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:

Wednesday, September 28, 2016

The Rehabilitation of Younger Stroke Patients

Your doctor can read the 68 pages here and update the young stroke protocols she has.

The Rehabilitation of Younger Stroke Patients
Key Points
The incidence rate of young stroke patients varies considerably due to differing population
demographics surveyed.
Approximately one third of young stroke victims suffered a stroke of unknown etiology.
Hypertension, arteriovenous ma
lformations, ruptured aneurysms, or a combination of these
factors are the most common causes for hemorrhagic strokes in young individuals.
The majority of strokes in young patients are ischemic.
Patients under 30 experience more uncommon etiologies. Pote
ntial causes of young strokes are
likely due to genetic factors or pre
existing conditions/diseases that increase the risk of strokes.
Modifiable risk factors for stroke include smoking, hypertension, hyperlipidemia, diabetes mellitus,
excessive alcohol co
nsumption, drug use, oral contraceptive use in women, and migraine with aura
in young females.
modifiable risk factors for stroke include family history, patent foramen ovale, age, race,
valve prolapse, and pregnancy/postpartum in young females.
Young stroke patients have a better recovery and prognosis when compared to older stroke
Young stroke rehabilitation differs when compared to the typical older stroke rehab because of a
better likelihood of neurological recovery and unique
social issues.
Improved recovery of young stroke patients tends to put less stress on caregivers; however,
struggles are often associated with changes in relationships and difficulty adjusting post
Institutionalization is required infrequently in y
oung stroke patients and is generally associated with
severe stroke and poor or limited social support.
Vocational issues are often neglected in young stroke patients’ rehabilitation.
Vocational issues in young patients are influenced by job type, cognitiv
e ability, functional recovery
and stroke severity.
Young patients post
stroke tend to have unique psychosocial and supportive needs rather than
specific health concerns.
Dr. Robert Teasell
Parkwood Institute, 550 Wellington Road, London, Ontario, Canada, N6C 0A7
Phone: 519.685.4000 ● Web:
● Email:

Tuesday, September 27, 2016

Identifying candidates for targeted gait rehabilitation after stroke: better prediction through biomechanics-informed characterization

With no protocols presented this research is not only totally useless but not repeatable.
Was this research from June 2015 not good enough to come to a conclusion to your question?

Paretic Propulsion and Trailing Limb Angle Are Key Determinants of Long-Distance Walking Function After Stroke

The latest here:

Identifying candidates for targeted gait rehabilitation after stroke: better prediction through biomechanics-informed characterization

  • Louis N. AwadEmail author,
  • Darcy S. Reisman,
  • Ryan T. Pohlig and
  • Stuart A. Binder-Macleod
Journal of NeuroEngineering and Rehabilitation201613:84
DOI: 10.1186/s12984-016-0188-8
Received: 11 June 2016
Accepted: 26 August 2016
Published: 23 September 2016



Walking speed has been used to predict the efficacy of gait training; however, poststroke motor impairments are heterogeneous and different biomechanical strategies may underlie the same walking speed. Identifying which individuals will respond best to a particular gait rehabilitation program using walking speed alone may thus be limited. The objective of this study was to determine if, beyond walking speed, participants’ baseline ability to generate propulsive force from their paretic limbs (paretic propulsion) influences the improvements in walking speed resulting from a paretic propulsion-targeting gait intervention.


Twenty seven participants >6 months poststroke underwent a 12-week locomotor training program designed to target deficits in paretic propulsion through the combination of fast walking with functional electrical stimulation to the paretic ankle musculature (FastFES). The relationship between participants’ baseline usual walking speed (UWSbaseline), maximum walking speed (MWSbaseline), and paretic propulsion (propbaseline) versus improvements in usual walking speed (∆UWS) and maximum walking speed (∆MWS) were evaluated in moderated regression models.


UWSbaseline and MWSbaseline were, respectively, poor predictors of ΔUWS (R 2  = 0.24) and ΔMWS (R 2  = 0.01). Paretic propulsion × walking speed interactions (UWSbaseline × propbaseline and MWSbaseline × propbaseline) were observed in each regression model (R 2 s  = 0.61 and 0.49 for ∆UWS and ∆MWS, respectively), revealing that slower individuals with higher utilization of the paretic limb for forward propulsion responded best to FastFES training and were the most likely to achieve clinically important differences.


Characterizing participants based on both their walking speed and ability to generate paretic propulsion is a markedly better approach to predicting walking recovery following targeted gait rehabilitation than using walking speed alone.

Spastic cocontraction of plantar flexors during swing phase of gait in chronic hemiparesis

No clue what use this is going to be in getting you to 100% recovery. Bet your doctor doesn't either. Lots of fucking data but no content.
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In spastic hemiparesis, quantify agonist recruitment of tibialis anterior and triceps surae spastic cocontraction during swing phase of gait.

Material/Patients and methods

Thirty-seven subjects with chronic hemiparesis (49 ± 14 years, mean ± SD; time since lesion, 8 ± 7 years) performed a 3D gait analysis, barefoot at comfortable speed (10 optoelectronic cameras, 6 dynamometric force plates, analysis of 9 cycles), with bilateral electromyography of tibialis anterior (TA), soleus (SO) and gastrocnemius medialis (GM). Speed, step length and maximal active dorsiflexion during swing were measured. Indices of agonist recruitment, IRATA, and spastic cocontraction, ICCSO and ICCGM, were calculated over 3 periods of swing phase (T1, [0–33%]; T2, [34–66%]; T3, [67–100%]), by the ratio of the RMS of the electromyogram in the period of interest over the RMS of the electromyogram of the same muscle over 100 ms around the maximal agonist isometric activity (measured on standing position by a maximal effort against resistance). IRA and ICC were compared between the 3 periods and between paretic and non paretic sides using repeated measures MANOVA (significant effect, P < 0.05).


Speed, 0.68 ± 0.26 m/s; paretic step length, 0.48 ± 0.12 m, non paretic, 0.43 ± 0.15 m; paretic maximal active dorsiflexion, −3 ± 8°, non paretic, 6 ± 4°.
On the paretic side: IRATA decreased between T1 and T2 (T1, 0.69 ± 0.59; T2, 0.48 ± 0.39, P = 2E-4) and then remained unchanged at T3 (0.47 ± 0.45; vs T1, P = 1E-4; vs T2, ns), while ICCSO and ICCGM increased at T3 only (ICCSO, T2, 0.25 ± 0.21; T3, 0.57 ± 0.50; P = 5E-8; ICCGM, T2, 0.39 ± 0.40; T3, 0.59 ± 0.50; P = 2E-4). On the non-paretic side, IRATA, ICCSO and ICCGM remained unchanged (IRATA, T1, 0.32 ± 0.20; T2, 0.23 ± 0.13; T3, 0.25 ± 0.10, ns; ICCSO, T1, 0.12 ± 0.12; T2, 0.13 ± 0.12; T3, 0.25 ± 0.18 ns; ICCGM, T1, 0.17 ± 0.31; T2, 0.19 ± 0.27; T3, 0.26 ± 0.25 ns). Side xperiod effect, P = 0.04.

Discussion - Conclusion

During comfortable gait in chronic hemiparesis, there is a decrease in tibialis anterior recruitment from mid-swing phase on and an increase in soleus and gastrocnemius spastic cocontraction at late swing were found.

changes in the muscle-tendon complex of triceps surae after 1 year of rehabilitation including a daily self-stretch program in patients with chronic hemiparesis

Totally worthless since they didn't even bother to measure spasticity and the effects of this program on that. Bet your doctor has no clue what a guided Self-rehabilitation contract is?

changes in the muscle-tendon complex of triceps surae after 1 year of rehabilitation including a daily self-stretch program in patients with chronic hemiparesis




To explore changes in muscle architectural parameters of the muscle-tendon unit of soleus and medial gastrocnemius (GM) in patients with chronic hemiparesis, after 1 year of rehabilitation.

Material/Patients and methods

In this prospective study, 20 chronic hemiparetic patients (8W, mean age: 56 [12], time since lesion 9 [8]) were evaluated. Muscle architectural parameters including muscle fascicle length, pennation angle, thickness, tendon and muscle belly lengths were evaluated in vivo using ultrasonography in passive condition (verified by electromyographic recording) in a seated patient with ankle, knee and hip on the paretic side at 90°. Following the biomechanical analysis, each patient benefited from the Five Step Assessment (FSA), involving the measure of XV1, angle of arrest at slow and strong stretch, which estimates soft tissue extensibility around each muscle. Four muscles of interest in the lower limb were selected for this measure: soleus (XV1Sol), medial gastro-soleus complex (XV1GSC), gluteus maximus (XV1GM) and rectus femoris (XV1RF). Biomechanical and clinical analyses were performed at the beginning and after 1 year of treatment. Two treatments were implemented:

– conventional rehabilitation (50%);

– guided Self-rehabilitation contract (GSC, 50%).

Patients in the GSC group were prescribed a daily self-stretch program with static (>10 min/muscle/day) and eccentric stretch. Changes in architectural parameters and clinical muscle extensibility of overall patients before and after 1 year of rehabilitation were analyzed (Student's).


After 1 year, muscle fascicle length and thickness increased respectively by 6.1mm (14.2%, P=0.05), 1.8mm (13.6%, P=0.06) in soleus, and by 2.9mm (9.1%, P=0.04) and 1.7mm (13.2%, P=0.03) in MG. Muscle belly length of MG increased by 2.9cm (17%, P=0.0001) and its tendon length decreased by 0.82cm (5%, P=0.04). XV1GSC increased by 4.8° (3.3%, P=0.07), XV1GM by 4.1° (3.3%, P=0.0004) and XV1RF by 7.2° (6%, P=0.02).

Discussion - Conclusion

Stretch of soleus and medial gastrocnemius practiced over the long term in patients with spastic hemiparesis allowed structural changes, increasing muscle fascicle length and thickness. Muscle belly length of medial gastrocnemius also increased significantly while its tendon length decreased, suggesting that the tendon may adapt its length to the muscle length changes.

National stroke awareness group honors local marketing campaign for innovation, creativity

Fucking, fucking awareness, NOT solving any of the many problems in stroke. Why the hell do you even have stroke in your name?  You as a stroke association should curl up and die from shame. I dare the president of the ASA to contact me to talk to their board of directors. Or are you too chickenshit to meet with a disabled stroke survivor?

A campus event at the University of South Florida St. Petersburg with national hip hop recording artist Dee-1 is not where you would expect the American Heart Association to promote its message about learning the warning signs of stroke.

But that’s exactly what the American Heart Association Tampa Bay chapter did this spring during National Stroke Month. And for that enterprising event, along with its creative use of social media and strategic partnerships with local businesses, hospitals and media, the chapter recently won a national award.

In September, the chapter received the American Stroke Association’s national award for Best Integrated Campaign for American Stroke Month 2016 among markets with a corporate sponsor. Frontier Communications is the Tampa Bay American Heart Association corporate partner.

According to Lily Conrad, communications director for the local AHA chapter, one of the goals for this year’s campaign was to engage millennials.

“We wanted to reach them with the message that stroke can affect anyone at any time and how important it is to know stroke’s warning signs,” says Conrad.

To accomplish that, the chapter organized the USFSP event with Rapper Dee-1, who is a spokesperson for the national American Heart Association. His rap song communicates the association’s healthy lifestyle message.

“The USFSP event was our kick-off event for the stroke campaign and having Dee-1 there, along with games and other activities for the students, made it very successful,” says Conrad.

Dee-1’s song, “Salle Mae Back” about paying back his student loans after graduating from Louisiana State University was a record hit with millennials concerned about student debt.

The chapter also reached the community through widespread use of Facebook, Twitter and Instagram. The results exceeded the chapter’s expectation.

“We’ve been using social media for a while, but for this year’s campaign, we really took it to the max and had our largest engagement numbers ever,” says Conrad. “This was also our first time using Instagram for the campaign.”

To create a personal connection with the dangers of strokes, the chapter worked with Jen Petit-Homme, marketing manager for Frontier Communications, Tampa Bay, and her mother, Yolande Petit, a stroke survivor.

Their images and story were used extensively to help promote the national stroke month theme:  “Stroke Hero – Stroke Heroes spot a stroke F.A.S.T.” Fast stands for face dropping, arm weakness, speech difficulty, and time to call 911.

“It is so meaningful to be nationally recognized for our efforts to raise stroke awareness,” says Kate Sawa, executive director of the American Heart Association Tampa Bay.

“Frontier Communications and the American Heart Association/American Stroke Association had a vision to equip our community with lifesaving education. We’ve been fortunate to accomplish this through unique community events, engaging corporate employees, and working closely with healthcare systems and incredible stroke survivors,” says Sawa.

The Tampa Bay Metro AHA chapter’s campaign was evaluated on the basis of creativity and innovation, planning, execution and evaluation. Judges noted the chapter’s “impressive” strategic alliance and volunteer engagement, as well as “expansive” market reach through social media posts, media coverage, sponsors and events. 

Interruptions to Rehab Are Common After Stroke or Brain Injury—but Many Are Preventable

I bet nothing gets done with this because our fucking failures of stroke associations do not consider it their responsibility to distribute current research and updated stroke rehab protocols to all stroke doctors. Fucking lazy assholes. You as a stroke survivor will need to be up-to-date on research and train your doctor in their job.
Article ID: 661647
Released: 27-Sep-2016 11:05 AM EDT
Source Newsroom: Wolters Kluwer Health: Lippincott Williams and Wilkins
Newswise — September 27, 2016 – Patients in inpatient rehabilitation after a stroke, brain injury, or spinal cord injury have significant rates of interruptions of their rehab program—often including being transferred back to the hospital for treatment of complications, reports a study in the American Journal of Physical Medicine & Rehabilitation, the official journal of the Association of Academic Physiatrists. The journal is published by Wolters Kluwer.
But at least ten percent of these interruptions and transfers are potentially preventable, suggesting opportunities to improve patient outcomes while lowering the costs of care, according to the new research by Addie Middleton, PhD, DPT and colleagues of University of Texas Medical Branch, Galveston.
Study Shows 'Room for Improvement' in Rehab Care for Neurological Conditions
The researchers analyzed Medicare data on patients undergoing inpatient rehabilitation for one of three neurological conditions: about 72,000 patients with stroke, 7,100 with traumatic brain injury, and 660 with spinal cord injury (SCI). All were admitted to rehab directly from the hospital.
The analysis focused on two types of issues indicating that the patient's rehab program wasn't completed as planned: program interruptions, defined as being transferred to another facility, then back to the rehab center within three days; and short-stay transfers, defined as being transferred to a hospital or other facility before the expected length of stay at the rehab center. "Program interruptions and short-stay transfers are undesirable outcomes that may impact patient recovery and healthcare expenditures," according to the authors.
The results showed that program interruptions occurred in about one percent of patients: 0.9 percent of those with stroke, 0.8 percent with brain injury, and 1.4 percent with SCI. In nearly all of these cases, the patient was transferred to an acute care hospital, usually because of some type of complication.
Short-stay transfers occurred in about 22 percent of patients with stroke or brain injury, and nearly 32 percent of those with SCI. About one-third of these patients were also transferred back to acute-care hospitals. (Others were transferred to skilled nursing facilities.)
Based on review, the researchers classified some of these events as "potentially preventable." Across groups, about 11 to 12 percent of program interruptions might have been preventable. Of the short-term transfers, about 15 percent were potentially preventable in the patients with stroke, ten percent with brain injury, and four percent with SCI. Preventable causes of short-term transfers included problems like dehydration, heart failure, pneumonia, and urinary tract infections.
Inpatient rehabilitation is a common focus of policy reforms seeking to improve quality while reducing the costs of healthcare. The new study is one of the first to focus on the impact of program interruptions and short-stay transfers in patients with stroke, brain injury, or SCI.
The results suggest that "Inpatient rehabilitation facilities are performing well in preventing complications," Dr. Middleton and coauthors write. "However," they add, "given that more than one in ten of the rehospitalized patients returned to acute care for a potentially avoidable condition, there is still room for improvement."
The researchers believe that potentially preventable rehospitalizations are a "clear target" for efforts to improve the quality of rehabilitation care. Future studies may identify modifiable risk factors that could be targeted for preventive efforts. Dr. Middleton and colleagues conclude, "Reducing rates of program interruptions and short-stay transfers will not just improve patient experiences of care, they will likely also translate to lower Medicare spending per beneficiary."
Click here to read “Program Interruptions and Short-Stay Transfers Represent Potential Targets for Inpatient Rehabilitation Care-Improvement Efforts.”
Article: “Program Interruptions and Short-Stay Transfers Represent Potential Targets for Inpatient Rehabilitation Care-Improvement Efforts” (doi: 10.1097/PHM.0000000000000629)

Review highlights urgent demand for tool to identify stroke survivors with visual impairments

Well there is NO standardized way to identify ANY stroke damage diagnosis because everyone uses impairment to try to guess where the damage was. Totally fucking useless. You have no way of knowing which of these 9 causes of deficits is responsible. Without knowing what caused the deficit your therapist is just whistling in the dark. We will never get stroke protocols properly correlated with damage until we get of objective damage diagnosis. Your doctor is totally incompetent for not coming up with a damage diagnosis and properly instructing your therapists in the stroke protocols that will get you back to 100%. Your doctor will whine and complain and give the fucking excuse: 'All strokes are different, all stroke recoveries are different'. If s/he gives you that load of bullshit, call up the hospital president and ask for someone competent. That probably means firing the complete stroke medical team, but we have to start cleaning out the deadwood sometime.

A University of Liverpool led review of the methods available to screen for post-stroke visual impairments has found there is an urgent demand for the development of a tool.
Currently, over 65% of stroke survivors will suffer from a visual impairment while 45% of stroke units do not assess vision.
Visual impairment significantly reduces the quality of life of stroke survivors with many being unable to return to work or drive and in some cases results in depression. The impairments can also have an impact on other people when it is not diagnosed or sufficiently communicated to patients.
Quality of life
Identifying visual impairment after stroke can aid general rehabilitation and thus, improve the quality of life for these patients.
The review, led by postgraduate researcher Kerry Hanna from the University's Institute of Psychology, Health and Society, examined the available literature about current screening methods to accurately identify stroke survivors with visual impairments.
This included reviews of randomised controlled trials, controlled trials, cohort studies, observational studies, systematic reviews and retrospective medical note reviews.
The review, published in 'The Journal of Disability and Rehabilitation' today, found that there is currently no standardised visual screening tool which can accurately assess all potential post stroke visual impairments.
Visual defects missed
Kerry Hanna, said: "The current tools screen for only a number of potential stroke-related impairments meaning many visual defects may be missed.
"The sensitivity of those which screen for all impairments is significantly lowered when patients are unable to report their visual symptoms.
"Future research is required to develop a tool capable of assessing stroke patients which encompasses all potential visual deficits and can also be easily performed by both the patients and administered by health care professionals in order to ensure all stroke survivors with visual impairment are accurately identified and managed."
University of Liverpool

Monday, September 26, 2016

PCSK9 Drug Regresses Coronary Plaque

But is it better than watermelon juice or pomegranate juice or coffee or aged garlic extract ? A simple question that will never be answered because we have NO fucking stroke leaders or strategy.

Watermelon juice reverses hardening of the arteries 

Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation 

Good News: Coffee Could Be Cleaning Out Your Arteries.

New study shows aged garlic extract can reduce dangerous plaque buildup in arteries



PCSK9 Drug Regresses Coronary Plaque 

The PCSK9 inhibitor evolocumab (Repatha) reduces atherosclerosis volume as measured by intravascular ultrasound (IVUS) compared with placebo atop statin therapy, Amgen announced in topline results from the GLAGOV trial.
Along with that positive finding for the primary endpoint at 78 weeks, the trial also met the secondary endpoints of percent and total atheroma volume regression from baseline.
The findings were encouraging, Pablo Corral, MD, a lipid specialist at the Instituto de Clinica Medica in Buenos Aires, and Sekar Kathiresan, MD, of Massachusetts General Hospital in Boston, agreed in a conversation on Twitter.
It might make positive findings more likely from the pending large cardiovascular outcomes trial, due out early in 2017, suggested Ethan Weiss, MD, of the University of California San Francisco, in the same conversation. "Anecdotally, IVUS correctly predicted torcetrapib results," whereas carotid intima-media thickness did not, Weiss added.
However, "I wouldn't declare victory too early," responded Harlan Krumholz, MD, of Yale University in New Haven, Conn., noting that the outcomes trials haven't been stopped prematurely for efficacy.
The phase III GLAGOV trial included 968 patients getting cardiac catheterization, who were on optimized background statin therapy and randomized to double-blind treatment with evolocumab (420 mg monthly) or placebo subcutaneous injections.
Amgen said no new safety concerns emerged in the trial nor was there a difference in treatment-emergent adverse events between groups.
Detailed results are slated for presentation at the American Heart Association meeting in November.term

6 Brain Boosting Foods You Need To Eat Now

How fucking long is it going to take before our medical establishment writes up brain food protocols. I'm guessing never, so you are once again completely on your own to guess how much of this stuff to eat and when. You can't depend on your doctor for anything.
Summer is coming to a close, which means school and work are ramping up again - and you want your brain to be in tip top shape to tackle important tasks and projects. Did you know that there are specific foods you can incorporate into your diet to increase your cognitive abilities such as focus, memory, problem solving skills and learning?
Research has shown that certain nutrients can enhance brain function by increasing blood flow to the brain, calming inflammation and battling fatigue.
Here are my top six brain boosting foods to keep you sharp, focused and on point.
1. Beets: These beautiful root vegetables have tremendous brain boosting potential because of the natural nitrates they contain. Some studies show that these nitrates increase blood flow to the brain, enhancing mental performance. My favorite way to eat beets is to roast (you lose much fewer nutrients this way than by boiling) and drizzle them with some extra virgin olive oil, Icelandic flake salt and fresh ground pepper.
2. Almonds: Nutritional powerhouses, almonds are high in Vitamin E, heart-healthy mono-unsaturated fats, fiber and protein. Vitamin E has been shown to help reduce the risk of cognitive impairment and potentially even the decline caused by Alzheimer’s. An easy way to eat almonds is to pre-portion them out (one small handful is the ideal serving size) and keep them in your car, desk and bag for a healthy snack or to swap out peanut butter for almond butter.
3. Celery: Fibrous, crunchy celery is a great source of luteolin, a plant compound that might lower rates of age-related memory loss. Luteolin calms inflammation and prevents degeneration by inhibiting inflammatory cytokines in the brain. Celery is an easy food to snack on, and for an added brain boost, you can add almond butter and goji berries to it - like a grown up version of bugs on a log.
4. Sardines: People either love or hate these little fishes but it’s undeniable that they are a super food: full of essential fatty acids (EFAs), calcium and protein, sardines are one of the best foods you can possibly consume. The EFAs they contain are EPA and DHA, omega-3 fatty acids that act to bolster communication among brain cells and assist in modulating neurotransmitters responsible for mental focus as well as calming inflammation in the brain. EPA and DHA also increase brain levels of the ‘good mood’ chemical, serotonin. Bonus: the mercury content in sardines is one of the lowest in any fish.
5. Dark chocolate: The key here is choosing good quality chocolate that has 70% or more cacao content. The flavonols in dark chocolate improve blood vessel function, and thus increase brain blood flow. This can enhance memory, cognitive function and alertness. Dark chocolate also boasts brain stimulating caffeine and theobromine, which can help with short term cognitive functioning.
6. Green Tea: Polyphenols in green tea are thought to be neuroprotective and are being studied as therapeutic agents with the potential to alter brain aging processes. Green tea contains caffeine, though only about a third of the amount in a cup of coffee, which can also provide a short term mental boost. My favorite way to increase my intake of green tea is by eating these natural mints that contain one cup of green tea in three mints.

Mascha Davis, MPH, RDN specializes in helping clients reach their goals.
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This Legal Drug Could Protect Brain From Ageing - Nicotine

I'm going to do the nicotine patch after my next stroke. What is your doctor having you do?
ANYTHING AT ALL? Does your doctor know anything at all about this? Or does your doctor read NO research at all?

Nicotine Holds Promise for Stronger Stroke Recovery

Nicotine Patch Appears To Help Mild Cognitive Loss

The latest here:

This Legal Drug Could Protect Brain From Ageing - Nicotine

Could cigarettes contain the latest clue to an anti-ageing drug?
Nicotine could help to protect the brain from Alzheimer’s and Parkinson’s disease, new research finds.
The substance — when given independently from tobacco — could help to protect the ageing brain.
The neuroprotective effect of nicotine could be down to its well-known quality of reducing appetite.
For the study, the researchers gave varying levels of nicotine to mice in their drinking water.
There was no evidence, though, that it caused anxiety, which the researchers were concerned would be the case.
Dr Ursula Winzer-Serhan, who led the research, said:
“Some people say that nicotine decreases anxiety, which is why people smoke, but others say it increases anxiety.
The last thing you would want in a drug that is given chronically would be a negative change in behavior.
Luckily, we didn’t find any evidence of anxiety: Only two measures showed any effect even with high levels of nicotine, and if anything, nicotine made animal models less anxious.”
The mice given the highest levels of nicotine ate the least and gained the least weight.
Dr Winzer-Serhan cautioned:
“I want to make it very clear that we’re not encouraging people to smoke.
Even if these weren’t very preliminary results, smoking results in so many health problems that any possible benefit of the nicotine would be more than cancelled out.
However, smoking is only one possible route of administration of the drug, and our work shows that we shouldn’t write-off nicotine completely.”
The next step for the researchers is to test whether nicotine has a an anti-ageing effect.
Dr Winzer-Serhan said:
“Although the results are intriguing, we would need large-scale clinical trials before suggesting anyone change their behavior.
At the end of the day, we haven’t proven that this addictive drug is safe — and it certainly isn’t during childhood or adolescence — or that the benefits outweigh the potential risks.”
The study was published in the Journal of Toxicology (Huang et al., 2016).

Could Nicotine Help Protect The Aging Brain?

I'm going to do the nicotine patch after my next stroke. What is your doctor having you do?
ANYTHING AT ALL? Does your doctor know anything at all about this? Or does your doctor read NO research at all?

Nicotine Holds Promise for Stronger Stroke Recovery

Nicotine Patch Appears To Help Mild Cognitive Loss

The latest here:

Could Nicotine Help Protect The Aging Brain? 

Summary: When given independently from tobacco, nicotine appears to help protect the aging brain, a new study reports.
Source: Texas A&M.
Texas A&M research shows how this component of cigarettes might actually be beneficial on its own.
Everyone knows that tobacco products are bad for your health, and even the new e-cigarettes may have harmful toxins. However, according to research at Texas A&M, it turns out the nicotine itself—when given independently from tobacco—could help protect the brain as it ages, and even ward off Parkinson’s or Alzheimer’s disease.
Ursula Winzer-Serhan, PhD, an associate professor at the Texas A&M College of Medicine, and her collaborators found that nicotine’s ability to be neuroprotective may be partly due to its well-known ability to suppress the appetite. Their research is published in the Open Access Journal of Toxicology.
Using animal models, Winzer-Serhan and her collaborators added nicotine to the animal’s drinking water. There were three different groups that received nicotine at three different concentrations (low, medium and high) corresponding to occasional, low and medium smokers, respectively, in addition to a control group that did not receive any nicotine.
The two groups that received nicotine at low and medium doses didn’t show any levels of the drug in their blood and they experienced no changes in food intake, body weight or number of receptors in the brain where nicotine acts. In contrast, the group getting the highest concentration of nicotine ate less, gained less weight and had more receptors, indicating that at higher doses, the drug gets into the brain where it can impact behavior. However, even at high doses, it didn’t seem to have worrying behavioral side effects like making the individuals more anxious, which the researchers were concerned could happen.
“Some people say that nicotine decreases anxiety, which is why people smoke, but others say it increases anxiety,” Winzer-Serhan said. “The last thing you would want in a drug that is given chronically would be a negative change in behavior. Luckily, we didn’t find any evidence of anxiety: Only two measures showed any effect even with high levels of nicotine, and if anything, nicotine made animal models less anxious.”
The next step is to test nicotine’s potential anti-aging effects using aged animal models. Although early results indicate that nicotine can keep older individuals from gaining weight like the control group does, Winzer-Serhan hasn’t yet determined whether this lower body mass index translates into less degeneration of the brain. It is also unclear if nicotine’s effects are related only to its ability to suppress appetite, or if there are more mechanisms at work.
Because there are still so many unknowns, Winzer-Serhan urges caution. “I want to make it very clear that we’re not encouraging people to smoke,” she said. “Even if these weren’t very preliminary results, smoking results in so many health problems that any possible benefit of the nicotine would be more than cancelled out. However, smoking is only one possible route of administration of the drug, and our work shows that we shouldn’t write-off nicotine completely.”
Still, Winzer-Serhan cautions people not to purchase nicotine-containing products just yet. “Although the results are intriguing, we would need large-scale clinical trials before suggesting anyone change their behavior,” she said. “At the end of the day, we haven’t proven that this addictive drug is safe—and it certainly isn’t during childhood or adolescence—or that the benefits outweigh the potential risks.”
About this neuroscience and aging research article
Source: Christina Sumners – Texas A&M
Image Source: This image is adapted from the Texas A&M press release.
Original Research: Full open access research for “Evaluation of Chronic Oral Nicotine Treatment in Food Consumption, Body Weight and [125I] Epibatidine Binding in Adult Mice” by Pei-San Huang, Louise C. Abbott and Ursula H Winzer-Serhan in Open Access Journal of Toxicology. Published online September 2016 doi:not available

Sunday, September 25, 2016

Pediatric stroke rehabilitation: A review of techniques facilitating motor recovery


Pediatric stroke rehabilitation: A review of techniques facilitating motor recovery



Paediatric stroke is a relatively rare medical condition, but it often leads to long lasting motor and cognitive impairments. Rehabilitation of motor impairments has been widely studied, with most studies performed in children with cerebral palsy (CP). However, CP covers a variety of medical conditions, including brain lesions due to paediatric stroke occurring early in life, but not stroke occurring later on during childhood. The specificity of rehabilitation after paediatric stroke remains understudied. This paper aims to present current motor rehabilitation practices (from birth to age 18) and examine which of these techniques are applicable and efficient for paediatric stroke.

Materials/Patients and methods

We first conducted searches using Ovid Database, for motor rehabilitation techniques used in childhood hemiplegia and/or CP. As a second step, a systematic search was conducted up to March 2016, combining the therapies retrieved in the first search AND key words referring to paediatric stroke. Separate searches were conducted for each rehabilitation technique previously identified, namely: constraint induced movement therapy (CIMT), hand arm bimanual training (HABIT), occupational therapy combined with botulinum toxin injections, non-invasive brain stimulation, virtual reality, robotics, action-observation therapy, functional electric stimulation and prismatic or mirror adaptations.


In paediatric stroke, studies on rehabilitation of lower limb present low or insufficient evidence, whereas most studies refer to rehabilitation of upper-limb disabilities. CIMT presents moderate to strong evidence, sometimes coupled with imaging studies examining the associated brain changes. Individual case studies propose CIMT for toddlers or infants, both for motor rehabilitation or unilateral spatial neglect. Contrary to CP literature, there is no available evidence on bimanual training or botulinum toxin injections, whereas there is a growing body of research on non-invasive brain stimulation, (tDCS or TMS) providing preliminary evidence on the efficacy, as well as safety and feasibility of such methods for older children. Novel approaches such as functional electric stimulation, robotic therapy, virtual reality and action–observation therapy present low or insufficient evidence, but may be promising for more severe upper limb deficits or early intervention.


Rehabilitation of motor deficits following paediatric stroke remains understudied, but a number of promising therapies are emerging.



Asking New Questions with Old Data: The Centralized Open-Access Rehabilitation Database for Stroke

With this amount of knowledge it should be damned easy to come up with a strategy to solve all the problems in stroke.
  • 1School of Kinesiology, Auburn University, Auburn, AL, USA
  • 2School of Biological and Health Systems Engineering, Arizona State University, Tempe, AZ, USA
  • 3Department of Health, Physical Education and Recreation, Utah State University, Logan, UT, USA
  • 4Department of Physical Therapy, University of British Columbia, Vancouver, BC, Canada
  • 5Program in Physical Therapy, Washington University School of Medicine in St. Louis, St. Louis, MO, USA
  • 6Program in Occupational Therapy, Washington University School of Medicine in St. Louis, St. Louis, MO, USA
  • 7Department of Neurology, Washington University School of Medicine in St. Louis, St. Louis, MO, USA
Background: This paper introduces a tool for streamlining data integration in rehabilitation science, the Centralized Open-Access Rehabilitation database for Stroke (SCOAR), which allows researchers to quickly visualize relationships among variables, efficiently share data, generate hypotheses, and enhance clinical trial design.
Methods: Bibliographic databases were searched according to inclusion criteria leaving 2,892 titles that were further screened to 514 manuscripts to be screened by full text, leaving 215 randomized controlled trials (RCTs) in the database (489 independent groups representing 12,847 patients). Demographic, methodological, and statistical data were extracted by independent coders and entered into SCOAR.
Results: Trial data came from 114 locations in 27 different countries and represented patients with a wide range of ages, 62 year [41; 85] [shown as median (range)] and at various stages of recovery following their stroke, 141 days [1; 3372]. There was considerable variation in the dose of therapy that patients received, 20 h [0; 221], over interventions of different durations, 28 days [10; 365]. There was also a lack of common data elements (CDEs) across trials, but this lack of CDEs was most pronounced for baseline assessments of patient impairment and severity of stroke.
Conclusion: Data integration across hundreds of RCTs allows clinicians and researchers to quickly visualize data from the history of the field and lays the foundation for making SCOAR a living database to which researchers can upload new data as trial results are published. SCOAR is a useful tool for clinicians and researchers that will facilitate data visualization, data sharing, the finding of relevant past studies, and the design of clinical trials by enabling more accurate and comprehensive power analyses. Furthermore, these data speak to the need for CDEs specific to stroke rehabilitation in randomized controlled trials.
PROSPERO 2014:CRD42014009010


The information architecture in rehabilitation science is poor (1). For example, randomized controlled trials (RCTs) are the basic “unit” of information that guide clinical practice. Yet when clinicians and scientists want to ask a very basic question of these data, they are published: (1) across a wide spectrum of journals and formats that often have limited access (e.g., payment required for access); (2) embedded potentially in text, tables, figures, or even supplemental materials; and (3) with very few common data elements (CDEs) reported across studies (2, 3). Thus, despite the tremendous time and financial burdens associated with even a single RCT, the resultant data lack a consistent structure. This lack of structure is an unnecessary barrier to integration in future scientific and clinical practice. Efforts to streamline data integration should increase the transparency and visibility of comprehensive bodies of evidence, rather than a single study, to better inform clinically relevant questions such as, “How do therapy outcomes change with increased time in therapy?” or “How variable are outcomes, historically, for specific parameters of therapy?”
We now introduce one such tool for streamlining data integration: the Centralized Open-Access Rehabilitation database for Stroke (SCOAR). In short, SCOAR is a central repository for summary statistics from RCTs. SCOAR currently contains data from a systematic review and extraction of papers from 1981 to early 2014 (described in detail below), but the goal of SCOAR is much bigger: to create a “living” database where new data can be added as clinical trials are completed. Imposing such an architecture (4) on clinical trial data would allow basic and clinical scientists to (1) quickly and easily visualize relationships among variables, (2) efficiently share data, (3) generate hypotheses based on noticeable patterns or even “gaps” in the current data, (4) search the current literature from the data up (rather than key-terms down), and (5) improve clinical trial design through more accurate and comprehensive power analyses.
Generally speaking, the goal of SCOAR is to improve the design of future clinical trials by giving researchers fast and easy access to the historical range of effect-sizes, based on thousands of stroke patients who received therapies of different types, different doses, at different times, and were measured on different outcomes. From our perspective, the effort associated with the design, implementation, and dissemination of randomized clinical trials deserves an information architecture that supports and increases their visibility. In the current paper, we (1) explain the systematic search and data extraction that led to the creation of SCOAR; (2) present summary statistics for the major variables in SCOAR, including the geographical reach, to understand how SCOAR data represent research in stroke rehabilitation; and (3) based on the lack of CDEs we find across many variables, we argue for a consistent set of CDEs in rehabilitation trials (CDEs to describe participants, methodology, and outcomes). SCOAR lays the foundation for an information architecture that captures some of the complex and multivariate nature of neurorehabilitation. Most importantly, this information architecture is scalable, making it easy to add new data as new trials are published.

How Neurons Talk to Each Other

Will this help your doctor get you to 100% recovery?
Summary: A new paper offers an overview as to how neurons ‘communicate’ with one another.
Source: Max Planck Institute.
Neurons are connected to each other through synapses, sites where signals are transmitted in the form of chemical messengers. Reinhard Jahn, Director at the Max Planck Institute for Biophysical Chemistry in Göttingen, has investigated precisely how the process works.
Our nervous system consists of about 100 billion interlinked neurons that are capable of carrying out complex computations. Each neuron has an antenna zone comprising the cell body and its extensions (dendrites). It is here that it receives signals from other neurons.
One cell talks, the other listens
The signals are then computed and forwarded by a “cable”, the axon, in the form of electrical impulses. In the emitter region, the axon branches to form contact sites, known as synapses, where the signals are transmitted to other neurons. At the synapse, electrical impulses arriving from the axon are converted into chemical signals. The information then flows in only one direction: one cell talks, the other listens. The number of synapses that a single neuron can develop varies considerably. Depending on its type, a neuron can have anything from just one to more than 100,000 synapses. On average, each neuron has around 1,000 synapses.
Synapses – elementary units of neuronal information transmission
Synapses consist of:
  • the nerve ending of the transmitting (presynaptic) neuron,
  • the synaptic cleft separating the transmitting and receiving neurons and
  • the membrane of the receiving (postsynaptic) neuron.
The presynaptic nerve endings contain signal molecules known as neurotransmitters, which are stored in small membrane-enclosed vesicles. Each nerve ending in the central nervous system contains an average of several hundred synaptic vesicles. However, synapses vary significantly. For example, some specialist synapses contain more than 100,000 vesicles. They include the synapses that control our muscles. At each synapse some vesicles are always in the starting position, “lurking”, as it were, on the presynaptic plasma membrane to which they have docked.
Molecular machines at work
An electrical signal arriving at the nerve ending activates calcium channels in the plasma membrane. Calcium ions from outside then flow through the channels into the interior of the synapse. There, the inflowing calcium ions encounter and activate a molecular machine located between the vesicle membrane and the plasma membrane. This machine causes the membranes of the vesicles in the starting position to fuse with the plasma membrane and release the neurotransmitters contained in the vesicles into the synaptic cleft.
Illustration of a neuron (left) and a synapse (right). image is credited to MPI for Biophysical Chemistry.

On the other side of the synaptic cleft, the neurotransmitters come into contact with docking sites on the membrane of the receiving neuron which regulate the electrical properties of that membrane. This alters the electrical resistance of the membrane. The receiving cell is able to process the resulting potential change rapidly. Only around one thousandth of a second elapses between the arrival of an impulse and the potential change on the other side of the synaptic cleft. In fact, synaptic transmission is one of the fastest biological processes known. Nevertheless, it is positively sluggish in comparison to a transistor.
Synaptic vesicles: not just storage organelles
A synaptic vesicle is not just a kind of membrane-bound “storage tank” for neurotransmitters. Its membrane contains a whole series of proteins that have barely changed over millions of years of evolution. A group of these proteins, the neurotransmitter transporters, are responsible for pumping neurotransmitters from the cytoplasm into the vesicles, where they accumulate. This process requires a great deal of energy, which is provided by another protein molecule, proton ATPase (V-ATPase), that pumps protons into the vesicles – a process that is fuelled by adenosine triphosphate (ATP). The pumps, in turn, use the resulting concentration gradient for the uptake of neurotransmitters.
In addition to these proteins required for “replenishing”, the membranes of synaptic vesicles contain other components that enable the vesicles to fuse with the plasma membrane (including the SNARE protein synaptobrevin and the calcium sensor synaptotagmin). Once membrane fusion has occurred, they are transported back into the nerve ending. The synaptic vesicles are then recycled back into the nerve ending via several intermediate steps and are refilled with neurotransmitters. This process is repeated again and again, thousands of times in the life cycle of a vesicle.
The process by which synaptic vesicles function at the molecular level is intricate. Several years ago, we created a comprehensive inventory of all vesicle components. Because vesicles are tiny and complex in composition, this undertaking was not easy. Several teams from Germany, Japan, Switzerland and the United States collaborated for years in order to identify the protein and fat components of vesicles and develop a quantitative molecular model of a standard vesicle.
First, problems had to be solved that were not as straightforward as one might suppose, for example counting the number of vesicles in a solution and determining the quantities of proteins and membrane lipids present. The results were surprising even for experts. It turned out that the structure of a biological transport vesicle is shaped to a far greater extent by proteins than was previously thought: If the vesicle model is looked at from the outside, the lipid membrane (yellow) can barely be seen for the sheer number of proteins. Yet the model only contains around 70 percent of the total quantity of protein present.

Temple scientists use hydrogen sulfide to restore stem cell-mediated blood flow in ischemic limbs of diabetic mice

Not that this directly helps stroke survivors but shit hydrogen sulfide research back to 2013 proved helpful for survivors. 7 posts on it here.  But shit once again nothing seems to have been done that might actually help stroke survivors. I blame our fucking failures of stroke associations, great at doing nothing for survivors.

Temple Health
Hydrogen sulfide is a noxious gas, but in the human body it serves important functions as a gaseous signaling molecule. Among those functions is to protect the tone and cell function of blood vessels, which according to scientists at the Lewis Katz School of Medicine at Temple University (LKSOM) could prove critical in preventing limb amputation in patients with diabetes, a major complication of which is a painful reduction in limb blood flow known as critical limb ischemia (CLI). In a new study, the researchers are the first to show in diabetic animals that induced hydrogen sulfide production in bone marrow stem cells can effectively repair vessel tone and limb circulation. The study was published online September 22 in the journal Circulation. To determine whether hydrogen sulfide deficiency predisposed diabetic stem cells to abnormalities that undermine their function, Dr. Kishore and colleagues isolated bone marrow cells from nondiabetic and diabetic mice and examined the cells for differences in levels of hydrogen sulfide–synthesizing enzymes. They found that protein levels of an enzyme known as cystathionine gamma–lyase (CSE) were significantly decreased in diabetic bone marrow cells, accounting for the animals' hydrogen sulfide deficiency. The researchers then introduced the CSE gene into bone marrow cells isolated from diabetic mice to induce CSE overexpression and injected the cells back into the animals. The treatment resulted in dramatic improvements in blood vessel formation and blood flow. Remarkably, simple dietary supplementation with a hydrogen sulfide donor compound likewise restored hydrogen sulfide levels and improved limb circulation, enabling partial limb rescue. Blood flow was further increased when the special diet was combined with conventional stem cell therapy for CLI.