Changing stroke rehab and research worldwide now.Time is Brain! 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:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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 lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.My back ground story is here:

Tuesday, February 25, 2014

Taking your brain for a walk: the secret to delaying dementia

I'll have to add this to my dementia presentation in the section - What Would Dean Do?
Regular brisk walks can slow down the shrinking of the brain and the faltering mental skills that old age often brings, scientists say.
Studies on men and women aged 60 to 80 found that taking a short walk three times a week increased the size of brain regions linked to planning and memory over the course of a year.
The prefrontal cortex and hippocampus increased in size by only 2% or 3%, but that was enough to offset the steady shrinkage doctors expected to see over the same period.
"It may sound like a modest amount but that's actually like reversing the age clock by about one to two years," said Professor Kirk Erickson, a neuroscientist at the University of Pittsburgh.
"While the brain is shrinking, we actually saw not a levelling out but an increase in the size of these regions. It was better than before we started the study."
People who took part in the study scored higher on spatial memory tests, and some reported feeling more mentally alert, according to Erickson. "They feel better, they feel as if the fog has lifted. Anecdotally, it seems to benefit these cognitive functions," he said.
Erickson recruited more than 100 adults who confessed to doing little if any exercise in their daily lives. Half were randomly assigned to walk for 30 to 45 minutes three days a week. The rest spent a similar amount of time doing stretching exercises.
Medical scans showed minor increases in the two brain regions in both groups. But the effect was greater in the walkers, Erickson said at the annual meeting of the American Association for the Advancement of Science.
"With modest amounts of exercise, we were able to increase the size of these structures that typically deteriorate and precede the cognitive complaints that often come in late adulthood," Erickson said.
"You don't need highly vigorous physical activity to see these effects. People are misled to believe they need years of vigorous physical exercise. But it only needs to be moderate, and not even for that long.
"The results suggest that brain and cognitive function of the older adults remain plastic and highly malleable. There is not this inevitable decline that we used to think it was."
Scientists are unsure what changes in the brain underpin the increases in size of the two regions, or how long the improvements last. Exercise is unlikely to stave off the brain's decline for long, but it could delay the inevitable decline and slow the onset of dementia.
There is a desperate need for any approach that could slow the rising epidemic of dementia. An estimated 44.4 million people now have dementia worldwide, and that number is expected to reach 75.6 million in 2030, according to figures from Alzheimer's Disease International.
Erickson said: "The prefrontal cortex is involved in a lot of higher-level cognitive functions and the hippocampus is involved in memory formation. And when it shrinks, it leads to Alzheimer's disease and dementias.
"If we measured these people for a long period of time, we'd probably be slowing the decline rather than completely mitigating it. But it might slow it down for a long period of time. We cannot say it's the magic-bullet cure for Alzheimer's. There isn't one."

Early strokes leave many young adults with long-lasting disability

These people writing this have no brains at all.
One-third of people who survive a stroke before age 50 are unable to live independently or need assistance with daily activities 10 years after their stroke, according to research in the American Heart Association journal Stroke.
About 10 percent of strokes occur in 18- and 50-year-olds.
“Even if patients seem relatively well recovered with respect to motor function, there may still be immense ‘invisible’ damage that leads to loss of independence,” said Frank-Erik de Leeuw, Ph.D., senior author of the study and associate professor of neurology at the Radboud University Nijmegen Medical Center in the Netherlands.
Researchers assessed the function of 722 people who had a first stroke when they were age 18-50. After an average follow-up of nine years, about one-third had at least moderate disability, requiring assistance for some activities. Many were also unable to conduct routine tasks independently, such as caring for themselves, doing household chores or looking after their finances.
Upon closer investigation, researchers found the rate of poor functional outcome and the ability to live independently varied by type of stroke:
  • After a transient ischemic attack (TIA, or ‘mini-stroke’), 16.8 percent had functional disability and 10.8 percent had poor skills for independence.
  • After an ischemic stroke, caused by a blood clot in the brain, 36.5 percent had functional disability and 14.6 were unable to live independently.
  • After a hemorrhagic stroke, caused by a brain bleed, 49.3 percent had functional disability and 18.2 percent didn’t have the skills for independent living.
“Most doctors view young stroke patients as a group with great recovery opportunities,” de Leeuw said. “But our study is the first to show these almost life-long effects of stroke on performance. This is important to communicate right from the start to patients and families.”
Patients fared worse if they experienced another stroke during the follow-up period. Of the 91 patients who did: 54.9 percent were at least moderately disabled, compared with 28.7 percent of those without a recurrent stroke; and 33.3 percent were dependent on others in activities of daily living, compared with 11.5 percent of those without a recurrent stroke.
The researchers are investigating factors most responsible for poor functional outcome.
“We don’t know if it’s cognition, depression, problems in their families or relationships or other factors, but once we do, we can develop more effective interventions,” de Leeuw said.
My God, the stupidity involved in that statement, you stop the neuronal cascade of death, less disability results - better outcomes.
Co-authors are Nathalie E. Synhaeve, M.D.; Renate M. Arntz, M.D.; Noortje A.M. Maaijwee, M.D.; Loes C.A. Rutten-Jacobs, M.Sc.; Hennie C. Schoonderwaldt, Ph.D.; Lucille D.A. Dorresteijn, M.D.; Paul L.M. de Kort, Ph.D.; and Ewoud J. van Dijk, Ph.D. Author disclosures are on the manuscript.
The Dutch Epilepsy Fund supported the study.

Monday, February 24, 2014

Global Bill of Rights for Stroke

A WSO initiative.  I'm going to be extremely blunt, we need stroke protocols for all deficits, 100% recovery.
Its a damned survey. Pathetic, no open-ended questions.  Trying to find an email address to contact them.

Siddharthan Chandran: Can the damaged brain repair itself?

He is mainly talking about TBI, MS and ALS. What is completely disgusting is that I don't think there is a single person in the world that can answer that question for stroke.

The effects of repetitive peripheral magnetic stimulation on upper-limb spasticity and impairment in patients with spastic hemiparesis: a randomized, double-blind, sham-controlled study

Damn, some on sensation, some on spasticity, none on motor.
Choose an option to locate/access this article:
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The aim of this study was to investigate short-term and long-term effects of repetitive peripheral magnetic stimulation (rpMS) on spasticity and motor function.


monocentric randomized, double-blind, sham-controlled trial.


neurologic rehabilitation hospital


66 patients with severe hemiparesis and mild to moderate spasticity due to a stroke or a traumatic brain injury. On average, time since injury was 26 or 37 weeks for the intervention groups with a standard deviation of 71 and 82, respectively.


rpMS for 20 min or sham stimulation with subsequently occupational therapy for 20 min, two times a day over a 2-week period
Main Outcome Measure(s): modified Tardieu scale and Fugl-Meyer assessment (arm score), assessed before therapy, at the end of the 2-week treatment period, and 2 weeks after study treatment. Additionally, the Tardieu scale was assessed after the 1st and before the 3rd therapy session to determine any short-term effects.


Spasticity (Tardieu >0) was present in 83% of wrist flexors, 62% of elbow flexors, 44% of elbow extensors, and 10% of wrist extensors. Compared to the sham stimulation group the rpMS group showed short-term effects on spasticity for wrist flexors (p=.048), and long-term effects for elbow extensors (p<.045). Arm motor function (rpMS group: median 5 (4-27); sham group: 4 (4-9)) did not significantly change over the study period in either group, whereas rpMS had a positive effect on sensory function.


Therapy with rpMS increases sensory function in patients with severe limb paresis. The magnetic stimulation has, however, limited effect on spasticity and no effect on motor function.

Intermittent fasting attenuates increases in neurogenesis after ischemia and reperfusion and improves recovery

What exactly will it take for your doctor to use this to create a stroke protocol? Or are they the stick in the mud type? What is the downside of doing this right now? You could just ask your patients if they are willing to try some neurogenesis possibilities that have only been tested in mice.  It might save/create neurons, isn't that worth trying?
Silvia Manzanero, Joanna R Erion, Tomislav Santro, Frederik J Steyn, Chen Chen, Thiruma V Arumugam and Alexis M Stranahan
Intermittent fasting (IF) is neuroprotective across a range of insults, but the question of whether extending the interval between meals alters neurogenesis after ischemia remains unexplored. We therefore measured cell proliferation, cell death, and neurogenesis after transient middle cerebral artery occlusion (MCAO) or sham surgery (SHAM) in mice fed ad libitum (AL) or maintained on IF for 3 months. IF was associated with twofold reductions in circulating levels of the adipocyte cytokine leptin in intact mice, but also prevented further reductions in leptin after MCAO. IF/MCAO mice also exhibit infarct volumes that were less than half those of AL/MCAO mice. We observed a 30% increase in basal cell proliferation in the hippocampus and subventricular zone (SVZ) in IF/SHAM, relative to AL/SHAM mice. However, cell proliferation after MCAO was limited in IF mice, which showed twofold increases in cell proliferation relative to IF/SHAM, whereas AL/MCAO mice exhibit fivefold increases relative to AL/SHAM. Attenuation of stroke-induced neurogenesis was correlated with reductions in cell death, with AL/MCAO mice exhibiting twice the number of dying cells relative to IF/MCAO mice. These observations indicate that IF protects against neurological damage in ischemic stroke, with circulating leptin as one possible mediator.

Medical Researchers Use Light to Quickly and Easily Measure Blood’s Clotting Properties

It doesn't say directly but I wonder if this would replace the blood draws for INR.

Stroke Rounds

I am pleased to announce that the AHA/ASA, along with our partner, MedPage Today, is re-launching Cardiovascular Daily to include a new feature-Stroke Rounds.
Stroke Rounds will be a dedicated section in the Tuesday and Thursday editions of Cardiovascular Daily, which is delivered to your email inbox each day from Monday to Friday.
Stroke Rounds will allow us to focus on the latest developments in research, treatment, quality of care, systems of care, and other topics relevant to stroke.
I hope you enjoy the "new" Cardiovascular Daily as much as we have enjoyed creating it.
Mariel Jessup, M.D.
American Heart Association/American Stroke Association

Congratulations Dr. Jessup,
Will you allow me to contribute the latest failures in stroke?  There are many.

What is the Unauthorized Practice of Medicine?

I'm just trying to make sure no one ever accuses me. Most of our doctors are obviously not  doing medicine, they are just practicing for the real game to come.
I think I would fall under this line.
Helping save a persons life falls under the Good Samaritan act and you are covered from lawsuits in most cases.
I do wonder about doing that in a hospital with a doctor standing by doing nothing. Can you get charged for practicing medicine on yourself?

New ideas change your brain cells: UBC research

This is probably where new intellectual pursuits prevent/delay dementia. But is your doctor going to put this into a stroke protocol? Fat chance!
A new University of British Columbia study identifies an important molecular change that occurs in the brain when we learn and remember.
Published this month in Nature Neuroscience, the research shows that learning stimulates our brain cells in a manner that causes a small fatty acid to attach to delta-catenin, a protein in the brain. This biochemical modification is essential in producing the changes in brain cell connectivity associated with learning, the study finds.
In animal models, the scientists found almost twice the amount of modified delta-catenin in the brain after learning about new environments. While delta-catenin has previously been linked to learning, this study is the first to describe the protein’s role in the molecular mechanism behind memory formation.
“More work is needed, but this discovery gives us a much better understanding of the tools our brains use to learn and remember, and provides insight into how these processes become disrupted in neurological diseases,” says co-author Shernaz Bamji, an associate professor in UBC’s Life Sciences Institute.
It may also provide an explanation for some mental disabilities, the researchers say. People born without the gene have a severe form of mental retardation called Cri-du-chat syndrome, a rare genetic disorder named for the high-pitched cat-like cry of affected infants. Disruption of the delta-catenin gene has also been observed in some patients with schizophrenia.
“Brain activity can change both the structure of this protein, as well as its function,” says Stefano Brigidi, first author of the article and a PhD candidate Bamji’s laboratory. “When we introduced a mutation that blocked the biochemical modification that occurs in healthy subjects, we abolished the structural changes in brain’s cells that are known to be important for memory formation.”
According to the researchers, more work is needed to fully establish the importance of delta-catenin in building the brain connectivity behind learning and memory. Disruptions to these nerve cell connections are also believed to cause neurodegenerative diseases such as Alzheimer’s and Huntington disease. Understanding the biochemical processes that are important for maintaining these connections may help address the abnormalities in nerve cells that occur in these disease states.

Marital status, dipping and nocturnal blood pressure: results from the Dietary Approaches to Stop Hypertension trial

Well, I'm sure this didn't apply to me.
The NYTimes blogging about it here; 
Marriage May Be Good for Your Blood Pressure
The abstract here;
 Marital status, dipping and nocturnal blood pressure: results from the Dietary Approaches to Stop Hypertension trial



Blood pressure normally declines during the night ('dipping'); a blunted nocturnal decline is an important cardiovascular risk factor. Marriage may be associated with lower ambulatory blood pressure, although this may be confounded by socio-economic and dietary factors. We examined the association of marital status with nocturnal dipping and night-time SBP amongst individuals on a controlled diet.


We analysed 325 individuals enrolled in the Dietary Approaches to Stop Hypertension trial who had available 24-h SBP data and who ingested a control diet. Logistic and linear regression models were fit to estimate the association of marital status with nocturnal dipping and mean night-time SBP.


Of the 325 individuals, 52.9% were men, the average age was 45.1 years and 48.9% reported being married. Compared with nonmarried individuals, those who were married had greater adjusted odds of dipping [odds ratio (OR) 2.26; 95% confidence interval (CI) 1.26-4.03; P = 0.01]. In adjusted models, being married was associated with lower night-time SBP (-2.4 mmHg; 95% CI -3.8 to -0.9 mmHg; P = 0.002), with the suggestion of a greater association in married men compared with married women (-3.1 vs. -1.7 mmHg); there was less difference for married nonblacks compared with married blacks (-2.7 and -2.4 mmHg, respectively).


Being married is independently associated with a greater likelihood of nocturnal dipping and with lower night-time SBP among individuals participating in a controlled dietary intervention; the association was particularly strong in married men. Marital status is a variable that may be considered in future analyses of ambulatory blood pressure.

National praise for £1.6 million Bradford strokes research

You in the UK will need to talk to her about preventing neuronal damage with much less disability by stopping the neuronal cascade of death. She is going down the rehab silo. That silo has a 10% full recovery rate and is a guarantee for failure. Have her push research into these 177 possibilities needing research. Or for an even faster turnaround these 31 things I will be demanding my doctor give me the first week.

A Letter from Your Future Self: What Day Is It Today?

You need to read this from Tiny Buddha.
A Letter from Your Future Self: What Day Is It Today?
You probably have 76 years of life, what are you doing with it?
And it has meditation in it Amy.

Omega 3 fatty acid for the prevention of cognitive decline and dementia

Your doctor will need to resolve the differences between this one and all the other research.
Fish Oil Fails to Stave Off Mental Decline 
Meta-analysis finds no CV benefit of omega-3 fatty acids
Monkeys That Eat Omega-3 Rich Diet Show More Developed Brain Networks
Vitamin D, Omega-3 May Help Clear Amyloid Plaques Found in Alzheimer's
Omega-3 fatty acids and traumatic neurological injury: from neuroprotection to neuroplasticity?
Protection against brain abnormalities provided by high serum omega-3 polyunsaturated fatty acid content 
Ask your doctor, whats the downside?
I will continue with this because waiting for proven answers is a recipe for disaster. So what if you have a little fish breath?

The abstract to compare these all against;
Omega 3 fatty acid for the prevention of cognitive decline and dementia



Evidence from observational studies suggests that diets high in omega-3 long-chain polyunsaturated fatty acids (PUFA) may protect people from cognitive decline and dementia. The strength of this potential protective effect has recently been tested in randomised controlled trials.


To assess the effects of omega-3 PUFA supplementation for the prevention of dementia and cognitive decline in cognitively healthy older people.


We searched ALOIS - the Cochrane Dementia and Cognitive Improvement Group's Specialized Register on 6 April 2012 using the terms: "omega 3", PUFA, "fatty acids", "fatty acid", fish, linseed, eicosapentaenoic, docosahexaenoic.


Randomised controlled trials of an omega-3 PUFA intervention which was provided for a minimum of six months to participants aged 60 years and over who were free from dementia or cognitive impairment at the beginning of the study. Two review authors independently assessed all trials.


The review authors sought and extracted data on incident dementia, cognitive function, safety and adherence, either from published reports or by contacting the investigators for original data. Data were extracted by two review authors. We calculated mean difference (MD) or standardised mean differences (SMD) and 95% confidence intervals (CI) on an intention-to-treat basis, and summarised narratively information on safety and adherence.


Information on cognitive function at the start of a study was available on 4080 participants randomised in three trials. Cognitive function data were available on 3536 participants at final follow-up.In two studies participants received gel capsules containing either omega-3 PUFA (the intervention) or olive or sunflower oil (placebo) for six or 24 months. In one study, participants received margarine spread for 40 months; the margarine for the intervention group contained omega-3 PUFA. Two studies had cognitive health as their primary outcome; one study of cardiovascular disease included cognitive health as an additional outcome.None of the studies examined the effect of omega-3 PUFA on incident dementia. In two studies involving 3221 participants there was no difference between the omega-3 and placebo group in mini-mental state examination score at final follow-up (following 24 or 40 months of intervention); MD -0.07 (95% CI -0.25 to 0.10). In two studies involving 1043 participants, other tests of cognitive function such as word learning, digit span and verbal fluency showed no beneficial effect of omega-3 PUFA supplementation. Participants in both the intervention and control groups experienced either small or no cognitive declines during the studies.The main reported side-effect of omega-3 PUFA supplementation was mild gastrointestinal problems. Overall, minor adverse events were reported by fewer than 15% of participants, and reports were balanced between intervention groups. Adherence to the intervention was on average over 90% among people who completed the trials. All three studies included in this review are of high methodological quality.


Direct evidence on the effect of omega-3 PUFA on incident dementia is lacking. The available trials showed no benefit of omega-3 PUFA supplementation on cognitive function in cognitively healthy older people. Omega-3 PUFA supplementation is generally well tolerated with the most commonly reported side-effect being mild gastrointestinal problems.Further studies of longer duration are required. Longer-term studies may identify greater change in cognitive function in study participants which may enhance the ability to detect the possible effects of omega-3 PUFA supplementation in preventing cognitive decline in older people.

Circulating omega-3 polyunsaturated fatty acids and subclinical brain abnormalities on MRI in older adults: the Cardiovascular Health Study

So how much fatty fish should we be getting while in the hospital? I just recently started buying tins of sardines in mustard sauce and making sandwiches of them.
This would seem to confirm the use of fish oil as a pretreatment and post treatment for concussions.
Monkeys That Eat Omega-3 Rich Diet Show More Developed Brain Networks

A Brain Posts blogger writing about it here:
Fish Consumption and Brain Health

The abstract here; I'm sure your doctor knows nothing of it, its only 4 months old.
 Circulating omega-3 polyunsaturated fatty acids and subclinical brain abnormalities on MRI in older adults: the Cardiovascular Health Study



Consumption of tuna or other broiled or baked fish, but not fried fish, is associated with fewer subclinical brain abnormalities on magnetic resonance imaging (MRI). We investigated the association between plasma phospholipid omega-3 polyunsaturated fatty acids (PUFAs), objective biomarkers of exposure, and subclinical brain abnormalities on MRI.


In the community-based Cardiovascular Health Study, 3660 participants aged ≥ 65 underwent brain MRI in 1992-1994, and 2313 were rescanned 5 years later. MRIs were centrally read by neuroradiologists in a standardized, blinded manner. Participants with recognized transient ischemic attacks or stroke were excluded. Phospholipid PUFAs were measured in stored plasma collected in 1992-1993 and related to cross-sectional and longitudinal MRI findings. After multivariable adjustment, the odds ratio for having a prevalent subclinical infarct was 0.60 (95% CI, 0.44 to 0.82; P for trend = 0.001) in the highest versus lowest long-chain omega-3 PUFA quartile. Higher long-chain omega-3 PUFA content was also associated with better white matter grade, but not with sulcal or ventricular grades, markers of brain atrophy, or with incident subclinical infarcts. The phospholipid intermediate-chain omega-3 PUFA alpha-linolenic acid was associated only with modestly better sulcal and ventricular grades. However, this finding was not supported in the analyses with alpha-linolenic acid intake.


Among older adults, higher phospholipid long-chain omega-3 PUFA content was associated with lower prevalence of subclinical infarcts and better white matter grade on MRI. Our results support the beneficial effects of fish consumption, the major source of long-chain omega-3 PUFAs, on brain health in later life. The role of plant-derived alpha-linolenic acid in brain health requires further investigation.

Sunday, February 23, 2014

The most important question - "Do they trust me enough to believe my promises?"

A great quote from Seth Godin. Apply this to your neurologist. Have any of their statements come true?


I used to be able to juggle three balls, but since the left hand is still useless I thought I'd try two balls in my right hand, something I used to be able to do. At a party, a daughter brought me two oranges and tried it with no practice, failed miserably. I used to use tennis balls but since they bounce and roll a lot when dropped I actually bought real juggling balls that stay put when dropped. So far  I can only get two balls to loop one time. Practice and I will succeed.

Saturday, February 22, 2014

What evidence does your doctor need to start using some hyperacute therapies that may stop the neuronal cascade of death?

The answer had better not be, ' When the Joint Commission includes it in their guidelines'
Or is the answer, 'I won't change anything from what I learned in medical school'
Or, 'I'm waiting for someone else to do the work to prove efficacy'
Is any of those answers a doctor worth trusting saving your neurons to?
177 possibilities needing research.
31 things I will be demanding my doctor give me. I will take charge of my own therapy because otherwise my doctor will just allow my neurons to die thru inaction. 
Don't do this because you will be practicing medicine, something your doctor obviously knows very little about. And you'll probably get arrested. So charge your doctor with murdering your neurons by medical neglect.

Tsunami of stroke

Its coming and no one is prepared. The existing number of neurologists and therapists will not be able to handle the workload coming. Two possibilities;
1. We just discharge them to home and instruct the caretakers like India is testing right now.
2. We revamp everything because we have figured out how to stop the neuronal cascade of death, that results in vastly less disability and the existing stroke infrastructure can handle that.
Anyone having a stroke in future years is totally screwed. Tell your parents right now to prepare to die or be disabled if they have a stroke because there is no planning or strategy  for stroke.
Tsunami statement came from  
The tsunami and stroke; two killer waves.

International Journal of Stroke

 February 2006
So 8 years and I bet nothing has been done. An example of nothing is the 

Roselinde Torres: What it takes to be a great leader

If we just look at the stroke world news in the last couple of weeks we can easily point out which ones do not have a great leader.
UC Neuroscience Institute at the University of Cincinnati and UC Health
Center for Innovation & Research at Memorial Hermann-Texas Medical Center
Mayo Clinic in Jacksonville, Fla.

Stanford marshmallow experiment

Where's the great stroke association or graduate student that will followup with these people to see if any of them had a stroke and their resilience and recovery? This I bet would map to the Mindset book,
Fixed mindset vs, growth mindset, which would also make a great graduate study, did those who delayed gratification have a growth mindset.
This link does try to sell you stuff.
T he Stanford marshmallow experiment explores the two different types of people in the world: (1) those who plan and think ahead and are able to delay immediate gratification if there is a substantially larger reward later and (2) those who grab a small reward at once (impatient decision making) rather than wait for a larger reward later. The way children as experimental subjects responded to an offered immediate reward (one marshmallow) as compared to a larger but delayed reward (two marshmallows) in the Stanford marshmallow experiment was significantly associated with very important outcomes in life such as educational attainment, income, SAT scores, body mass index, and other measures of general success in life.
The Marshmallow Experiment
The study took place in the late 60’s and early 1970’s, led by Walter Mischel, who was at that time a professor of psychology at Stanford University.A1 Children (4–6 years old) were left with a marshmallow and told that if they didn’t eat the marshmallow and waited for the experimenter to return in about 15 minutes, they would get two marshmallows (the original one plus another). The simple choice was between a small reward immediately (if the child ate the marshmallow before the experimenter returned) or a greater reward if the child waited for 15 minutes. Of 600 children that participated in the experiments, a minority ate the marshmallow immediately and of those that tried to wait for the fifteen minutes, one third of them succeeded in getting the second marshmallow. It was reported that age had a lot to do with the ability to wait for the larger reward.
The Difference Between Those Who Waited And Those Who Didn’t
J. Adam Fenster / University of Rochester
A follow-up study in 1988C reported that, “preschool children who delayed gratification longer in the self-imposed delay paradigm, were described more than 10 years later by their parents as adolescents who were significantly more competent.” The second follow-up in 1990 reported that delayed gratification was associated with higher SAT scores. Especially interesting was the result of a 2011 brain imaging study of a sample from the original child research subjects (now in middle age), which found that those who had delayed gratification longer had more activity in the prefrontal cortex (importantly involved in executive functions such as planning). Scientists know far more about the brain mechanisms involved in delaying gratification now than they did when these experiments were done. Interestingly, an important enzyme that degrades dopamine, a major constituent of the brain’s reward and reward seeking systems is involved and people with different versions of the gene encoding the enzyme have been identified to differ in their ability to delay gratification. Moreover, food components that can alter the function of the enzyme specified by that gene have also been identified, that have been shown to increase the ability to defer gratification.

Friday, February 21, 2014

Abstract T P262: Door to Needle Times Reduced With Enhanced Brain Attack Activation

These people have absolutely no idea what the hell they are doing. Its so f*cking simple you stop the need for expensive time-consuming scans and the neurologist needed to read the scan. You idiots need to be reading research papers, there are already 17 possible ways to objectively diagnose a stroke.  With that you could deliver ineffective tPA in 5 minutes.
The damned goal is wrong, door-to-needle is not the goal, Saving neurons is the goal.
 GAHHHH!!! The Stupidity.
  1. Mary Bilotta
+ Author Affiliations
  1. Reading Health System, West Reading, PA


Background: Current guidelines for care of the acute stroke patient demonstrate that the benefits of tissue plasminogen activator (tPA) are time dependent and recommend it be given within 60 minutes from arrival to the Emergency Department (ED).
Hypothesis: Door to tPA times would be reduced by using a multidisciplinary approach to acute stroke patients and by transporting them directly to the CT scanner.
Methods: The community hospital restructured its Brain Attack process after creating a Door to Needle team to evaluate and expedite the care of the acute stroke patient. This multidisciplinary team was assembled in order to plan, implement, and study the new Brain Attack alert process. The team is activated via a touchscreen in the ED, many times prior to patient arrival. Stable patients who do not require airway intervention are taken directly to a newly renovated CT scan anteroom for initial assessment, point of care anticoagulation testing, and initial NIH stroke scale. In addition, education concerning the new process, as well as acute stroke care in general was presented to 35 local EMS services by emergency physicians and an EMS outreach coordinator.
Results: In July of 2012, 54 Brain Attacks were evaluated with a median door to CT time of 41 minutes and door to CT interpretation time of 51 minutes. The new Brain Attack process was implemented on December 3, 2012. During the first month of the new process, 51 Brain Attacks were evaluated with median door to CT time of 28 minutes and door to CT interpretation time of 38 minutes. This represents a decrease in time to CT acquisition and interpretation of 13 minutes. tPA was given to 4 patients in July 2012 with only one patient (25%) receiving the medication in <60 minutes. In December, 4 patients received tPA, 3 (75%) within the 60 minute window.
Conclusions: Patients who received tPA were treated more expeditiously after implementation of the restructured activation process. 75% of tPA patients were treated within the 60 minute timeframe as recommended by current guidelines. EMS also provided extremely positive feedback concerning the education and restructured Brain Attack activation.

Taking Stroke Tx on the Road

Damn, damn, damn, going down the failure path again. While this might help in the short term it's just delaying the search for something that actually works. A 12% tPA efficacy rate is not a success by any stretch of the imagination. This is why no one in the stroke medical world should be making decisions about stroke. They fail almost every time. You notice they are using a portable CT scanner rather than seeing if one of the fast and objective possibilities are worth using.  Cost a hell of a lot less than 1M.
"My prediction is that 10 years from now every city in the country will have imaging on their ambulances,"
You are going to be so wrong with that stupid prediction, the tricorder will be used to diagnose stroke long before then. Do you even know about anything newer than 30 years ago?  Turn in your medical license now.

“An apple a day keeps the doctor away,”

A UK vascular mortality of all adults over 50 years old being prescribed either a statin or an apple a day.
What does your doctor think of the results or is the pressure from drug compnies too high?
  1. Adam D M Briggs, academic clinical fellow,
  2. Anja Mizdrak, researcher,
  3. Peter Scarborough, senior researcher
Author Affiliations
  1. Correspondence to: A D M Briggs
  • Accepted 27 November 2013


Objective To model the effect on UK vascular mortality of all adults over 50 years old being prescribed either a statin or an apple a day.
Design Comparative proverb assessment modelling study.
Setting United Kingdom.
Population Adults aged over 50 years.
Intervention Either a statin a day for people not already taking a statin or an apple a day for everyone, assuming 70% compliance and no change in calorie consumption. The modelling used routinely available UK population datasets; parameters describing the relations between statins, apples, and health were derived from meta-analyses.
Main outcome measure Mortality due to vascular disease.
Results The estimated annual reduction in deaths from vascular disease of a statin a day, assuming 70% compliance and a reduction in vascular mortality of 12% (95% confidence interval 9% to 16%) per 1.0 mmol/L reduction in low density lipoprotein cholesterol, is 9400 (7000 to 12 500). The equivalent reduction from an apple a day, modelled using the PRIME model (assuming an apple weighs 100 g and that overall calorie consumption remains constant) is 8500 (95% credible interval 6200 to 10 800).
Conclusions Both nutritional and pharmaceutical approaches to the prevention of vascular disease may have the potential to reduce UK mortality significantly. With similar reductions in mortality, a 150 year old health promotion message is able to match modern medicine and is likely to have fewer side effects.

Gallup-Healthways State Well-Being Index

And I willingly moved from Minnesota - 4th to Michigan - 37th. But I dodged a bullet. I had a provisional job offer based in West Virginia - 50th, that fell through because McDonnell-Douglas did not get the government contract.
Details from here:
I can't get it to display properly so you'll have to click on the link here.

Seasonal flu vaccine may cut stroke risk

So is this because of reduction of inflammation? Inquiring minds want to know.
Having the seasonal flu jab could reduce the risk of suffering a stroke by almost a quarter, researchers have found.

Academics from the University of Lincoln and The University of Nottingham in the UK discovered that patients who had been vaccinated against influenza were 24% less likely to suffer a stroke in the same flu season.

Their findings are reported in the scientific journal Vaccine.

In 2010, the same research team showed a similar link between flu vaccination and reduced risk of heart attack.

Lead investigator Professor Niro Siriwardena, who is Professor of Primary and Pre-hospital Healthcare in the School of Health and Social Care at the University of Lincoln and also a GP and Research Lead with Lincolnshire Community Health Services NHS Trust, said: "The causes of stroke are not fully understood. Classical risk factors like age, smoking and high blood pressure can account for just over half of all cases.
"We know that cardiovascular diseases tend to hit during winter and that the risks may be heightened by respiratory infections such as flu.
"Our study showed a highly significant association between flu vaccination and reduced risk of stroke within the same flu season.  The results were consistent with our previous research into heart attack risk."

Dr Zahid Asghar, statistician on the project, supported by Dr Carol Coupland (University of Nottingham) analysed records of more than 47,000 patients who had suffered a stroke or TIA (transient ischaemic attack, or "mini stroke") between 2001 and 2009. Data were drawn from the UK's national General Practice Research Database (now the Clinical Practice Research Datalink). Alongside flu vaccine take-up, they also looked at take-up of pneumococcal vaccination, which protects against infections like pneumonia.

They found flu vaccination was associated with a 24% reduction in risk of stroke. The reduction was strongest if the vaccination was given early in the flu season. There was no statistically significant change in risk of TIA with flu vaccination. Pneumococcal vaccination did not appear to reduce risks of either stroke or TIA.

The study, called IPVASTIA, used a matched case-control design. Actual cases of stroke were compared against 'control' patients, adjusted for other factors that might explain the differences in risk associated with flu vaccination such as age, existing diseases and treatment history. This type of analysis is widely used in health research to identify risk factors in large samples, although it cannot prove direct cause-and-effect relationships.

Professor Siriwardena added: "Further experimental studies would be needed to better understand the relationship between flu vaccination and stroke risk. However, these findings reinforce the value of the UK’s national flu vaccination programme with reduced risk of stroke appearing to be an added health benefit."

In the UK the seasonal flu vaccination is recommended for everyone over 65 years of age and other at-risk groups, such as those with disabilities or chronic illnesses. Take-up of the vaccine across England is lower than national targets at 74% for over-65s in 2011/12 and around 52% for under-65s in at-risk groups.

The study by Professor Siriwardena and his co-researchers features on a new website,, launched today (20th February 2014) by the UK’s National Institute for Health Research. The site aims to give the public an insight into the great work being done in the NHS to tackle stroke.

Thursday, February 20, 2014

Hot Topics: Advances in Stroke

If these three guys are supposed to be experts, we are totally screwed. Not one of them mentioned any of the prevention ideas I've written about and whats worse is no mention of the neuronal cascade of death. All it was about is status quo stuff. That is nowhere close to being able to handle the upcoming tsunami of stroke. They should be hanging their heads in shame. If I was a real bastard I'd be writing to their institutions demanding to know when someone intelligent and innovative takes over.
Only 3min 13 seconds of blah.
What works and what doesn't work in stroke? We asked three experts in the field for their take: Joseph Broderick, MD, director of the UC Neuroscience Institute at the University of Cincinnati and UC Health, James C. Grotta, MD, director of stroke research in the Center for Innovation & Research at Memorial Hermann-Texas Medical Center, and Thomas G. Brott, MD, of the Mayo Clinic in Jacksonville, Fla. In this video, they discuss stents, tPA, and artery bypass. What's not working includes clot removal and some recent devices.
F*CK it all - There is absolutely nothing working in stroke. If you don't know that get the hell out and let some intelligent people solve the stroke problems.

Damage to dead cell disposal system may increase heart disease

Is your doctor willing to look into this to see about preventing your next stroke or heart attack?
efferocytosis (from efferre, Latin for 'to take to the grave', 'to bury')
Conducting studies in mice with atherosclerosis, the researchers showed that loss of a candidate gene at this locus leads to impaired “efferocytosis” - from the Latin for “take to the grave” – the process by which dead or necrotic cells are removed. Literally, the burying of dead cells. Mice with this genetic variation showed an increase in buildup of these dead cells, further advancing their atherosclerosis as opposed to those that did not have the genetic variation.

In other words, a commonly inherited genetic variant, which is found in 20 percent of the population, contributes to the development of coronary artery disease (also known as coronary atherosclerosis) by stimulating the accumulation of necrotic debris within the evolving plaque. Coronary atherosclerosis is the process by which plaque builds up in the wall of heart vessels, eventually leading to chest pain and potentially lethal heart attacks. Leeper explained it to me further:

    If you were born with genetic variation at the 9p21 locus, your risk of heart disease is elevated, though we haven’t understood why. This research gets at that hidden risk. You can be a non-smoker, be thin, have low blood pressure, and still be at risk for a heart attack if you were born with this variant. This work may help explain that inherited risk factor, and more importantly help develop a new therapy to prevent the heritable component of cardiovascular disease. 

Rest at link. 
Conducting studies in mice with atherosclerosis, the researchers showed that loss of a candidate gene at this locus leads to impaired “efferocytosis” - from the Latin for “take to the grave” – the process by which dead or necrotic cells are removed. Literally, the burying of dead cells. Mice with this genetic variation showed an increase in buildup of these dead cells, further advancing their atherosclerosis as opposed to those that did not have the genetic variation.
In other words, a commonly inherited genetic variant, which is found in 20 percent of the population, contributes to the development of coronary artery disease (also known as coronary atherosclerosis) by stimulating the accumulation of necrotic debris within the evolving plaque. Coronary atherosclerosis is the process by which plaque builds up in the wall of heart vessels, eventually leading to chest pain and potentially lethal heart attacks. Leeper explained it to me further:
If you were born with genetic variation at the 9p21 locus, your risk of heart disease is elevated, though we haven’t understood why. This research gets at that hidden risk. You can be a non-smoker, be thin, have low blood pressure, and still be at risk for a heart attack if you were born with this variant. This work may help explain that inherited risk factor, and more importantly help develop a new therapy to prevent the heritable component of cardiovascular disease.
- See more at:

Iron deficiency may increase stroke risk through sticky blood

No self-prescription here, you would need some type of blood test to determine if you are deficient. Another thing for your doctor to know to prevent your next stroke.
Scientists at Imperial College London have discovered that iron deficiency may increase stroke risk by making the blood more sticky.
The findings, published in the journal PLOS ONE, could ultimately help with stroke prevention.
Every year, 15 million people worldwide suffer a stroke. Nearly six million die and another five million are left permanently disabled. The most common type, ischaemic stroke, occurs because the blood supply to the brain is interrupted by small clots.
In the last few years, several studies have shown that iron deficiency, which affects around two billion people worldwide, may be a risk factor for ischaemic stroke in adults and in children.  How iron deficiency could raise stroke risk has been a puzzle for researchers.
The Imperial team found that iron deficiency increases the stickiness of small blood cells called platelets, which initiate blood clotting when they stick together. Although a link between iron deficiency and sticky platelets was first discovered almost 40 years ago, its role has been overlooked until now.
The researchers studied a group of patients with a rare disease called hereditary haemorrhagic telangiectasia (HHT) that often leads to enlarged blood vessels in the lungs, similar to varicose veins.  Normally, the lungs’ blood vessels act as a filter to remove small clots before blood goes into arteries. In patients with abnormal lung vessels, blood is able to bypass the filter, so small blood clots can travel to the brain.
The patients in the study who were short of iron were more likely to have a stroke.  In addition, the researchers looked at platelets in the lab and found that when they treated these with a substance that triggers clotting, platelets from people with low iron levels clumped together more quickly.
Dr Claire Shovlin, from the National Heart and Lung Institute at Imperial College London, said: “Since platelets in the blood stick together more if you are short of iron, we think this may explain why being short of iron can lead to strokes, though much more research will be needed to prove this link.
 “The next step is to test whether we can reduce high-risk patients’ chances of having a stroke by treating their iron deficiency.  We will be able to look at whether their platelets become less sticky.  There are many additional steps from a clot blocking a blood vessel to the final stroke developing, so it is still unclear just how important sticky platelets are to the overall process.  We would certainly encourage more studies to investigate this link.”
The researchers studied data on 497 patients with abnormal blood vessels in the lung, known as pulmonary arteriovenous malformations, who were treated at a specialist HHT clinic at Hammersmith Hospital. The study found that even moderately low iron levels, around 6 micromoles per litre, approximately doubled the risk of stroke compared with levels in the middle of the normal range of 7-27 micromoles per litre.
Besides this group of patients, many other people have conditions that can allow blood clots to bypass the filter in the lungs. One in four people have a hole in the heart called a patent foramen ovale.  Holes in the heart also allow blood to bypass the lung filter from time to time, though not as often as for the lung patients.
The research was supported by donations from family and friends of HHT patients.

Peri Infarct N-Acetylaspartic Acid Predicts White Matter Atrophy After Ischemic Stroke

Finally someone thinking about objectively measuring white matter damage. What does your doctor think of that?
  1. Stephen M Davis1
+ Author Affiliations
  1. 1Melbourne Brain Cntr, Univ of Melbourne, Parkville, Australia
  2. 2Priority Rsch Cntr for Translational Neuroscience and Mental Health, Univ of Newcastle, Newcastle, Australia
  3. 3Univ of Melbourne, Parkville, Australia
  4. 4Dept of Radiology, Univ of Melbourne, Parkville, Australia


Objective: Cerebral volume changes post stroke have recently been described and may correlate with clinical outcome. We aimed to determine whether peri infarct measurement of the neuronal marker N-Acetylaspartic acid (NAA) on Magnetic Resonance Spectroscopy (MRS) predicts progressive cerebral volume change after stroke.
Methods: 11 patients (7 male) with supratentorial ischemic stroke underwent serial MRI within 1 week of onset, and at 1 and 3 months. Imaging was performed on a 3T Siemens Trio scanner. Structural imaging utilized a T1-weighted axial MPRAGE acquisition (1mm slices, TR1.9sec, TE2.82msec). NAA estimation was performed at the baseline scan using single voxel MRS (TE30msec, 3x3x3cm voxels). The voxel was placed in the peri infarct region as determined by assessment of the diffusion weighted image. Quantitative MRS analysis was performed using LCmodel using water referencing. Brain tissue volume, normalized for subject head size, was estimated with SIENAX, part of FSL. Due to anticipated effects of edema on initial cerebral volume, changes in grey, white and total brain volume were assessed as percentage change between the 1 and 3 month scans.
Results: Mean age was 71yr (IQR 62-79yr). Median baseline NIHSS was 11 (IQR 6-14). Mean baseline grey, white and total brain volume were 713ml (IQR 683-749), 731mL (IQR 721-747) and 1444mL (IQR 1384-1503) respectively. There was a significant correlation between age and baseline grey matter volume (r2=0.73, p=0.001) and total brain volume (r2=0.74, p=0.001). Mean peri infarct NAA concentration was 6.2mM (SD 1.3) compared with 7.0mM (SD 1.2) in the contralateral hemisphere (p=0.09, paired t-test). Mean percentage grey, white and total brain volume changes were 1.2% (IQR -1.8-4.1), 0.4% (IQR -2.2-3.7) and 0.8% (IRQ -1.0-2.6) respectively. There was a significant correlation between baseline NAA in the peri infarct region and change in white matter volume between the 1 and 3 month time points (r2=0.26, p=0.008).
Conclusions: Estimation of the neuronal marker NAA using MRS may signify varying degrees of neuronal damage after stroke which may correlate with the severity of axonal degeneration and subsequent white matter volume changes. Further validation and correlation with clinical outcomes is required.

Predicting Future Atrophy from White Matter Connectivity Disruption in Ischemic Stroke

Finally someone thinking about objectively measuring white matter damage. What does your doctor think of that?
  1. Ashish Raj1
+ Author Affiliations
  1. 1Radiology, Weill Cornell Med College, New York, NY
  2. 2Neurology, Weill Cornell Med College, New York, NY


Background: The Network Modification (NeMo) Tool uses a library of brain connectivity maps from normal subjects to quantify the amount of structural connectivity loss caused by focal brain lesions. We hypothesized that the NeMo Tool could predict remote brain tissue loss caused by Wallerian degeneration after stroke.
Methods: Baseline and follow-up MRIs from 27 patients with acute ischemic stroke were collected (74±14 years, initial NIHSS 2±3, 5.7±2.8 months b/w scans). Diffusion-weighted image derived lesion masks were superimposed on the NeMo Tool’s connectivity maps in order to predict changes to the structural connectivity network and to investigate correlations with future atrophy. Regional connectivity losses were estimated via the Change in Connectivity (ChaCo) score, i.e. the percent of “injured” tracks going through lesions that connect to a given region. ChaCo scores and longitudinal tissue changes were calculated using a standard 116 region atlas.
Results: Lesion location and size varied greatly, but they occurred more frequently in the left hemisphere. The ChaCo scores, which were generally higher in regions near stroke lesions, reflected this heterogeneity. In general, ChaCo was higher in the left hemisphere than the right and was high in the postcentral and precentral gyri, insula, middle cingulate, thalami, putamen, caudate nuclei, and pallidum. Moderate correlations were found between ChaCo scores at baseline and measures of subsequent tissue loss (change in volume and average mean diffusivity [MD] from baseline to follow-up, see Figure 1).
Conclusions: ChaCo scores varied greatly, but the most affected regions included those with sensorimotor, perception, learning and memory functions. Moderate correlations were found between ChaCo scores at baseline and subsequent tissue loss. These results suggest that the NeMo Tool could enable more accurate prognosis, as it may identify regions most susceptible to degeneration from remote infarcts.

Abstract T MP46: Stroke-Related Neuroplasticity During Steering of Human Gait

It seems to me that if your are going to get better at 'steering' you have to get a lot closer to falling by massive number of perturbations in your gait. Like this;
Motorized Shoes Help Elderly Prepare for Walking Accidents
Or this;
The effect of vibrotactile feedback on postural sway during locomotor activities
Or this;
Clinic helps stroke patients recover balance, avoid future falls
Or these;
1. Unstable Shoes Increase Energy Expenditure of Obese Patients
2. Compelled BodyWeight Shift Technique to Facilitate Rehabilitation of Individuals with Acute Stroke
3. Documenting abnormal anticipatory control prior to gait initiation in sub-acute stroke
4.  spnKiX motorized shoes edge closer to production
5. Motivation through Inclusion of Failure in Stroke Rehabilitation 
Or this;
Training to walk amid uncertainty with Re-Step: measurements and changes with perturbation training for hemiparesis and cerebral palsy
And the newest one here; 
  1. Jean-Paul Soucy2
+ Author Affiliations
  1. 1Kinesiology and Physical Education, McGill Univ, Montreal, Canada
  2. 2Neurology &Neurosurgery, McGill Univ, Montreal, Canada


Background: The risk of falling is higher in stroke survivors than among the general population. These falls are more frequent during walking and transfers or during turning. The neuronal substrates involved in steering of locomotion are poorly understood due to methodological limitations in quantifying brain activations during whole-body movements. Thus, no data is currently available to study the mechanisms of post-stroke brain plasticity for steering of gait. This study tested the hypothesis that stroke-induced neuroplastic changes for steering of gait can be quantified using 18F- fluorodesoxy-glucose (18F-FDG) Positron Emission Tomography (PET) in-vivo in humans
Methods: PET imaging with 18F-FDG tracer was used to quantify cerebral glucose metabolism (CMRGlc) during two locomotor tasks (straight walking and turning) measured on separate days. Immediately prior to each walking task, a 5 mCi bolus of 18F-FDG was injected. Subjects walked for 40 minutes (duration of 18F-FDG uptake). Subjects were scanned on an ECAT HR+ scan (20min emission followed by 10min transmission) within 10 minutes of completing the walking task, well within reaching the 2h half-life of 18F. Images obtained during straight walking were subtracted from the ones acquired during steering
Results: Subjects post-stroke showed an asymmetrical pattern of CMRGlc in sensorimotor areas and superior parietal lobule where the affected hemisphere shows no increase in CMRGlc. Differences between groups were also observed in the cerebellum where CMRGlc was increased in the vermis for controls, an area predominant for the control of trunk and gait. Stroke subjects, in contrast, showed increased CMRGlc in the hemishperes, associated with goal-directed leg movements.
Conclusions: Neuroplasticity in complex locomotor tasks such as steering can be quantified using 18F-FDG PET in subjects post-stroke. This study showed that changes affect several brain regions remote to the infarct. Understanding stroke-related changes in brain activity during steering of locomotion is crucial for improving rehabilitative strategies to minimize falls and injuries in stroke survivors.

“Senior coolness”: Living well as an attitude in later life

Nonchalance toward the problems in your life. I aspire to that.
Examples from the interviews.
The researchers cite many examples from the interviews to make their case. Here is a sample:

Mrs B (aged 87), a former nursing assistant, is no longer able to keep up with her housework. "Whenever I think: 'Oh, you ought to tidy things up again!', I don't do it every time, it doesn't bother me."

Mrs M (aged 88), a retired school teacher who uses a walking frame, reflects on how she will never be able to travel abroad again. "I'll never get there [to the ocean] again - never mind. That's just the thing, you make the most of the things you've had […] Of course, it's a shame I've never been to Greece. But: so what? As a child I saw half the world." [words in italics were uttered in English.]

Mrs H (aged 86), a former laundry shop worker, speaking about her incontinence: "I can think of more pleasant things."

Mrs L (aged 84), a former unskilled assistant at trade auctions, suffers from chronic pain. "… [Y]ou take what comes. What else can you do? I can still take pleasure in this and that."
Abstract here:
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Public perceptions of old age (80 +) focus largely on deficiency and loss.
By contrast, elderly people (80 +) report ways in which they are able to live well.
Living well in old age can be associated with the capacity to “keep cool”.
This “senior coolness” renders personal and societal problems manageable.


With demographic change becoming an ever more pressing issue in Germany, old age (80 +) is currently talked about above all in terms of being a problem. In mainstream discourse on the situation of the oldest old an interpretive framework has emerged that effectively rules out the possibility of people living positively and well in old age. With regard to both individual (personal) and collective (societal) spheres, negative images of old age dominate public debate. This is the starting point for an interdisciplinary research project designed to look at the ways in which people manage to “live well in old age in the face of vulnerability and finitude” — in express contrast to dominant negative perspectives. Based on the results of this project, the present article addresses an attitudinal and behavioral mode which we have coined “senior coolness”. Coolness here is understood as both a socio-cultural resource and an individualized habitus of everyday living. By providing an effective strategy of self-assertion, this ability can, as we show, be just as important for elderly people as for anyone else. “Senior coolness” is discussed, finally, as a phenomenon that testifies to the ways elderly people retain a positive outlook on life — especially in the face of difficult circumstances and powerful socio-cultural pressures.