the prognosis for severe stroke patients is poor,” says Sven Jacobson, CEO of Remedy Pharmaceuticals, the sponsor of the GAMES-PILOT study. “Decompressive surgery has improved the bleak outlook for many of these patients, yet numerous factors limit its usefulness. Some patients may get back to being functional, but many are left with very severe deficits. Clearly preventing brain swelling is a better strategy than attempting to relieve its deleterious effects. We hope that one day our drug will offer stroke patients a chance for a fuller recovery.”
Dr. Sheth’s poster presentation, titled “GAMES (Glyburide Advantage in Malignant Edema and Stroke) Pilot: Initial Design and Enrollment” will be presented at Poster CT P35, Hall B (Poster Hall) on Thursday Feb 2, 2012 at 6:15 PM.
Detailed information on the GAMES Pilot Study is available at:
About RP-1127
Remedy’s lead drug candidate, RP-1127, is a high affinity, well tolerated inhibitor of NCCa-ATP channels, which are key upstream mediators of the development of brain swelling (edema) and hemorrhage following ischemic and traumatic injury.
About Remedy Pharmaceuticals
Remedy Pharmaceuticals, Inc. is a clinical stage pharmaceutical company focused on the development and commercialization of small molecule drugs for acute central nervous system disorders including stroke, traumatic brain injury, and spinal cord injury. RP-1127 has not yet been approved for use by the FDA.

2012 Neuro Film Festival from the American Academy of Neurology Foundation

My submitted video,its rather unsophisticated:
Title - Time is Brain
submissions due Jan. 31, results in April.
Other submitted ones are here:

Statins Equally Effective in Women and Men

Cholesterol-lowering drugs known as statins are equally effective in men and women, a new study finds.

For both males and females, these drugs lowered the risk of a heart attack by about 20 percent, the researchers say. Previously, some thought that statins, which include Lipitor, Lovastatin and Crestor, benefited women less than men.

"Statin therapy should be used to treat all appropriate patients, regardless of gender," said lead researcher Dr. William Kostis, of the cardiology division at Massachusetts General Hospital in Boston.

"Despite prior concerns in the literature, the benefits of statin therapy pertain to both women and men," he added.

The report was published in the Jan. 30 online edition of the Journal of the American College of Cardiology.

Cardiovascular disease remains the leading cause of death among women and men in the United States. Statins are designed to lower bad cholesterol levels, which increase the risk of heart attack and stroke, and raise good cholesterol levels.

To compare statins' effectiveness in men and women, Kostis' team analyzed data from 18 clinical trials that involved more than 140,000 patients, including more than 40,000 women.

Researchers use this kind of study, called a meta-analysis, to look for common patterns that might have been overlooked in the original report.

Kostis' group found fewer cardiovascular events and fewer deaths from any cause among those taking statins, regardless of gender.

Dr. Lori Mosca, director of preventive cardiology at New-York Presbyterian Hospital in New York City and author of an accompanying journal editorial, said that "women and men have the same relative benefit with statins as far as reducing the future risk of a heart problem is concerned, but because women often start off at a lower risk level than men the net benefit is likely less."

But there isn't enough data to make solid conclusions about gender differences in the risk-to-benefit ratio for patients who don't have definite heart disease, she said.

"However, even among patients without heart disease, statins can be considered for prevention in women, but the net benefit and risks, including potential for side effects such as muscle problems and possible increased risk of diabetes, should be taken into consideration," Mosca said.

Another expert, Dr. Gregg C. Fonarow, a professor of cardiovascular medicine and science at the University of California, Los Angeles, said many trials have shown statin treatment reduces fatal and nonfatal cardiovascular events in apparently healthy people as well as those with cardiovascular disease.

While national guidelines recommend that men and women receive statin medications to prevent and treat cardiovascular disease, some experts felt there was insufficient evidence to make strong recommendations for statin use in women, particularly in regards to preventing cardiovascular disease, Fonarow said.

But this study answers those concerns, he said.

"Statin therapy, together with a healthy diet and exercise, provides substantial cardiovascular protection to women and men," Fonarow said. "The answer to the question as to whether statins work equally well for both sexes, is a definitive yes."

15 Things Your Walk Reveals About Your Health

You will have to read the complete article at the link. See #3 and 13. Check out the ones that apply to you.
Walk into an exam room and a trained eye can tell a lot about you in seconds: Your stride, gait, pace, and posture while walking can reveal surprising information about your overall health and well-being.

Walking clue #1: A snail's pace

May reveal: Shorter life expectancy

Walking clue #2: Not too much arm swing

May reveal: Lower back trouble

Walking clue #3: One foot slaps the ground

May reveal: Ruptured disk in back, possible stroke

Walking clue #4: A confident stride (in a woman)

May reveal: Sexual satisfaction

Walking clue #5: A short stride

May reveal: Knee or hip degeneration

Walking clue #6: Dropping the pelvis or shoulder to one side

May reveal: A back problem

Walking clue #7: Bowlegged stride

May reveal: Osteoarthritis

Walking clue #8: Knock-kneed appearance

May reveal: Rheumatoid arthritis

Walking clue #9: A shortened stride on turns and when maneuvering around things

May reveal: Poor physical condition

Walking clue #10: A flat step without much lift

May reveal: Flat feet, bunions, neuromas

Walking clue #11: Shuffling

May reveal: Parkinson's disease

Walking clue #12: Walking on tiptoes, both feet

May reveal: Cerebral palsy or spinal cord trauma

Walking clue #13: Walking on tiptoes, one foot

May reveal: Stroke

Walking clue #14: A bouncing gait

May reveal: Unusually tight calf muscles

Walking clue #15: One higher arch and/or a pelvis that dips slightly

May reveal: One leg is shorter than the other

Monday, January 30, 2012

CMS says? More data needed on best management of blocked carotid arteries

For those who need more information on the possibilities for their carotid arteries.
The Centers for Medicare & Medicaid Services (CMS) held a meeting Jan. 25 with the hope of strengthening carotid atherosclerosis management. During said meeting, the Medicare Evidence Development & Coverage Advisory Committee (MEDCAC) voted on evidence, procedures and the most beneficial strategies for the management of atherosclerosis to prevent stroke with most members agreeing that more data are necessary.

Currently, CMS covers coronary artery stenting for patients at a high risk of adverse events from carotid endarterectomy (CEA) for:
  • Symptomatic patients with ? 70 percent stenosis;
  • Symptomatic patients with a 50 to 70 percent stenosis when procedures are performed in FDA approved category B IDE trials or FDA approved post approval studies; and
  • In asymptomatic patients with ? 80 percent stenosis when procedures are performed in FDA approved trials.

Members looked at both symptomatic and asymptomatic patients population to discuss whether carotid artery stenting (CAS), CEA and optimal medical therapy (OMT) improved outcomes in atherosclerotic patients. Additionally, CMS looked to understand whether previously published data on the topic is generalizable to the Medicare population.

Members voted on six questions and used the following responses: low confidence, intermediate confidence or high confidence. Questions dealt with whether CAS or CEA is the favored treatment strategy in various patient populations, previous data outlining the benefits/risks of CAS or CEA as opposed to OMT and what should be done in the future, among others.

During the meeting, William A. Gray, MD, an associate professor of Medicine at the Columbia University Medical Center in New York City, said the “concept of a ‘low-risk’ patient has not clearly been defined, nor identified.” Additionally, Gray said that to date, there are no trials that assess patients who are at a high surgical risk, and that post-trial CEA outcomes cannot be generalize to those who were not enrolled in the trial.

Gray went on to say that in symptomatic patients, CEA and CAS “appears equivalent” in terms of outcomes and stroke in the CREST trial, but noted women did better with CAS compared with CEA in the EVA-3S and ICSS trials.

Lastly, Gray said that the “correct cocktail of medical class” is missing in asymptomatic patients to determine the most optimal medical therapy to treat those with carotid artery disease. “The role of medical therapy remains a tantalizing but unproven alternative to revascularization in patients with established severe carotid stenosis,” Gray said in a statement.

Meanwhile, Robert M. Zwolak, MD, PhD, of the Dartmouth-Hitchcock Medical Center in Lebanon, N.H., looked at the real-world results of CAS and CEA during a presentation at the meeting, concluding that real-world results are not always comparable to what is found in randomized controlled trials.

Zwolak used 30-day stroke and death rates post-CAS and CEA from the SVS Registry as an example. Of 1,450 CAS patients and 1,368 CEA patients, the combined rates of stroke, death and MI was nearly 6 percent for CAS patients compared with nearly 3 percent in CEA patients. The 30-day stroke rates for CAS and CEA for asymptomatic patients was 2.11 percent vs. 1.28 percent, and 5.27 percent vs. 2.37 percent in symptomatic patients. Based on a Nationwide Inpatient Sample analysis, Zwolak reported that stroke and death rates in high surgical risk patients to be nearly two times higher after CAS vs. CEA.

“Even after risk-factor adjustment, stroke risk likely greater after CAS in population based studies,” Zwolak said.

When asked to vote on whether there is accurate evidence to determine whether or not CEA or CAS is the favored treatment as compared to optimal medical therapy in the Medicare population, the majority of the voting body said they had low- to intermediate- confidence about the data. This question was asked about asymptomatic patients not considered high risk for adverse events with CEA.

All voting members said that they had a low confidence that CAS would be the favored treatment strategy in asymptomatic carotid atherosclerosis patients who were not at high risk for stroke. However, many said they had a high confidence that optimal medical therapy alone should be the favored treatment strategy in this patient population.

All in all, the majority of the panelists agreed that more data are necessary to better define the best treatment strategy—CEA, CAS or OMT—for atherosclerotic Medicare patients.

Scientists shift on brain speech centre

We need this kind of specificity if we are ever to get a decent damage diagnosis.
The part of the brain used for speech processing is in a different location than originally believed, according to a US study that researchers say will require a rewrite of medical texts.

Wernicke's area, named after the German neurologist who proposed it in the late 1800s, was long believed to be at the back of the brain's cerebral cortex, behind the auditory cortex which receives sounds.

But a review by scientists at Georgetown University Medical Center of more than 100 imaging studies has shown it is actually three centimetres closer to the front of the brain, and is in front of the auditory cortex, not behind.

"Textbooks will now have to be rewritten," said neuroscience professor Josef Rauschecker, lead author of the study which appears in the Proceedings of the National Academy of Sciences.

"We gave old theories that have long hung a knockout punch."

Rauschecker and colleagues based their research on 115 previous peer-reviewed studies that investigated speech perception and used brain imaging scans - either MRI (functional magnetic resonance imaging) or PET (positron emission tomography).

An analysis of the brain imaging coordinates in those studies pointed to the new location for Wernicke's area, offering new insight for patients suffering from brain damage or stroke.

"If a patient can't speak, or understand speech, we now have a good clue as to where damage has occurred," says Rauschecker.

Humans and primates 'more similar'

It also adds an intriguing wrinkle to the origins of language in humans and primates, who have also been shown to process audible speech in the same region of the brain.

"This finding suggests the architecture and processing between the two species is more similar than many people thought."

Lead author Iain DeWitt, a PhD candidate in Georgetown's Interdisciplinary Program in Neuroscience, says the study confirms what others have found since brain imaging began in earnest in the 1990s, though some debate has persisted.

"The majority of imagers, however, were reluctant to overturn a century of prior understanding on account of what was then a relatively new methodology," he says.

"The point of our paper is to force a reconciliation between the data and theory."

Proximal balloon superior to distal protection in carotid artery stenting

For those needing their arteries cleaned out, read for stroke prevention strategies so you can ask your doctor.
Proximal balloon occlusion provides significantly greater embolic protection during carotid artery stenting (CAS) for internal artery stenosis when compared with a filter protection device, research shows [1]. Proximal balloon-occlusion devices do not cross the lesion before it is stented, which helps to significantly reduce embolic load in the brain during the carotid procedure, according to researchers.

To heartwire, senior investigator Dr Joachim Schofer (University Cardiovascular Center, Hamburg, Germany) said that while the question can't be answered clinically from these data, he believes there is connection between the asymptomatic "spots" observed on diffusion-weighted magnetic resonance imaging (DW-MRI) in their study and the risk of stroke. "I'm pretty convinced that proximal balloon occlusion is more effective than distal protection and would result in a lower rate of stroke," he said.

The results of the study, known as the Prevention of Cerebral Embolization by Proximal Balloon Occlusion Compared to Filter Protection During Carotid Artery Stenting (PROFI), are published online January 25, 2012 in the Journal of the American College of Cardiology.

Spots on the brain

The study included 62 consecutive symptomatic and asymptomatic patients undergoing CAS with embolic protection who were randomly assigned proximal balloon occlusion (MO.MA, Invatec) or filter protection (Emboshield Protection System, Abbott Vascular). Compared with the filter, which crosses the lesion before the stent is implanted and is deployed to catch debris during the procedure, the balloon-occlusion device is placed proximal to the lesion and inflated to occlude the external and common carotid arteries. Flow is reversed in the target vessel before the lesion is crossed and treated.

Using DW-MRI, the researchers found that the incidence of new cerebral ischemic lesions per patient was significantly greater among patients who underwent distal protection (87.1% in the filter group vs 45.2% in the balloon-occlusion group; p=0.001). The incidence of new ischemic lesions was significantly higher with filter protection in symptomatic and asymptomatic patients, and there was a trend toward more lesions in patients >80 years of age. Regarding the secondary end points, the researchers report that the number of lesions per patient and the volume of lesions per patient were significantly higher among those who received the filter device compared with balloon occlusion.

One patient had a minor stroke in the filter-protection group, while no major adverse cardiovascular or cerebrovascular events (MACCE) were observed in the balloon-occlusion patients. Schofer noted, however, the study is underpowered for clinical events.

Schofer told heartwire that filter-protection devices are relatively easy to use, and the risk they pose is related to the crossing of the lesion, which results in some dislodging of emboli. In addition, some particles might be too small to be captured by the filter or might pass by the filter if it is not placed properly against the vessel wall. The filters can also become overloaded, which can cause some debris to spill during retrieval. The proximal balloon-occlusion device does not have similar downsides, although it is slightly harder to use and does require more training, said Schofer.

Not all patients are good candidates for proximal balloon occlusion, either. Patients with contralateral occlusion were not included in this study, but balloon intolerance was still noted in 13% of patients. Contralateral new ischemic lesions that develop are likely caused by emboli dislodged when the catheters navigate through the aortic arch, said Schofer.

More data needed on carotid atherosclerosis, CMS advisers agree

Finally someone agrees we need a much better data collection and registry. In this case for carotid problems, which would have meant my doctors should have sent my data to them except that they didn't find my blockage.
The panel that advises the Centers for Medicare & Medicaid Services (CMS) on coverage issues is still unsure how to answer several key questions about the treatment of carotid atherosclerosis [1].

"If there was ever a moving-target problem in assessing healthcare interventions, this is one," committee chair Dr Clifford Goodman (The Lewin Group, Falls Church, VA) said during the Medicare Evidence Development & Coverage Advisory Committee (MEDCAC) January 25, 2012 meeting at CMS headquarters. "The epidemiology is changing, the patient population is changing accordingly, all of the interventions continue to change, and we've not been keeping up in our data collection for the safety and effectiveness of these interventions as they continue to evolve. This means that to the extent that the CMS is going revisit this as a coverage decision over time, this is an ongoing data-collection issue."

The panel met to discuss the latest data on carotid stenting, carotid endarterectomy surgery, and best medical management for carotid atherosclerosis. The panel did not address the CMS's national coverage policy for these therapies, but the agency is expected to reopen the policy for reconsideration later this year. Currently, Medicare covers carotid stenting with embolic protection only in patients with carotid stenosis >70% who would be at high risk for complications during carotid endarterectomy.

The seminal Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST) trial showed similar composite outcomes with stenting or carotid endarterectomy in 2502 high-risk patients. Many interventionalists see the CREST results as justification for discussing both options with their patients, but some physicians argue that surgery is still the best option in these patients, because the 30-day stroke rate was significantly higher with stenting than surgery (4.1% vs 2.3%) in CREST. Those in favor of at least offering stenting to these patients point out that the rate of major strokes was about the same—under 1%—for both therapies and that MI was higher with surgery than stenting (2.3% vs 1.1%).

This diversity of opinion was reflected by MEDCAC. The panel was asked to rate, on a scale of 1 to 5, their confidence in the evidence comparing stenting, surgery, or best medical therapy to decrease stroke or death in asymptomatic, standard-risk patients with carotid stenosis over 60% by angiography (>70% by ultrasound). Several panelists voted 1, indicating they believe the available data are inadequate to determine which of these therapies is best for these patients. On the other end of the spectrum, neurologist Dr J David Spence (University of Western Ontario, London) voted 5 on this question, but overall, the panel's confidence in this evidence was 2 out of 5, so they didn't discuss which therapy they believe is best for these patients.

The panel did discuss the different therapies for symptomatic carotid-atherosclerosis patients at standard risk during surgery. For that group, the panel gave the highest score (3.44) to endarterectomy surgery as the favored option, while stenting scored a 2 and best medical therapy scored a 1.56.

For asymptomatic patients at standard risk for stroke in either cerebral hemisphere, the panel agreed that optimal medical therapy is best option, although a few panelists said they are not confident in the evidence on any therapy in this population.

An ongoing data-collection problem

Dr Kenneth Rosenfield (Massachusetts General Hospital, Boston), who spoke on behalf of the American College of Cardiology (ACC) at the MEDCAC meeting, told heartwire, "The take-away lesson [from the meeting] is that carotid artery disease and the management of it is a moving target. . . . We have really good evidence from 10 to 15 years ago on the management at that time," but results for surgery, medical management, and stenting have all improved over the years, and the data collection hasn't caught up to contemporary practice, he said.

"Some of us say that in the absence of pure clarity, are these treatments pretty darn close? Yes, they are," Rosenfield said. "Given that these are pretty even treatments, patients should be aware of that, and the treatment should be individualized to each patient and the patients should have access to everything.

"But everyone agrees we need to develop better evidence that is timelier and applies to today's results." Rosenfield expects one of the manufacturers of carotid stents to ask the CMS to reopen its coverage policy on carotid-atherosclerosis treatment. He said that the ACC will argue that the CMS should require Medicare-covered carotid procedures to be recorded in a national registry. "If [Medicare] is going to pay for it, shouldn't they and the doctors doing it be responsible for collecting the data on what they are doing? Shouldn't everyone be mandated to look at their own outcomes? It's also unbelievable that it doesn't happen now."

Several panelists also pushed for more ongoing data collection from carotid-atherosclerosis patients. "We need some high-quality registries, of both the procedures and the patients, to figure out what is going on in the real world," Dr Mark Hlatky (Stanford University, CA) said.

Will there be another CREST trial?

Rosenfield and several MEDCAC panelists also expressed support for the proposed CREST II trial, currently spearheaded by neurologist Dr Thomas Brott (Mayo Clinic, Jacksonville, FL). The investigators are currently discussing plans for the study with the National Institutes of Health.

CREST II would randomize about 950 asymptomatic patients with high-grade stenosis to either best medical management or revascularization. Patients randomized to revascularization would work with their doctors to choose either surgery or stenting. The primary outcome of CREST II would be the composite of stroke or death within 30 days of enrollment or ipsilateral stroke up to four years thereafter. The trial is designed to show a 4.8% (1.2% per year) treatment difference between revascularization and medical management, Brott explained during a presentation at the MEDCAC meeting.

Rosenfield is concerned that CREST II may have trouble enrolling patients. "I imagine that a lot of doctors and patients have preconceived notions such that if [patients] have [for example] a 90% narrowing, they want to get it fixed. They won't want to enroll in a randomized trial that might just leave them on best medical therapy. Some doctors might believe, in their own mind, 'This patient is higher risk, so I don't want to randomize them,' " he said. "If you get a lot of people in the trial who have 70% to 75% narrowing but none with higher degrees of narrowing, then you may not be able to show a difference. The trial shows something only about the people it enrolls, not the ones it doesn't enroll, so it will be important to track those patients who aren't enrolled."

Where should stroke research go next?

A two pronged approach.
1. Prevention - The whole goal here is to save brain cells, not necessarily prevent strokes. Figure out how to stop the neuronal cascade of death due to glutamate poisoning, excitotoxicity, closed capillaries due to pericytes. This alone can probably reduce the death and disability on a massive scale. See my hyperacute posts for ideas.
2. Until #1 occurs we will need to figure out exactly how and why neuroplasticity occurs.
Until we know that there is really no reason for researchers to keep proving that neuroplasticity works, we already know that, stop reinventing the wheel.

Where are the thought leaders in this space that should have thought of this 20 years ago?

Association of a difference in systolic blood pressure between arms with vascular disease and mortality: a systematic review and meta-analysis

So get your blood pressure checked in both arms.


Differences in systolic blood pressure (SBP) of 10 mm Hg or more or 15 mm Hg or more between arms have been associated with peripheral vascular disease and attributed to subclavian stenosis. We investigated whether an association exists between this difference and central or peripheral vascular disease, and mortality.


A difference in SBP of 10 mm Hg or more, or of 15 mm Hg or more, between arms might help to identify patients who need further vascular assessment. A difference of 15 mm Hg or more could be a useful indicator of risk of vascular disease and death.

Saturday, January 28, 2012

Portable Neurorobotics for the Severely Affected Arm in Chronic Stroke: A Case Study

A chronic case study, I may need to see if my health insurance will cover this when I get employed again. Pictures at the lower url.


Background and Purpose: Few motor therapies increase active movement in the severely impaired arm of individuals with chronic stroke. Existing robotic devices to address this need are large and expensive. This case study describes the application and reports outcomes associated with a repetitive task-specific training (RTP) program incorporating a portable robotic device. We assessed outcomes related to affected arm impairment, ability to perform valued activities, satisfaction with movement performance, and quality of life in a participant with chronic stroke exhibiting severe arm hemiparesis.

Case Description: The participant was a 53-year-old man, 30 months after hemorrhagic stroke. At the time of enrollment, he exhibited some active shoulder and elbow flexion, but no active elbow extension, and no active movement at any joint below the elbow.

Intervention: The participant engaged in RTP incorporating a portable, electromyography-triggered neurorobotic device in 1-hour sessions, 3 days/week for 8 weeks using the affected arm.

Outcomes: The upper extremity section of the Fugl-Meyer Impairment scale (FM), the Canadian Occupational Performance Measure (COPM), and the Stroke Impact Scale (SIS) were administered before and after training. After intervention, the subject exhibited reduced affected arm impairment (+2 points on the FM), increased ability to perform valued activities, increased satisfaction with performance of these activities (indicated by score increases of +2 and +1.8 points on the COPM Performance and Satisfaction scales, respectively), improved strength, performance of activities of daily living, hand function, participation, and physical function (as indicated by increases in respective SIS scores).

Discussion: The RTP incorporating the neurorobotic device appears promising. To our knowledge, this is the first study documenting a portable robotic-based RTP strategy in a person exhibiting this severity of hemiparesis.

Effects of gait rehabilitation with a footpad-type locomotion interface in patients with chronic post-stroke hemiparesis: a pilot study

I think I found what this looks like, check out the lower url.


Objective: We developed a footpad-type locomotion interface called the GaitMaster. The purpose of this pilot study was to examine the effects of gait rehabilitation using the GaitMaster in chronic stroke patients.

Design: Randomized cross-over design.

Setting: An outpatient department.

Subjects: Twelve patients with chronic post-stroke hemiparesis.

Intervention: In group A, patients underwent an ‘intervention phase’ followed by a ‘non-intervention phase’, whereas in group B, patients underwent the non-intervention phase first, followed by the intervention phase. In the four- or six-week intervention phase, participants underwent twelve 20-minute sessions of gait rehabilitation using the GaitMaster4.

Main outcome measures: We measured gait speed and timed up-and-go test.

Results: No differences between the two groups were observed in the baseline clinical data. For the combined groups A and B, the maximum gait and timed up-and-go test speeds improved significantly only in the intervention phase (P = 0.0001 and P = 0.003, respectively). The percentages of improvement from baseline at the end of GaitMaster training were 16.6% for the maximum gait speed and 8.3% for the timed up-and-go test. The effect size for GaitMaster4 training was 0.58 on the maximum gait speed and 0.43 on the timed up-and-go test.

Conclusions: This pilot study showed that gait rehabilitation using the GaitMaster4 was a feasible training method for chronic stroke patients. Calculation of the sample size indicated that a sample size of 38 participants would be adequate to test a null hypothesis of nil benefit additional to routine rehabilitation for chronic stroke patients in a future randomized controlled trial.

GaitMaster 5: The Mechanical Physical Therapist of the Future

Neuroprotection by the Metabolic Antioxidant α-Lipoic Acid

A hypothesis paper from 1996.


Reactive oxygen species are thought to be involved in a number of types of acute and chronic pathologic conditions in the brain and neural tissue. The metabolic antioxidant α-lipoate (thioctic acid, 1, 2-dithiolane-3-pentanoic acid; 1, 2-dithiolane-3 valeric acid; and 6,8-dithiooctanoic acid) is a low molecular weight substance that is absorbed from the diet and crosses the blood–brain barrier. α-Lipoate is taken up and reduced in cells and tissues to dihydrolipoate, which is also exported to the extracellular medium; hence, protection is afforded to both intracellular and extracellular environments. Both α-lipoate and especially dihydrolipoate have been shown to be potent antioxidants, to regenerate through redox cycling other antioxidants like vitamin C and vitamin E, and to raise intracellular glutathione levels. Thus, it would seem an ideal substance in the treatment of oxidative brain and neural disorders involving free radical processes. Examination of current research reveals protective effects of these compounds in cerebral ischemia-reperfusion, excitotoxic amino acid brain injury, mitochondrial dysfunction, diabetes and diabetic neuropathy, inborn errors of metabolism, and other causes of acute or chronic damage to brain or neural tissue. Very few neuropharmacological intervention strategies are currently available for the treatment of stroke and numerous other brain disorders involving free radical injury. We propose that the various metabolic antioxidant properties of α-lipoate relate to its possible therapeutic roles in a variety of brain and neuronal tissue pathologies: thiols are central to antioxidant defense in brain and other tissues. The most important thiol antioxidant, glutathione, cannot be directly administered, whereas α-lipoic acid can. In vitro, animal, and preliminary human studies indicate that α-lipoate may be effective in numerous neurodegenerative disorders.


  • α-Lipoate;
  • α-Lipoic acid;
  • Thioctic acid;
  • Dihydrolipoic acid;
  • 1, 2-Dithiolane-3-pentanoic acid;
  • 6,8-Dithiooctanoic acid;
  • Antioxidant;
  • Neuroprotection;
  • Ischemia;
  • Free radicals

β-Lactam antibiotics offer neuroprotection by increasing glutamate transporter expression

Not sure how I would create something like this for my ER kit for my next stroke.

Letters to Nature

Glutamate is the principal excitatory neurotransmitter in the nervous system. Inactivation of synaptic glutamate is handled by the glutamate transporter GLT1 (also known as EAAT2; refs 1, 2), the physiologically dominant astroglial protein. In spite of its critical importance in normal and abnormal synaptic activity, no practical pharmaceutical can positively modulate this protein. Animal studies show that the protein is important for normal excitatory synaptic transmission, while its dysfunction is implicated in acute and chronic neurological disorders, including amyotrophic lateral sclerosis (ALS)3, stroke4, brain tumours5 and epilepsy6. Using a blinded screen of 1,040 FDA-approved drugs and nutritionals, we discovered that many β-lactam antibiotics are potent stimulators of GLT1 expression. Furthermore, this action appears to be mediated through increased transcription of the GLT1 gene7. β-Lactams and various semi-synthetic derivatives are potent antibiotics that act to inhibit bacterial synthetic pathways8. When delivered to animals, the β-lactam ceftriaxone increased both brain expression of GLT1 and its biochemical and functional activity. Glutamate transporters are important in preventing glutamate neurotoxicity1, 9, 10, 11. Ceftriaxone was neuroprotective in vitro when used in models of ischaemic injury and motor neuron degeneration, both based in part on glutamate toxicity11. When used in an animal model of the fatal disease ALS, the drug delayed loss of neurons and muscle strength, and increased mouse survival. Thus these studies provide a class of potential neurotherapeutics that act to modulate the expression of glutamate neurotransmitter transporters via gene activation.

Neurosphere-derived multipotent precursors promote neuroprotection by an immunomodulatory mechanism

More neuroprotection from 2005. So many research projects to run in humans.
In degenerative disorders of the central nervous system (CNS), transplantation of neural multipotent (stem) precursor cells (NPCs) is aimed at replacing damaged neural cells1, 2. Here we show that in CNS inflammation, NPCs are able to promote neuroprotection by maintaining undifferentiated features and exerting unexpected immune-like functions. In a mouse model of chronic CNS inflammation, systemically injected adult syngeneic NPCs use constitutively activated integrins and functional chemokine receptors to selectively enter the inflamed CNS. These undifferentiated cells survive repeated episodes of CNS inflammation by accumulating within perivascular areas where reactive astrocytes, inflamed endothelial cells and encephalitogenic T cells produce neurogenic and gliogenic regulators. In perivascular CNS areas, surviving adult NPCs induce apoptosis of blood-borne CNS-infiltrating encephalitogenic T cells, thus protecting against chronic neural tissue loss as well as disease-related disability. These results indicate that undifferentiated adult NPCs have relevant therapeutic potential in chronic inflammatory CNS disorders because they display immune-like functions that promote long-lasting neuroprotection.

Neuroprotection by Aspirin and Sodium Salicylate Through Blockade of NF-κB Activation

Just think, regular aspirin can be used against the neuronal cascade of death. And my doctor only had 10 years to be able to incorporate this into hyperacute therapy. Written in 1996. I don't care if it was only tested in rats.
Aspirin (acetylsalicylic acid) is a commonly prescribed drug with a wide pharmacological spectrum. At concentrations compatible with amounts in plasma during chronic anti-inflammatory therapy, acetylsalicylic acid and its metabolite sodium salicylate were found to be protective against neurotoxicity elicited by the excitatory amino acid glutamate in rat primary neuronal cultures and hippocampal slices. The site of action of the drugs appeared to be downstream of glutamate receptors and to involve specific inhibition of glutamate-mediated induction of nuclear factor kappa B. These results may contribute to the emerging theme of anti-inflammatory drugs and neurodegeneration.

Subarachnoid Hemorrhage Risk Factors In Pregnant Women

Be careful out there.
Approximately 1 in every 15,000 pregnant women will develop subarachnoid hemorrhage (SAH) - bleeding in the area between the brain and the thin membranes that cover the brain, according to a study published in the February issue of Anesthesiology.

Friday, January 27, 2012

Needleless sensor patch aims to replace frequent bloodwork

Now all they have to do is monitor INR readings for those on warfarin and you could have a running tally of it rather than the stupid two week blood draws. And getting cholesterol levels so you could see on a daily basis what your eating habits do.
Does anyone know how to contact Sano to suggest these items?

What if people who have a condition that requires frequent bloodwork could have continuous access to their basic metabolic panel readings without ever having to be poked by a needle?

Early-stage startup Sano Intelligence is taking this concept and running with it, developing a transdermal sensor patch that its founders think could continuously monitor metabolic panels and deliver that data to software platforms or mobile devices.

Founded by Raj Gokal and Ashwin Pushpala — and springboarding off a college project Pushpala worked on — Sano Intelligence is hoping to provide digitalized blood chemistry information to patients and providers through a variety of applications. The original idea was intended for use in diabetes patients, but the founders said they have decided instead to focus on less crowded spaces in healthcare.

Gokal and Pushpala will participate in the Rock Health acceleration program this spring.

To prescribe or not to prescribe: That is the statin question, experts debate

I have 29 posts on statins covering a lot of the plusses and minuses. I do take mine, although I have no idea what my level is without taking them. My opinion on this is that while cholesterol is a problem because it attaches itself to artery walls, the attachment is what is needed to be stopped. Statins do not address the real problem. You brain needs cholesterol to function properly. Ask your doctor, I'm just a stupid stroke survivor. You do know that patients are as smart as laboratory rats.
Are statins one of the greatest advances since the introduction of antibiotics, capable of preventing cardiovascular disease in a wide range of patients, even healthy ones, or are clinicians relying too heavily on the lipid-lowering medications, using the drugs too frequently in individuals who would be better treated with an overhaul of their diet and exercise habits?
The two very different sides of the statin argument are debated today in the Wall Street Journal [1], with Dr Roger Blumenthal (Johns Hopkins University Medical Center, Baltimore, MD) arguing the drugs prevent heart disease in patients with cardiovascular risk factors as well as in those who have already had a cardiovascular event. Good diet and exercise are the foundations of good health, says Blumenthal, but they're simply not enough sometimes, especially in patients with increased LDL-cholesterol levels or other cardiovascular risk factors.
"Every major medical guideline calls for doctors to prescribe a statin to certain seemingly healthy people with high levels of 'bad' cholesterol, which signals elevated risk for a heart attack," according to Blumenthal. "Doing so is one of the certainties of life, like the Cubs falling out of the pennant race by Labor Day."
Dr Rita Redberg (University of California, San Francisco), on the other hand, argues against the current practice of prescribing statins to patients with cardiovascular risk factors, including individuals with elevated cholesterol levels. To heartwire, she said that there are too many low-risk individuals taking statins, and they simply don't get a benefit. In these low-risk/low-benefit patients, given the residual risk of statins, benefit is exceeded by harm.
"Despite research that has included tens of thousands of people, there is no evidence that taking statins prolongs life, although cholesterol levels do decrease," she writes in the Journal. "Using the most optimistic projections, for every 100 healthy people who take statins for five years, one or two will avoid a heart attack. One will develop diabetes. But, on average, there is no evidence that the group taking statins will live any longer than those who don't."

Stanford/Packard scientists find new uses for existing drugs by mining gene-activity data banks

Drug repositioning, lets use this to identify drugs that might stop the cascade of neuronal death.
Who is going to ask these researchers to look into this? I'm just a pathetic laboratory rat.

Researchers at the Stanford University School of Medicine have paired up medicines and maladies with help from a molecular “” When the scientists applied an “opposites attract” algorithm to publicly available databases, surprising sparks flew: They found potential compatibilities between numerous existing drugs and diseases for which those drugs had never before been thought to be beneficial.

So far, preclinical tests have borne out at least two of these findings: Cimetidine — a widely used, cheap, over-the-counter anti-ulcer drug — may be a good fit for a form of lung cancer; and topiramate — an off-patent anti-seizure drug with a solid safety profile — may be therapeutic for inflammatory bowel disease.

Scientists led by Atul Butte, MD, PhD, associate professor of systems medicine in pediatrics, combed public databases with a sophisticated computer algorithm and identified numerous drug-and-disease pairs that may have a therapeutic future together. The coupling is based on the opposing directions in which a given disease and a given drug alter various genes’ activity in tissues.

The results of this new study establish proof of principle for an approach that could significantly speed progress in combating difficult diseases with drugs that are already approved for other indications (a procedure called drug repositioning). They were published online Aug. 17 in two separate studies (one each for the cimetidine and topiramate findings) in Science Translational Medicine. Butte, who is also director of the Center for Pediatric Bioinformatics at Lucile Packard Children’s Hospital, is the senior author of both studies.

What may be most counterintuitive of all, Butte said, is the degree to which a drug that is effective in a disorder, for instance epilepsy, may prove effective in one disorder as seemingly different as, say, Crohn’s disease. Likewise, one wouldn’t ordinarily assume an ulcer drug might be useful in fighting lung cancer.

But such leaps do occur in the medical world, albeit typically by accident instead of by systematic search. To name one popular example, a compound originally developed for heart problems turned out to be effective for erectile dysfunction and, eventually, for a severe lung disorder called pulmonary hypertension. That drug, sildenafil, is more commonly known by its brand name, Viagra.

In the early 2000s, Butte began assembling a systematic way to mine the wealth of underused information in public databases. “I was wondering: Can we predict these intersections, instead of stumbling across them?” he said.

The working hypothesis was simple, said Butte: “If a drug exerts a change on gene-activity pattern that is opposite to that exerted by a disease, then that drug may have a therapeutic effect on that disease.”

Many studies aim to determine which of the approximately 30,000 genes contained in each cell of a given tissue are working hardest and which are quiescent. Every disease or drug affects cells’ overall pattern of gene activity in its own way, pointing at genes that may be important in that disease’s or drug’s effects on that tissue.

New technologies have rendered routine the simultaneous measurement of activity levels of every gene in a cell or tissue. Today there are 750,000 results of such analyses in publicly available databases, nearly a 30-fold increase since 2004, said Butte. “For various reasons, very few scientists use the data that’s already entered. So we thought we’d make use of this info.”

The Stanford researchers restricted their database search to analyses in which human biopsy samples and normal tissues, or drugged and non-drugged samples, were compared in the same experiment, yielding more-accurate comparisons. About 100 diseases and 164 approved drugs met this narrow criterion. (That was five years ago, when the search now being reported began. The same screen initiated today, Butte said, would deliver profiles on about 1,500 diseases and more than 300 drugs.)

Butte’s algorithm grouped diseases by how they changed gene activity instead of by the organ affected, and then paired them off against drugs whose gene-activity effects opposed those changes. Just like that celebrated little old lady of yore, the yenta, the algorithm suggested matches that, however startling, would prove to be made in heaven.

Butte’s team chose two seemingly oddball pairings: cimetidine, an ulcer drug, for adenocarcinoma of the lung, which accounts for about 30-40 percent of all lung cancers; and topiramate, an anti-seizure drug, for Crohn’s disease, an inflammatory bowel disorder.

The first author of the cimetidine study was Butte’s graduate student Marina Sirota, PhD, now at Pfizer. Cimetidine’s “matching score” vis-à-vis lung adenocarcinoma compared favorably with that of an approved lung-cancer drug, gefitinib. So the Stanford researchers tested its therapeutic potential in a classic animal model obtained from the Stanford Cancer Institute. They showed that cimetidine inhibited the growth of tumors formed by lung-cancer cells grafted onto mice that lack immune systems and are therefore unable to reject cancer-cell grafts. Applied directly to lung-cancer cells in a dish, cimetidine diminished those cells’ proliferation and increased their tendency to die spontaneously.

The topiramate study’s first author was Joel Dudley, PhD. Crohn’s disease is one of the most common and serious manifestations of inflammatory bowel disease, which affects more than 1 million individuals in North America. There are no known cures for Crohn’s, and current treatments for relieving symptoms can have severe side effects or be quite costly. Topiramate scored about as well as steroids, a well-known existing treatment, on Butte’s drug-disease algorithm. The team then tested this drug in a rodent model of Crohn’s disease, assessing topiramate’s healing effect as measured by inspecting the tissue by endoscopy or microscopy. By these measures, topiramate clearly had a beneficial effect. Physical symptoms such as diarrhea also improved.

Butte serves on the scientific advisory board of NuMedii, a startup company that aims to commercialize some of the technologies used in this research. Co-founded by Dudley, the company hopes to use the results of this pair of studies to help find funding sources that will enable it to use the new approach to get both on- and off-patent compounds into the right clinical trials.

The National Institute of General Medical Sciences, Howard Hughes Medical Institute and PhRMA Foundation provided funding for the studies. Other Stanford co-authors were Pankaj Jay Pasricha, MD, professor of gastroenterology; Mohan Shenoy, MD, basic life science research associate; assistant professor Alejandro Sweet-Cordero, MD, and associate professor Julien Sage, PhD, both of pediatric cancer biology; assistant professor of pathology Reetesh Pai, MD; Minnie Sarwal, MD, PhD, professor of pediatric nephrology; pediatrics postdoctoral researcher Silke Roedder, PharmD, PhD; graduate student Alex Morgan; research associate Jeewon Kim, PhD; and Annie Chiang, PhD, a former postdoctoral researcher.

Information about Stanford medical school’s departments of Pediatrics and of Medicine, which supported the work, is available at and, respectively.

Thursday, January 26, 2012

United Kingdom Stroke Forum Conference Dec. 2011

This page contains the various presentations or you can open the links below. I didn't find anything useful in them, except for Pippa Tyrrell.

2011 Speaker Presentations

Conference presentations, where speakers have given their permission, can be viewed below and are listed each day in alphabetical order of speaker surname. Some sessions are therefore missing. Unfortunately the UKSF is not able to provide hard copies of slides.

Tuesday 29 November 2011

British Association of Stroke Physicians' Training

John Potter - Managing Blood Pressure after Acute Stroke Adobe Acrobat file

MDT Rehabilitation Training

Therese Jackson - Delivering rehabilitation in a changing economic climate Adobe Acrobat file

NSNF/SSNF Training

Gill Cluckie - Risk Communication in Thrombolysis Adobe Acrobat file

Jennifer Davies - Stroke Survivor Speech Adobe Acrobat file

Maree Hackett - Return To Work (results embargoed) Adobe Acrobat file

Charlotte Lee - Advocacy and Stroke Adobe Acrobat file

NHS Stroke Improvement Programme Training

Sarah Gillham - Knowing where you are Adobe Acrobat file

Ian Golton - Making a difference Adobe Acrobat file

Jill Lockhart - Making a difference Adobe Acrobat file

Barbara Zutshi - Maintaining Momentum Adobe Acrobat file

Wednesday 30 November 2011

Cognitive Workshop Breakfast - All Slides Adobe Acrobat file

Rhoda Allison - Integrating ESD with community services Adobe Acrobat file

Bev Bennett - Enhancing dysphagia management: facilitated e-learning works and offers value for money (Oral Abstract) Adobe Acrobat file

Adrian Brady - AF and anti-coagulation Adobe Acrobat file

Michelle Brogan & Mark Smith - Telerehabilitation Adobe Acrobat file

Archibald Coulter - Extracranial stenosis causes overestimation of tissue at risk on CT perfusion imaging of acute stroke (Oral Abstract)Adobe Acrobat file

Fiona Coupar - Home-based therapy programmes for upper limb functional recovery after stroke: a Cochrane systematic review (Oral Abstract) Adobe Acrobat file

Pooja Dassan - Cerebral microbleeds in acute ischaemic stroke are associated with higher serum levels of vascular endothelial growth factor (Oral Abstract) Adobe Acrobat file

David Davis - The pre-hospital paradigm Adobe Acrobat file

Matthew Fay - Commissioning for stroke Adobe Acrobat file

Joanna Fletcher Smith - A survey to explore the acceptability of the treatment approaches used in the DRESS study (Oral Abstract)Adobe Acrobat file

Gary Ford - Pre hospital Stroke Research Adobe Acrobat file

Vijeya Ganesan - Managing childhood stroke in adulthood Adobe Acrobat file

Ian Golton - Introduction to Shaping Community Stroke Services Adobe Acrobat file

Caroline Haw - Making information about stroke more accessible (Oral Abstract) Adobe Acrobat file

Martin James - Will delays in treatment jeopardise the population benefit from extending the time window for stroke thrombolysis? (Oral Abstract) Adobe Acrobat file

Louise Johnson - Observation of Physiotherapy for Gait Re-education Post Stroke – How Do Therapists Use Instructions and Feedback? (Oral Abstract)Adobe Acrobat file

Stephanie Jones - Training call handlers to recognise stroke – the evaluation and impact of a training package (Oral Abstract)Adobe Acrobat file

Nicol Korner-bitensky - Implementing Research Evidence Adobe Acrobat file

Peter Langhorne - Researching Telehealth Systems Adobe Acrobat file

Jill Lockhart - Shaping Community Stroke Services Adobe Acrobat file

Kate McArthur - Central adjudication of modified Rankin Scale disability assessments in acute stroke trials (Oral Abstract) Adobe Acrobat file

Natalie Mohr - Analysis of the implementation of a validated swallowing screening tool for acute stroke: The Modified Mann Assessment of Swallowing Ability (MMASA) (Oral Abstract) Adobe Acrobat file

Amit Mistri - Patent Foramen Ovale Adobe Acrobat file

Helen O'Kelly - Accessing more than rehabilitation after stroke Adobe Acrobat file

Rebecca Palmer - Cost effectiveness of aphasia computer therapy compared with usual stimulation for people with long standing aphasia (CACTUS): results of a pilot study (Oral Abstract) Adobe Acrobat file

Valerie M Pomeroy - Advances in Upper Limb Rehabilitation Adobe Acrobat file

Cathy Price - Predicting Language after Stroke Adobe Acrobat file

Kristiina Rannikmae - Genetic associations of cerebral amyloid angiopathy - a systematic review and meta-analysis (Oral Abstract) Adobe Acrobat file

Christine Roffe - BASP Survey of interventional treatments for stroke in the UK (Oral Abstract) Adobe Acrobat file

Peter Sandercock - Third International stroke trial of intravenous thrombolysis with RTPA in acute ischaemic stroke: baseline characteristics of the 3035 patients randomised (Oral Abstract) Adobe Acrobat file

Penny Standen - WiiSTAR Adobe Acrobat file

Katie Thomson - The use of commercial gaming in stroke upper limb rehabilitation: a systematic review (Oral Abstract) Adobe Acrobat file

Hilary Walker - The London Stroke Model: Impact on quality of hyperacute care (Oral Abstract) Adobe Acrobat file

Caroline Watkins - UK practice (pre-hospital admission) Adobe Acrobat file

David Werring - Clinical Relevance of Microbleeds in Stroke (CROMIS-2): Microbleeds and genetic risk factors to predict the risk of intracranial haemorrhage after anticoagulation for cardioembolic stroke due to atrial fibrillation (Oral Abstract) Adobe Acrobat file

Thursday 1 December 2011

Myzoon Ali - Recovery from Post-Stroke Visual Impairment Adobe Acrobat file

Ann Ashburn - Activity levels post stroke: a three year follow up study (Oral Abstract) Adobe Acrobat file

Liz Cullen - Community Stroke Reviews – A Stroke Review Tool to deliver Quality Marker 14 of the Stroke Strategy (Oral Abstract) Adobe Acrobat file

Brid Farrell - Improving stroke care in Northern Ireland Adobe Acrobat file

Rebecca Fisher - Community Rehabilitation Adobe Acrobat file

Sarah Gillham - National work in improving access to psychological care in stroke Adobe Acrobat file

Louise Johnson - Observation of Physiotherapy for Gait Re-education Post Stroke – How Do Therapists Use Instructions and Feedback? (Oral Abstract)Adobe Acrobat file

Andrew Jones - Improving stroke care in Wales Adobe Acrobat file

Fiona Jones - 'We already do that in our practice’: changes in attitudes and beliefs towards stroke self-management amongst health and social care practitioners (Oral Abstract)Adobe Acrobat file

Micky Kerr - A qualitative investigation of Early Supported Discharge Services: moving beyond the evidence base (Oral Abstract) Adobe Acrobat file

Ian Kneebone - Anxiety Management post stroke Adobe Acrobat file

Caroline Lecko - Development of the national descriptors for texture modification Adobe Acrobat file

Nadina Lincoln - Measuring Change in Psychological Outcomes Adobe Acrobat file

Amit Mistri - Does labetalol increase short term blood pressure variability after acute stroke? (Oral Abstract) Adobe Acrobat file

Deborah Parkinson - Visual perception defects following stroke Adobe Acrobat file

David Saunders - Physical Fitness Training for Stroke Patients: a systematic review of the evidence (Oral Abstract) Adobe Acrobat file

John Sinden - Human Neural Stem Cells: CTX0E03 therapy Adobe Acrobat file

Mirek Skrypak - Quality of life measures and their use in stroke services: insight into appropriate use and careful selection (Oral Abstract)Adobe Acrobat file

Catherine Stevenson - part 1 - Introduction of stroke assessment bay to improve access to stroke unit (Oral Abstract) Adobe Acrobat file

Catherine Stevenson - part 2 - Introduction of stroke assessment bay to improve access to stroke unit (Oral Abstract) Adobe Acrobat file

Pippa Tyrrell - The Interleukin-1 receptor antagonist story Adobe Acrobat file

Geert Verheyden - Assessing motor and functional performance after stroke Adobe Acrobat file

Elizabeth Weekes - Evidence supporting the role of dietetic intervention in acute stroke Adobe Acrobat file

Luke Williams - Distress management post stroke Adobe Acrobat file