Traumatic brain injury incidence could be six times higher than previously estimated

If this holds up, that would mean millions more people worldwide need some kind of treatment. What is your countries stroke association going to do about it? Or are you planning on relying on the WSO failure?
http://www.news-medical.net/news/20121122/Traumatic-brain-injury-incidence-could-be-six-times-higher-than-previously-estimated.aspx

The first study to estimate rates of traumatic brain injury (TBI), without relying on official figures, suggests the worldwide incidence of TBI could be six times higher than previously estimated. The New Zealand population-based study, published Online First in The Lancet Neurology, found that rates of TBI (790/100 000 people per year), and particularly mild TBI (749/100 000), were far higher than in other high-income countries in Europe (47–453/100 000) and North America (51–618/100 000).
“Our estimates are the first to include more mild cases of TBI that are not usually treated in hospital and, thus, are often overlooked in official estimates,” explains Professor Valery Feigin, who heads AUT University’s National Institute for Stroke and Applied Neurosciences in New Zealand and led the research.
“It is the first study to show that 95% of all TBI cases are mild and that the true annual incidence of mild TBI is substantially higher than recent World Health Organisation (WHO) estimates (100–300/100 000 people per year). Based on these findings, we estimate that some 54–60 million people worldwide sustain a TBI each year, of which some 2.2–3.6 million people incur moderate or severe TBI. This is almost six times higher than previous estimates and means that every second two people in the world are struck by a new TBI.”
TBI occurs when an external force such as a bump or blow to the head disrupts the normal function of the brain. Leading causes include falls, motor vehicle accidents, and assaults.
TBI is the leading cause of long-term disability among children and young adults and cost the USA alone an estimated $406 billion in 2000. TBI is projected to become the third largest cause of disease burden worldwide by 2020.
The BIONIC (Brain Injury Outcomes New Zealand In the Community) study examined multiple overlapping sources of information (eg, public hospitals, family doctors, rehabilitation centres, coroner/autopsy records, rest homes, ambulance services, and prisons) to record all new cases of TBI that occurred over a one-year period (1 March 2010 to 28 February 2011) in an area (173,205 residents) representative of the New Zealand population in terms of demographic, ethnic, socioeconomic, and urban and rural structure.
Rates of TBI were highest in children (0–14 years old) and younger adults (15–34 years old), accounting for almost 70% of cases, far higher than the 40–60% reported in previous studies.

next page at the link

Chocolate Consumption, Cognitive Function, and Nobel Laureates

Various takes on this story. Do not self-medicate.

The New England Journal of Medicine: This is paywalled.
http://www.nejm.org/doi/full/10.1056/NEJMon1211064
Chocolate consumption could hypothetically improve cognitive function not only in individuals but in whole populations. Could there be a correlation between a country's level of chocolate consumption and its total number of Nobel laureates per capita?

Chocolate-loving countries produce more Nobel laureates

Chocolate consumption, cognitive function & nobel laureates

If Eating Chocolate Increases My Chances of Winning a Nobel Prize, Why Haven't I Won?

 

 

 

 

 

Back seat driving: hindlimb corticospinal neurons assume forelimb control following ischaemic stroke.

Who is going to take this and determine applicability to humans and then create a therapy protocol?
Don't just tell me it occurs, tell me exactly how to make it occur. Otherwise I'll know you are lazy and wish to leave the hard work to us stroke-addled patients.

http://feedproxy.google.com/~r/nih/bxxu/~3/Q_ujIq_Y6A4/display.cgi
Whereas large injuries to the brain lead to considerable irreversible functional impairments, smaller strokes or traumatic lesions are often associated with good recovery. This recovery occurs spontaneously, and there is ample evidence from preclinical studies to suggest that adjacent undamaged areas (also known as peri-infarct regions) of the cortex 'take over' control of the disrupted functions. In rodents, sprouting of axons and dendrites has been observed in this region following stroke, while reduced inhibition from horizontal or callosal connections, or plastic changes in subcortical connections, could also occur. The exact mechanisms underlying functional recovery after small- to medium-sized strokes remain undetermined but are of utmost importance for understanding the human situation and for designing effective treatments and rehabilitation strategies. In the present study, we selectively destroyed large parts of the forelimb motor and premotor cortex of adult rats with an ischaemic injury. A behavioural test requiring highly skilled, cortically controlled forelimb movements showed that some animals recovered well from this lesion whereas others did not. To investigate the reasons behind these differences, we used anterograde and retrograde tracing techniques and intracortical microstimulation. Retrograde tracing from the cervical spinal cord showed a correlation between the number of cervically projecting corticospinal neurons present in the hindlimb sensory-motor cortex and good behavioural recovery. Anterograde tracing from the hindlimb sensory-motor cortex also showed a positive correlation between the degree of functional recovery and the sprouting of neurons from this region into the cervical spinal cord. Finally, intracortical microstimulation confirmed the positive correlation between rewiring of the hindlimb sensory-motor cortex and the degree of forelimb motor recovery. In conclusion, these experiments suggest that following stroke to the forelimb motor cortex, cells in the hindlimb sensory-motor area reorganize and become functionally connected to the cervical spinal cord. These new connections, probably in collaboration with surviving forelimb neurons and more complex indirect connections via the brainstem, play an important role for the recovery of cortically controlled behaviours like skilled forelimb reaching.

Why is it that after a stroke, some patients recover faster and better than others?

This should have been done decades ago.  So you in the Thunder Bay area contact her and volunteer.
http://www.netnewsledger.com/2012/11/22/healthbeat-why-is-it-that-after-a-stroke-some-patients-recover-faster-and-better-than-others/

Dr. Jane Lawrence-Dewar of the Thunder Bay Regional Research Institute (TBRRI) will be investigating how the brain re-maps itself after a stroke. This baseline research will help future scientists develop better ways of helping stroke patients recover.

THUNDER BAY – Health News – Why is it that after a stroke, some patients recover faster and better than others? And are there ways we can help that process?
Those are two of the questions that Dr. Jane Lawrence-Dewar of the Thunder Bay Regional Research Institute (TBRRI) will be investigating shortly. At first, her research will concentrate on hand coordination, how that coordination is affected by stroke, and how it recovers or adapts after stroke.
“We know that following a stroke injury, many patients can recover some hand function, but that amount is always variable,” Dr. Lawrence-Dewar said. “We really just don’t know what is happening in the brain in order to make that happen.”
Generally speaking, the brain is often able to “re-map” itself after an injury, creating new pathways around the injured area. But this happens differently in each patient.
“I’m interested in what changes in the patterns of brain activity in order to facilitate that recovery.”
Dr. Lawrence-Dewar uses a method called functional Magnetic Resonance Imaging or fMRI. This method detects brain activity based on changes in blood flow and blood oxygenation. It is a non-invasive technique that doesn’t require a contrast or radiation.
The study itself will measure the brain activity of a stroke patient while they are simply lying down inside the MRI. Then, the patient will be asked to do some sort of task, at which point certain areas of the brain will light up.
“What I aim to do is try to piece together the differences in the patterns laid out when people recover well versus when they aren’t as well,” she said. “If we can learn what areas of the brain we need to get active, perhaps we can use that knowledge in order to make our rehab methods more effective or develop new tools that can better target that re-mapping.”
What makes the research even more complex is that every stroke patient will be different, both in injury and recovery.
“This is one of the challenges – and one of the arguments for having techniques that enable personalized medicine,” Dr. Lawrence-Dewar said.
In other words, once you are able to study the patient’s particular injury and get insight based on previous cases to see what treatment approach might work best, doctors can create a rehab routine that is custom-made for that patient. (Duh, this is so obvious why did it take so long to come to this conclusion, I thought this immediately after my stroke and I'm stroke-addled)
Right now, Dr. Lawrence-Dewar is waiting for additional equipment, including a projection screen and a specialized all-plastic trackball that can safely enter the MRI unit with the patient (steel and other metals are not allowed within the strong magnetic field) so the patient can see and react to events on the screen. These tools will help her determine hand function while simultaneously observing fMRI images of the brain to see which areas are lighting up – and which aren’t.
The current project will take about two years to complete, Dr. Lawrence-Dewar said, though she expects it will evolve into other areas of study. This research will provide a scientific “baseline” for future studies that could investigate ways of helping patients improve recovery by assisting with the brain re-mapping in some way.
“Right now I’m at Step 1,” Dr. Lawrence-Dewar said.

IRCM researchers discover a nerve cell's internal clock

I couldn't help it, another reference to the sonic hedgehog. Ask your doctor if this could help your neurogenesis.
http://www.news-medical.net/news/20121122/IRCM-researchers-discover-a-nerve-cells-internal-clock.aspx

A team of IRCM researchers, led by Dr. Fr-d-ric Charron, recently uncovered a nerve cell's internal clock, used during embryonic development. The discovery was made in collaboration with Dr. Alyson Fournier's laboratory at the Montreal Neurological Institute. Published today in the prestigious scientific journal Neuron, this breakthrough could lead to the development of new tools to repair and regenerate nerve cells following injuries to the central nervous system.
Researchers in Dr. Charron's laboratory study neurons, which are the nerve cells that make up the central nervous system (brain and spinal cord). They want to better understand how neurons navigate through the developing embryo to arrive at their correct destination.
"To properly form neural circuits, developing axons (long extensions of neurons that form nerves) follow external signals to reach the right targets," says Dr. Fr-d-ric Charron, Director of the Molecular Biology of Neural Development research unit at the IRCM. "We discovered that nerve cells also have an internal clock, which changes their response to external signals as they develop over time."
For this research project, IRCM scientists focused on the Sonic Hedgehog (Shh) protein, which gives cells important information for the embryo to develop properly and plays a critical role in the development of the central nervous system.
"It is known that axons follow the Shh signal during their development," explains Dr. Patricia Yam, research associate in Dr. Charron's laboratory and first author of the study. "However, axons change their behaviour once they reach this protein, and this has been a mystery for the scientific community. We found that a nerve cell's internal clock switches its response to external signals when it reaches the Shh protein, at which time it becomes repelled by the Shh signal rather than following it."

next page at the link.

Tirofiban effectively prevents strokes in high risk patients

See if your doctor thinks this may be useful for your prevention. At least find out if you are considered high risk.
http://www.news-medical.net/news/20121122/Tirofiban-effectively-prevents-strokes-in-high-risk-patients.aspx

Scientists may have discovered a new way to prevent strokes in high risk patients, according to research from the University of Warwick and University Hospitals Coventry and Warwickshire (UHCW).
Work by a new research group, led by Professor Donald Singer, Professor of Therapeutics at Warwick Medical School and Professor Chris Imray from UHCW, has now been published in US journal Stroke.
The group is using ultrasound scanning to look at patients with carotid artery disease, one of the major causes of stroke. Clots can form on diseased carotid arteries in the neck. Small parts of these clots can released to form microemboli, which can travel to block key brain arteries and lead to weakness, disturbed speech, loss of vision and other serious stroke syndromes. Standard anti-platelet drugs such as aspirin may not prevent the formation of harmful microemboli.
The scanning process can be used to find patients at very high risk of stroke because microemboli have formed despite prior anti-platelet drugs. Using scanning, the team has found that tirofiban, another anti-platelet drug designed to inhibit the formation of blood clots, can suppress microemboli where previous treatment such as aspirin has been ineffective. In their study, tirofiban was more effective than other 'rescue' treatment.
Professor Singer said: "These findings show that the choice of rescue medicine is very important when carotid patients develop microemboli despite previous treatment with powerful anti-platelet drugs such as aspirin. We now need to go on to further studies of anti-microemboli rescue treatments, to aim for the right balance between protection and risk for our patients."
Professor Imray said: "These findings show the importance of ultrasound testing for micro-emboli in carotid disease patients. These biomarkers of high stroke risk cannot be predicted just from assessing the severity of risk factors such as smoking history, cholesterol and blood pressure."

DocGuide

DG Apps brings the best of the world of medical apps to the physicians and healthcare professionals. Focused 100% on professional practice (rather than apps for the general public), it saves time and keeps users up-to-date with apps of most interest in a particular specialty area(s).
You can register as a patient to see what is out there for your neurologist and even get the free ones for yourself.  And then see what your doctor should know about your condition.  Your doctor should know more than you about your condition  but I bet s/he doesn't.
http://dgapps.docguide.com/
The ones highlighted for stroke;
http://dgapps.docguide.com/appsearch/ios/latest/stroke

National Disability Insurance Scheme (NDIS)

This will never happen in the US, they would rather we be reduced as part of the surplus population. Great for Australia though. My former Senator Hubert Humphrey had this saying,
"The moral test of government is how it treats those who are in the dawn of life . . . the children; those who are in the twilight of life . . . the elderly; and those who are in the shadow of life . . . the sick . . . the needy . . . and the disabled." Our people/government just dodged a bullet.
http://www.strokefoundation.com.au/blog/?p=2428
To date, the funding for people with a disability has been a cruel lottery
The amount of support and services for people with a disability, their families and carers has depended on where they live, what disability they have, and how they attained that disability. The NDIS aims to change all of that.
The Prime Minister released the Productivity Commission’s report on 10 August 2011 and all governments agreed with the recommendation to establish an NDIS. Rather than funding based on historical budget allocations, a funding pool will be
based on actuarial assessment of need.
It will recognise that disability is for a lifetime, and so it will take a lifelong approach to providing care and support. This means that assessment will look beyond the immediate need, and across the course of a person’s life. Taking a lifelong approach also means focusing on intensive early intervention, particularly for people where there is good evidence that it will substantially improve functioning or delay or lesson a decline in functioning.
Importantly, an NDIS will support choice for people with disability, their families and carers, and put people in control of the care and support they receive, based on need. An NDIS will ensure people are no longer “shut out” from opportunities and from independence by providing the appropriate and necessary supports that allow people with disability to reach their full potential.
It will nurture and sustain the support of families, carers and friendship groups – the very communities of support that are
critical to improving the lives of people with disability.
And it will include a comprehensive information and referral service, to help people with a disability who need access to mainstream, disability and community supports.
Latest updates
The first stage of a National Disability Insurance Scheme (NDIS) will become real for people with significant disabilities in South Australia, Tasmania, the ACT, the Hunter in NSW and the Barwon region of Victoria.
ACT: the timing for the launch of the NDIS may start in July 2013 or July 2014 and take a phased-in approach.
NSW: the first stage will begin in the Hunter region during 2013-14 for eligible residents from the local government areas of Newcastle, Lake Macquarie and Maitland.
Victoria: the first stage starts in the Barwon region on 1 July 2013 for eligible residents from the local government areas of the City of Greater Geelong, Surf Coast Shire, Borough of Queenscliffe and Colac-Otway Shire.
South Australia: From July 2013, an NDIS will be launched across the State, focusing on children aged 0-5 with significant and permanent disability. By 2014 the age limit will be extended to 13 years and in year 3 all children up to 14 years. A total of
around 4,800 children with significant and permanent disability are expected to benefit from the first stage of the scheme.
Tasmania: The first stage of National Disability Insurance Scheme in Tasmania will cover all eligible adolescents aged 15-24.
This approach has been chosen because it represents an opportunity to examine and improve the range of supports that need to be in place for young people with disability to ensure a smooth transition between school and work or higher education.
As more detailed information becomes available it will be posted on the NDIS website at www.ndis.gov.au.
This story was first seen in the Synapse bridge magazine Vol 8

Citicoline - Agent No Help in Brain Trauma

This is what is in CerAxon that Diane from Pink House on the Corner thought helped Bob.
A positive review for stroke here:
So ask your doctor why it would be helpful for stroke but not TBI.
http://www.medpagetoday.com/CriticalCare/HeadTrauma/36050
Citicoline -- a chemical that occurs naturally in the body and is available in the U.S. as a nutraceutical -- did not improve outcomes among patients with traumatic brain injury, the randomized COBRIT trial showed.
Functional and cognitive outcomes assessed with a battery of tests 90 days after the injury were not significantly different between the patients who received citicoline and those who received placebo, according to Ross Zafonte, DO, of Harvard Medical School in Boston, and colleagues.
There were also no differences in any secondary outcome, including survival, the researchers reported in the Nov. 21 issue of the Journal of the American Medical Association.
The findings call into question the use of citicoline around the world, they said.
The agent is approved for use in patients with traumatic brain injuries in 59 countries. Preclinical studies and some small clinical trials have suggested that citicoline has potential neuroprotective effects and may enhance neurological repair after a brain injury, but most randomized trials in patients with traumatic brain injury have failed to show any benefit.
"The absence of an effect in prior trials and in COBRIT may be attributable either to the therapy simply being ineffective or to the heterogeneous pathophysiological nature of traumatic brain injury," Zafonte and colleagues wrote. "This would suggest that the mechanisms of action of drugs used in future ... trials would need to be tested in specific subtypes of traumatic brain injury, where they are likely to have a positive effect."
The COBRIT trial was a phase III, double-blind, randomized trial that included 1,213 patients treated at one of eight U.S. level 1 trauma centers for a nonpenetrating traumatic brain injury. The seriousness of the injuries ranged from complicated mild traumatic brain injury to severe injury.
The patients received either daily enteral or oral citicoline 2,000 mg or matching placebo starting within 24 hours of the injury.
The primary outcome was a global measure of functional and cognitive status -- the TBI Clinical Trials Network Core Battery, which includes nine scales -- at 90 days.
The trial was stopped for futility at the fourth interim analysis. The primary outcome was no different between the citicoline and placebo groups at 90 days (OR 0.98, 95% CI 0.83 to 1.15). The severity of injury did not affect the results.
The rate of a favorable outcome for each of the nine scales of the assessment ranged from 35.4% to 86.5% in the citicoline group and from 35.6% to 84% in the placebo group, with no between-group differences.
In an accompanying editorial, Robert Ruff, MD, PhD, and Ronald Riechers II, MD, of the Cleveland VA Medical Center, noted that among the possible reasons citicoline did not improve outcomes was the fact that there are many different mechanisms of injury involved in brain trauma.
"Traumatic brain injury can have regional pathology attributable to hematomas, edema, infarction, penetrating injury, and cerebral contusions. Diffuse injury mechanisms include diffuse edema, activation of inflammatory cytokines, release of excitatory neurotransmitters, extracellular potassium-induced membrane depolarization, and diffuse axonal injury," they wrote.
"Hence, optimal treatment ... may require that multiple agents and modalities be used to address all of the regional and widespread injury processes that occur in traumatic brain injury," they wrote.

Telomerase reverses ageing process

I could sure have used something like this after my instant decreptitude of my stroke.
http://www.nature.com/news/2010/101128/full/news.2010.635.html
Premature ageing can be reversed by reactivating an enzyme that protects the tips of chromosomes, a study in mice suggests.
Mice engineered to lack the enzyme, called telomerase, become prematurely decrepit. But they bounced back to health when the enzyme was replaced. The finding, published online today in Nature¹, hints that some disorders characterized by early ageing could be treated by boosting telomerase activity.
It also offers the possibility that normal human ageing could be slowed by reawakening the enzyme in cells where it has stopped working, says Ronald DePinho, a cancer geneticist at the Dana-Farber Cancer Institute and Harvard Medical School in Boston, Massachusetts, who led the new study. "This has implications for thinking about telomerase as a serious anti-ageing intervention."
Other scientists, however, point out that mice lacking telomerase are a poor stand-in for the normal ageing process. Moreover, ramping up telomerase in humans could potentially encourage the growth of tumours.

Eternal youth

After its discovery in the 1980s, telomerase gained a reputation as a fountain of youth. Chromosomes have caps of repetitive DNA called telomeres at their ends. Every time cells divide, their telomeres shorten, which eventually prompts them to stop dividing and die. Telomerase prevents this decline in some kinds of cells, including stem cells, by lengthening telomeres, and the hope was that activating the enzyme could slow cellular ageing.
Two decades on, researchers are realizing that telomerase's role in ageing is far more nuanced than first thought. Some studies have uncovered an association between short telomeres and early death, whereas others have failed to back up this link. People with rare diseases characterized by shortened telomeres or telomerase mutations seem to age prematurely, although some tissues are more affected than others.

“They are not studying normal ageing, but ageing in mice made grossly abnormal.”

When mice are engineered to lack telomerase completely, their telomeres progressively shorten over several generations. These animals age much faster than normal mice — they are barely fertile and suffer from age-related conditions such as osteoporosis, diabetes and neurodegeneration. They also die young. "If you look at all those data together, you walk away with the idea that the loss of telomerase could be a very important instigator of the ageing process," says DePinho.
To find out if these dramatic effects are reversible, DePinho's team engineered mice such that the inactivated telomerase could be switched back on by feeding the mice a chemical called 4-OHT. The researchers allowed the mice to grow to adulthood without the enzyme, then reactivated it for a month. They assessed the health of the mice another month later.
"What really caught us by surprise was the dramatic reversal of the effects we saw in these animals," says DePinho. He describes the outcome as "a near 'Ponce de Leon' effect" — a reference to the Spanish explorer Juan Ponce de Leon, who went in search of the mythical Fountain of Youth. Shrivelled testes grew back to normal and the animals regained their fertility. Other organs, such as the spleen, liver and intestines, recuperated from their degenerated state.
The one-month pulse of telomerase also reversed effects of ageing in the brain. Mice with restored telomerase activity had noticeably larger brains than animals still lacking the enzyme, and neural progenitor cells, which produce new neurons and supporting brain cells, started working again.
"It gives us a sense that there's a point of return for age-associated disorders," says DePinho. Drugs that ramp up telomerase activity are worth pursuing as a potential treatment for rare disorders characterized by premature ageing, he says, and perhaps even for more common age-related conditions.

Cancer link

The downside is that telomerase is often mutated in human cancers, and seems to help existing tumours grow faster. But DePinho argues that telomerase should prevent healthy cells from becoming cancerous in the first place by preventing DNA damage.
David Sinclair, a molecular biologist at Harvard Medical School in Boston, agrees there is evidence that activating telomerase might prevent tumours. If the treatment can be made safe, he adds, "it could lead to breakthroughs in restoring organ function in the elderly and treating a variety of diseases of aging."

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Other researchers are less confident that telomerase can be safely harnessed. "Telomere rejuvenation is potentially very dangerous unless you make sure that it does not stimulate cancer," says David Harrison, who researches ageing at the Jackson Laboratory in Bar Harbor, Maine.
Harrison also questions whether mice lacking telomerase are a good model for human ageing. "They are not studying normal ageing, but ageing in mice made grossly abnormal," he says. Tom Kirkwood, who directs the Institute for Ageing and Health at Newcastle University, UK, agrees, pointing out that telomere erosion "is surely not the only, or even dominant, cause" of ageing in humans.
DePinho says he recognizes that there is more to ageing than shortened telomeres, particularly late in life, but argues that telomerase therapy could one day be combined with other therapies that target the biochemical pathways of ageing. "This may be one of several things you need to do in order to extend lifespan and extend healthy living," he says.

Embryonic neuron transplants could effectively treat brain diseases

I don't see why this couldn't be used in stroke also.
http://www.medical-blogs.org/blog-crawler?bci=824553&url=http://www.news-medical.net/news/20121015/Embryonic-neuron-transplants-could-effectively-treat-brain-diseases.aspx

The unexpected survival of embryonic neurons transplanted into the brains of newborn mice in a series of experiments at the University of California, San Francisco (UCSF) raises hope for the possibility of using neuronal transplantation to treat diseases like Alzheimer's, epilepsy, Huntington's, Parkinson's and schizophrenia.
The experiments, described this week in the journal Nature, were not designed to test whether embryonic neuron transplants could effectively treat any specific disease. But they provide a proof-of-principle that GABA-secreting interneurons, a type of brain cell linked to many different neurological disorders, can be added in significant numbers into the brain and can survive without affecting the population of endogenous interneurons.
The survival of these cells after transplantation in numbers far greater than expected came as a shock to the team, which was led by UCSF professor Arturo Alvarez-Buylla, PhD, and former UCSF graduate student Derek Southwell, MD, PhD.
The prevailing theory held that the survival of developing neurons is something like a game of musical chairs. The brain has limited capacity for these cells, forcing them to compete with each other for the few available slots. Only those that find a place to "sit" (and receive survival signals derived from other cell types) will survive when the music stops. The rest die a withering death.
Based on this theory, the UCSF team had expected only a fixed and small number of transplanted embryonic interneurons would survive in the brains of older recipient mice, regardless of how many they transplanted. What they found was very different: Regardless of how many they transplanted, a consistent percentage always survived.
"[This constant rate of survival] suggests that these cells, which other collaborative studies have shown have great therapeutic promise, can be added to cortex in significant numbers," said Alvarez-Buylla, who is the Heather and Melanie Muss Professor of Neurological Surgery and a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF.
Past work at UCSF and elsewhere has shown that transplanting these cells can create a new critical period of plasticity in the recipient brain, reduce seizures in animal models of epilepsy, and reduce Parkinson's-like movement disorders in laboratory rats. The activity of these cells is often disrupted in Alzheimer's disease, and their number is altered in the brains of people with schizophrenia. When transplanted into the spinal cord, they also help decrease pain sensation.
In the current study, the UCSF team found that as they altered the number of cells they transplanted, a constant proportion of these cells survived - rather than a constant number - suggesting that a fraction of the cells is destined to die by cell-autonomous mechanisms or that a survival factor is secreted by the inhibitory neurons themselves. The work shows that these interneurons may be transplanted in far greater numbers than previously thought - an observation that could have important implications for the use of these cells to correct defects in the excitatory/inhibitory valance in the disease brain.
Survival of Cells Depends on Unknown "Signals
GABAergic interneurons are essential for brain function because they balance the action of "excitatory" neurons in the cerebral cortex by producing inhibitory signals. Diseases like epilepsy, Alzheimer's, Huntington's, Parkinson's and schizophrenia are all variously linked to disruptions in this excitatory/inhibitory balance, and problems with the GABAergic interneurons have been documented in all these diseases.

Next page at the link.

For the continuously sleepy, a new treatment shows promise

For us continually fatigued survivors maybe you want to have your doctor check for this.
http://www.latimes.com/news/science/sciencenow/la-sci-sn-continuously-sleepy-treatment-shows-promise-20121121,0,5849003.story

In 2005, a woman showed up at Emory University's sleep center in Atlanta complaining of being sleepy just about every moment of every day. She slept for 14, then 16, then 18 hours a night, but still woke up feeling drowsy. Doctors had prescribed her stimulants, which worked for a bit. But when they wore off, she would go on a sleeping binge, becoming unarousable for days at a time.
Her diagnosis? Hypersomnia, a rare and debilitating condition in which people sleep excessively, are extremely drowsy while awake, and respond poorly to existing anti-sleep treatments. The condition can make people unable to work or maintain relationships.
When the woman showed up at the sleep center, researchers did a range of tests and finally took samples of her cerebrospinal fluid. They discovered it had some unusual properties. Namely, something in it caused GABA, the main neurotransmitter molecule responsible for reducing the activity of brain cells, to have an outsized effect. In essence, a mystery molecule appeared to be working with GABA to tamp down brain activity, acting as a sort of constant sleeping pill.
There's another class of molecules that has a similar effect on GABA’s action in the brain. They are called benzodiazepines, which include Valium and Ambien.
The research team wondered whether something similar was at work in this patient, so they checked to see whether a drug used to counteract benzodiazepines, called flumazenil, would neutralize the effect of whatever was floating around in her cerebrospinal fluid. And it worked -- at least in a dish: Applying flumazenil to the woman's cerebrospinal fluid eliminated that strange effect of GABA.
But would it work in people? That's what the team, led by sleep expert Dr. David Rye, has been investigating since their discovery. And according to a study published Wednesday in the journal Science Translational Medicine, the answer is yes.
For the study, Rye and his team recruited seven people with various forms of hypersomnia and analyzed their cerebrospinal fluid. All had the same GABA-enhancing effect as the initial patient. And when the researchers treated the study subjects with flumazenil, they all became more alert.
According to an article on the project’s early days in Emory’s alumni magazine, that first Atlanta patient turned to her doctors after receiving the drug and exclaimed, after months of listlessness and days of nothing but sleeping, “I feel alive!” The moment brought her physicians to tears.
The finding is particularly noteworthy because flumazenil is not a stimulant and does not make normal people more alert.
Though flumazenil does appear to counteract the activity of the mysterious sleep-promoting molecule in the brains of these patients, laboratory analyses presented in the report suggest the molecule is not a benzodiazepine, and the researchers are still unsure just what it is.
That leaves the possibility that a better drug might come along for those with hypersomnia once researchers can identify what exactly causes the disorder. But for now, flumazenil appears to work well enough to get many with hypersomnia back to their lives.
Return to the Science Now blog.

Positive Outlook on Aging Helps Seniors Heal

So you will need to ignore your doctors negative thoughts and nocebo pronouncements.
http://www.medpagetoday.com/Geriatrics/GeneralGeriatrics/36043
Older patients with positive attitudes on aging may be more likely to fully recover from severe disability compared with those who can't see the bright side of life, researchers found.
A positive stereotype about aging was associated with a 44% greater likelihood of recovery from severe disability versus negative stereotypes (95% CI 1.01 to 2.06, P=0.04), according to Becca Levy, PhD, from the Yale School of Public Health, and colleagues.
Holding positive stereotypes in older age was also significantly associated with a slower rate of decline in activities of daily living (P=0.001), they wrote in a research letter in the Journal of the American Medical Association online.
"Further research is needed to determine whether interventions to promote positive age stereotypes could extend independent living in later life," the authors noted.
The researchers sampled patients through the Precipitating Events Project study and included 598 mostly female patients (63.3%), with an average age of 79, who belonged to a Connecticut health plan. All participants lived in a community, were nondisabled, and experienced at least 1 month of disability from active daily life during the follow-up period.
The participants were interviewed monthly for up to 129 months and filled out home-based assessments every 18 months over 10 years.
The researchers established age stereotypes by asking participants for five terms or phrases they associated with older individuals and coding those descriptors on a five-point scale, with 1 being most negative (such as decrepit) and 5 being most positive (such as spry). The participants scored a mean 2.12 on this scale.
Participants' severity of disability was based on the number of activities of daily living compromised by disability, including bathing, dressing, transferring, and walking. Three or four compromised activities were considered severely disabled; mild to severe disability required assistance with one to two activities, and mild to no disability required no assistance with activities of daily life.
The researchers grouped patients on whether they held positive or negative age stereotypes and compared rates of recovery from severe or mild injury to no or mild disability. Patients between groups were well-matched for age, sex, nonwhite ethnicity, frailty, education, chronic conditions, mental status, depression, and whether or not they lived alone. The nature of the disabling events was not described.
Patients were significantly more likely to recover from any state of injury to either no or mild disability if they fit positive age stereotypes, including from severe disability to no disability, severe disability to mild disability (HR 1.23, 95% CI 1.03 to 1.46, P=0.02), and mild disability to no disability (HR 1.15, 95% CI 1.02 to 1.29, P=0.02).
The researchers also noted that the positive age-stereotyped patients "showed an advantage in the absolute risk increase percentages" in likelihood of recovery, in addition to "a significantly slower rate of [activities of daily life] decline."
Study limitations included recruitment from a single community and an undersampling of black patients.

Speech Therapy Apps: A New Rehabilitation Choice for People with Aphasia

Commercial products but check them out and write up your impressions.
http://www.aphasia.com/blog/2012/11/15/speech-therapy-apps-a-new-rehabilitation-choice-for-people-with-aphasia

Scientists at Mainz University identify inhibitor of myelin formation in the central nervous system

So we first need to find out from our doctors if loss of myelin occurs during a stroke. 

Scientists at Mainz University identify inhibitor of myelin formation in the central nervous system

Possible implication for various neurological illnesses
Scientists at the Mainz University Medical Center have discovered another molecule that plays an important role in regulating myelin formation in the central nervous system. Myelin promotes the conduction of nerve cell impulses by forming a sheath around their projections, the so-called axons, at specific locations – acting like the plastic insulation around a power cord. The research team, led by Dr. Robin White of the Institute of Physiology and Pathophysiology at the University Medical Center of Johannes Gutenberg University Mainz, recently published their findings in the prestigious journal EMBO reports.
Complex organisms have evolved a technique known as saltatory conduction of impulses to enable nerve cells to transmit information over large distances more efficiently. This is possible because the specialized nerve cell axonal projections involved in conducting impulses are coated at specific intervals with myelin, which acts as an insulating layer. In the central nervous system, myelin develops when oligodendrocytes, which are a type of brain cell, repeatedly wrap their cellular processes around the axons of nerve cells forming a compact stack of cell membranes, a so-called myelin sheath. A myelin sheath not only has a high lipid content but also contains two main proteins, the synthesis of which needs to be carefully regulated.
The current study analyzed the synthesis of myelin basic protein (MBP), a substance which is essential for the formation and stabilization of myelin membranes. In common with all proteins, MBP is generated in a two-stage process originating from basic genetic material in the form of DNA. First, DNA is converted to mRNA, which, in turn, serves as a template for the actual synthesis of MBP. During myelin formation, the synthesis of MBP in oligodendrocytes is suppressed until distinct signals from nerve cells initiate myelination at specific "production sites". To date, the mechanisms involved in the suppression of MBP synthesis over relatively long periods of time have not been understood. This is where the current work of the Mainz scientists comes in, as they were able to identify a molecule that is responsible for the suppression of MBP synthesis.
"This molecule, called sncRNA715, binds to MBP mRNA, thus preventing MBP synthesis," explains Dr. Robin White. "Our research findings show that levels of sncRNA715 and MBP inversely correlate during myelin formation and that it is possible to influence the extent of MBP production in oligodendrocytes by artificially modifying levels of sncRNA715. This indicates that the recently discovered molecule is a significant factor in the regulation of MBP synthesis."
Understanding the molecular basis for myelin formation is essential with regard to various neurological illnesses that involve a loss of the protective myelin layer. For example, it is still unclear why oligodendrocytes lose their ability to repair the damage to myelin in the progress of multiple sclerosis (MS). "Interestingly, in collaboration with our Dutch colleagues, we have been able to identify a correlation between levels of sncRNA715 and MBP in the brain tissue of MS patients," Robin White continues. "In contrast with unaffected areas of the brain in which the myelin structure appears normal, there are higher levels of sncRNA715 in affected areas in which myelin formation is impaired. Our findings may help to provide a molecular explanation for myelination failures in illnesses such as multiple sclerosis."

Inpatient sleeping drug quadrupled fall risk

I know that  Ambien was used in the hospital I was at and I used it because of all the light and noise of the hospital floor. I never did fall while there. So ask your doctor if they are using other techniques for sleep aid.

 

Zolpidem (Brand names: Ambien, Edluar, Intermezzo, Zolpimist)

 

http://www.alphagalileo.org/ViewItem.aspx?ItemId=125952&CultureCode=en

A drug commonly prescribed to help patients sleep in hospitals has been associated with an increased risk of falls, according to a study published in the Journal of Hospital Medicine.
U.S. sleep specialists from the Mayo Clinic found that the fall rate among the 4,962 patients who took zolpidem during their hospital stay was more than four times as high as the 11,358 who did not take the drug.
They also found that the risk posed by the drug was greater than the risks posed by factors such as age, cognitive impairment, delirium or insomnia, regardless of the dosage used.
“Ensuring that people get enough sleep during their hospital stay is very important, but it can also prove very challenging,” says the Clinic’s Chief Patient Safety Officer Dr. Timothy I. Morgenthaler, who specializes in sleep disorders and pulmonary and critical care.
“Patient falls are also a significant patient safety issue in hospitals and one that has been quite difficult to tackle, despite considerable efforts. That is why it is one of the target aims of the U.S. Department of Health and Human Services Partnership for Patients project.”
“Discovering that zolpidem, which is commonly used in hospitals, is a significant risk factor for patient falls provides us with additional knowledge to help tackle this problem.”
Key findings of the study include:

• Just under 39 percent of eligible admissions during 2010 were prescribed zolpidem (16,320 patients) but 88 percent of the prescriptions were issued on an “as needed basis.”
• Zolpidem was administered to 30.4 percent of patients who were prescribed it and to 11.8 percent of all Mayo Clinic admissions in 2010.
• Just over three percent of the patients on zolpidem fell during their in-patient hospital stay, compared with 0.7 percent of the patients who did not take zolpidem.
• Zolipdem use continued to be associated with an increased fall risk when other key factors, including health, length of hospital stay and assessed fall risk, were taken into consideration.

“Our hospitals have an overall fall rate of about 2.5 per 1000 patient days, which is lower than many national benchmarks. However, we have not been able to significantly reduce this rate in recent years. Now, we calculate that for every 55 patients who received zolpidem, there was one additional fall that may have been avoided by not administering the drug,” says Dr. Morgenthaler.
“As a result of our study, we are now phasing out zolpidem and moving toward sleep enhancement techniques that are not based on drugs and which we believe are safer and probably as effective.”

 

Hand-Clapping Songs Improve Motor and Cognitive Skills, Research Shows

I would love to be able to clap my hands to improve my cognitive and motor skills. Has your therapist been trained for this? What is the coding for reimbursement for this ADL? But first I need the spasticity in my fingers gone. And you'd get double benefit from the music.
http://www.sciencedaily.com/releases/2010/04/100428090954.htm
A researcher at Ben-Gurion University of the Negev (BGU) conducted the first study of hand-clapping songs, revealing a direct link between those activities and the development of important skills in children and young adults, including university students.

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"We found that children in the first, second and third grades who sing these songs demonstrate skills absent in children who don't take part in similar activities," explains Dr. Idit Sulkin a member of BGU's Music Science Lab in the Department of the Arts. "We also found that children who spontaneously perform hand-clapping songs in the yard during recess have neater handwriting, write better and make fewer spelling errors."
Dr. Warren Brodsky, the music psychologist who supervised her doctoral dissertation, said Sulkin's findings lead to the presumption that "children who don't participate in such games may be more at risk for developmental learning problems like dyslexia and dyscalculia. There's no doubt such activities train the brain and influence development in other areas. The children's teachers also believe that social integration is better for these children than those who don't take part in these songs."
As part of the study, Sulkin went to several elementary school classrooms and engaged the children in either a board of education sanctioned music appreciation program or hand-clapping songs training -- each lasting a period of 10 weeks.
"Within a very short period of time, the children who until then hadn't taken part in such activities caught up in their cognitive abilities to those who did," she said. But this finding only surfaced for the group of children undergoing hand-clapping songs training. The result led Sulkin to conclude that hand-clapping songs should be made an integral part of education for children aged six to 10, for the purpose of motor and cognitive training.
During the study, "Impact of Hand-clapping Songs on Cognitive and Motor Tasks," Dr. Sulkin interviewed school and kindergarten teachers, visited their classrooms and joined the children in singing. Her original goal, as part of her thesis, was to figure out why children are fascinated by singing and clapping up until the end of third grade, when these pastimes are abruptly abandoned and replaced with sports.
"This fact explains a developmental process the children are going through," Dr. Sulkin observes. "The hand-clapping songs appear naturally in children's lives around the age of seven, and disappear around the age of 10. In this narrow window, these activities serve as a developmental platform to enhance children's needs -- emotional, sociological, physiological and cognitive. It's a transition stage that leads them to the next phases of growing up."
Sulkin says that no in-depth, long-term study has been conducted on the effects that hand-clapping songs have on children's motor and cognitive skills. However, the relationship between music and intellectual development in children has been studied extensively, prompting countless parents to obtain a "Baby Mozart" CD for their children.
This study also demonstrates that listening to 10 minutes of Mozart music (.i.e., the 'Mozart Effect') does not improve spatial task performance more than 10 minutes hand clapping songs training or 10 minutes exposure to silence.
Sulkin also found that hand-clapping song activity has a positive effect on adults: University students who filled out her questionnaires reported that after taking up such games, they became more focused and less tense. "These techniques are associated with childhood, and many adults treat them as a joke," she said. "But once they start clapping, they report feeling more alert and in a better mood."
Sulkin grew up in a musical home. Her father, Dr. Adi Sulkin, is a well-known music educator who, in the 1970s and 1980s, recorded and published over 50 cassettes and videos depicting Israeli children's play-songs, street-songs, holiday and seasonal songs, and singing games targeting academic skills.
"So quite apart from the research experience, working on this was like a second childhood," she noted.

KLF4 genetic factor prevents blood vessels from blockages

So ask your doctor if your genetic factors are correct. They should know about this before you bring it up. 

KLF4 genetic factor prevents blood vessels from blockages

Researchers at Case Western Reserve University School of Medicine have identified a genetic factor that prevents blockages from forming in blood vessels, a discovery that could lead to new therapies for cardiovascular diseases.
The findings are described in the Nov. 19 issue of the Journal of Clinical Investigation.
Researchers led by Mukesh K. Jain, MD, FAHA, professor of medicine, Ellery Sedgwick Jr. Chair and director of Case Cardiovascular Research Institute at Case Western Reserve School of Medicine, found that a shortage of the genetic factor KLF4, which regulates endothelial cells lining the interior of blood vessels, makes the lining more prone to the buildup of harmful plaque and fat deposits. In addition they showed that the deficiency of KLF4 also made the blood vessel more susceptible to clot formation. The plaque buildup (called atherosclerosis) narrows vessels and provides the foundation for clot formation (called thrombosis) that leads to heart attack and stroke.
Conversely, sufficient levels of KLF4, protect the inner lining of blood vessels, from toxins and other harmful agents that trigger the buildup of plaque and clot formation.
"This research answers a fundamental question in blood vessel health, identifying KLF4 as a master regulator of the most cardinal functions of endothelial cells," says Jain, who is also chief research officer of Harrington Heart & Vascular Institute at University Hospitals Case Medical Center.
"The fact that the level of these genetic factors can be altered in human disease suggests that targeting them may be a viable therapeutic strategy," Jain says.
The researchers are now developing tools to identify small molecules that increase KLF4 levels. Long-term, the goal is to identify a new class of molecules to develop a drug that works with those already used to treat heart disease. Another possibility is to modify existing drugs that can boost KLFs levels.
"It is possible," Jain says, "that chemical modification of the current statins will create super-statins that are more potent at inducing KLF levels, providing additional benefit."
Studies have shown that the earliest lesions of atherosclerosis typically begin at points where blood vessels branch out to different parts of the body, such as the brain, heart and legs.
Researchers hypothesized that mechanical forces may irritate the lining at these intersections, making them more prone to atherosclerosis than straighter lengths of the vessel system. In addition, toxins and harmful cytokines - cell secretions that can trigger inflammation - can further injure the endothelium and speed the development of disease.
However, the molecular reasons for this have remained elusive until now.

Another page at the link.

Severe Stroke Tied to Aspirin Resistance

Ask your doctor if you fall into this category.
http://www.medpagetoday.com/Cardiology/Strokes/36024
Individuals who are resistant to aspirin's antiplatelet effects appear to have more severe ischemic strokes than those who respond to the drug, researchers found.
Among patients admitted with an acute stroke, those shown to be resistant to aspirin with a platelet function assay were significantly more likely to have an NIH Stroke Scale (NIHSS) score of 16 or higher on admission (OR 7.49, 95% CI 1.49 to 48.00), the cutoff for severe stroke, according to Bernard Yan, MD, of Royal Melbourne Hospital in Parkville, Australia, and colleagues.
In addition, resistant patients were more likely to have an Alberta Stroke Program Early CT Score (ASPECTS) of less than 7 (OR 60.0, 95% CI 10.5 to 343.2), indicating a large area of infarction, the researchers reported online in Archives of Neurology.
"Our results support the need for a randomized controlled study to investigate alternative antiplatelet therapy in patients with aspirin resistance," they wrote.
The use of aspirin before a stroke has been associated with less severe symptoms at admission and improved functional outcomes at discharge. And short-term aspirin therapy has been shown to significantly reduce the risks of death and dependency at 6 months following an acute ischemic stroke.
Resistance to aspirin, however, may contribute to poor clinical outcomes in some patients.
Yan and colleagues explored the issue using data from 90 adult patients admitted with an acute ischemic stroke at their center. All had been using aspirin for at least 7 days before stroke onset (median 5 years).
The mean age of the patients was 75, and 64.4% were male.
At admission, the median NIHSS score was 4, indicating minor symptoms. The median ASPECTS was 9, indicating a small area of infarction (the maximum score of 10 indicates a normal CT scan).
As measured by the VerifyNow assay, 28.9% of the patients were resistant to aspirin, defined as an aspirin reaction unit (ARU) of 550 or higher. The median ARU for the entire cohort was 486.
Each 1-point increase in ARU was associated with a 0.03-point increase in NIHSS score (P=0.001) and a 0.02-point decrease in ASPECTS (P less than 0.001). That works out to a 1-point increase in NIHSS score for a 33-point increase in ARU and a 1-point decrease in ASPECTS for a 50-point increase in ARU.
The presence of aspirin resistance was associated with a worse stroke according to both the NIHSS and ASPECTS.
"Platelets are critical to thrombus formation, contributing as much as 50% of the total thrombus volume. Antiplatelet agents decrease platelet aggregation and, in turn, the size and frequency of thrombolytic emboli," the authors wrote.
Thus, they said, "the increased severity and infarct size observed in the present study may be due to larger thrombus formation as a result of inadequate platelet inhibition."
"Aspirin also reduces platelet microaggregates and platelet-derived vasoconstricting products," they added. "This may ease ischemic injury by improving local blood flow. Aspirin-resistant patients may not experience the same therapeutic effect and, as a result, sustain a larger stroke."
Alternatively, other neuroprotective or anti-inflammatory processes could be involved in the observed relationship, Yan and colleagues noted.
They acknowledged that their study was limited by the small sample size, the slight selection bias favoring patients with milder symptoms, and the possible insensitivity of ASPECTS to early ischemic changes.

Stroke survivor triathlete Anthony Connor admits fraudulent benefits claim

We need this guy to writeup what he did to recover. Do you know him? Ask him.
http://www.bbc.co.uk/news/uk-england-manchester-20167396

A Manchester man who said he could barely walk, but was filmed competing in a triathlon, has admitted falsely claiming more than £17,000 in benefits.

Anthony Connor, 39, of Wythenshawe, received the money after informing officials he had difficulty walking.
But he was filmed running and cycling in Cheshire in September 2010.
Manchester magistrates sentenced Connor to 12 weeks in prison, suspended for a year, and ordered him to carry out 100 hours of community service.
Officials for the Department for Work and Pensions (DWP) investigated Connor after he claimed a stroke had left him unable to go up or downstairs or climb in and out of the bath without help.
'Not straggling' He also told officials he was not capable of walking more than 75m in five minutes.
Connor had originally made a legitimate claim in 2006 after he suffered a stroke but had not informed the DWP of his return to health.
Following a tip-off, investigators filmed Connor cycling and running in the Tatton Park Triathlon on 19 September 2010.
The DWP's Andrew Wood said the film clearly showed Connor had been lying about his health.
"He wasn't straggling behind everyone else, he was in with the pack," he said.
In court, Connor admitted failing to declare a change in circumstances and receiving £17,093.17 in benefit overpayments between June 2010 and July 2011.