Video games 'help dyslexic pupils'

28 February 2013 Last updated at 12:38 ET

Boys playing computer games

Playing video games may help children with dyslexia improve their reading skills, research suggests.

A study of 10-year-olds who played 12 hours of an “action” video game found it improved their reading speed without any cost to accuracy.

The effects were equivalent to more than a year’s worth of reading development, the Italian team reported in Current Biology.

But more research was needed before games could be considered a treatment.

Their work builds on earlier research in which they linked dyslexia with early problems in visual attention rather than language skills.

They selected a fast-moving game requiring a high degree of perceptual, cognitive, and motor skills as well as being unpredictable and involving peripheral processing.

Ten children spent nine 80-minute sessions playing the video game, which consisted of a series of mini-games.

And their reading and attention skills were compared before and after with 10 children not exposed to the game.

Speed and accuracy

The researchers found those who had played the video games had better attention skills than before.

And they were able to read faster without losing any accuracy, the team from the University of Padua reported.

Study leader, Dr Andrea Facoetti, said: “Action video games enhance many aspects of visual attention, mainly improving the extraction of information from the environment.

“Dyslexic children learned to orient and focus their attention more efficiently to extract the relevant information of a written word more rapidly.”

He explained that attention should be thought of as a “spotlight” that can be moved, and adjusted in its size, in the visual field.

When the spotlight is on a portion of the visual field, the details will be enhanced, the contrast improved and so on, while everything that is outside of this spotlight will be inhibited.

The video games may be working to train the part of the brain responsible for attention and motion perception, he added.

“These results are very important in order to understand the brain mechanisms underlying dyslexia, but they don’t put us in a position to recommend playing video games without any control or supervision,” he said.

The team are now planning to look at the effects of video games on the prevention of dyslexia in children before they learn to read.

Dr Kate Saunders, chief executive of the British Dyslexia Association, said it was a complex condition but for some individuals part of the problem may include difficulty with aspects of visual perceptual skills, and visuo-motor coordination and attention.

She added that more research was needed to establish whether repeated play on some targeted computer games could help build certain visual and attention related skills.

“There are questions, however, as to the extent that skills transfer from one situation to another and would be retained in the longer term.”

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Video games ‘help dyslexic pupils’

28 February 2013 Last updated at 12:38 ET

Boys playing computer games

Playing video games may help children with dyslexia improve their reading skills, research suggests.

A study of 10-year-olds who played 12 hours of an “action” video game found it improved their reading speed without any cost to accuracy.

The effects were equivalent to more than a year’s worth of reading development, the Italian team reported in Current Biology.

But more research was needed before games could be considered a treatment.

Their work builds on earlier research in which they linked dyslexia with early problems in visual attention rather than language skills.

They selected a fast-moving game requiring a high degree of perceptual, cognitive, and motor skills as well as being unpredictable and involving peripheral processing.

Ten children spent nine 80-minute sessions playing the video game, which consisted of a series of mini-games.

And their reading and attention skills were compared before and after with 10 children not exposed to the game.

Speed and accuracy

The researchers found those who had played the video games had better attention skills than before.

And they were able to read faster without losing any accuracy, the team from the University of Padua reported.

Study leader, Dr Andrea Facoetti, said: “Action video games enhance many aspects of visual attention, mainly improving the extraction of information from the environment.

“Dyslexic children learned to orient and focus their attention more efficiently to extract the relevant information of a written word more rapidly.”

He explained that attention should be thought of as a “spotlight” that can be moved, and adjusted in its size, in the visual field.

When the spotlight is on a portion of the visual field, the details will be enhanced, the contrast improved and so on, while everything that is outside of this spotlight will be inhibited.

The video games may be working to train the part of the brain responsible for attention and motion perception, he added.

“These results are very important in order to understand the brain mechanisms underlying dyslexia, but they don’t put us in a position to recommend playing video games without any control or supervision,” he said.

The team are now planning to look at the effects of video games on the prevention of dyslexia in children before they learn to read.

Dr Kate Saunders, chief executive of the British Dyslexia Association, said it was a complex condition but for some individuals part of the problem may include difficulty with aspects of visual perceptual skills, and visuo-motor coordination and attention.

She added that more research was needed to establish whether repeated play on some targeted computer games could help build certain visual and attention related skills.

“There are questions, however, as to the extent that skills transfer from one situation to another and would be retained in the longer term.”


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FDA staff say two non-hormonal hot flashes drugs show some efficacy

A view shows the U.S. Food and Drug Administration (FDA) logo at the lobby of its headquarters in Silver Spring, Maryland August 14, 2012. REUTERS/Jason Reed

A view shows the U.S. Food and Drug Administration (FDA) logo at the lobby of its headquarters in Silver Spring, Maryland August 14, 2012.

Credit: Reuters/Jason Reed

Thu Feb 28, 2013 1:44pm EST

(Reuters) – Food and Drug Administration staff said experimental drugs by Depomed Inc and Hisamitsu Pharmaceutical Co Inc showed efficacy in reducing menopausal hot flashes, and highlighted no new risks in comments issued on Thursday.

Depomed’s shares rose 8 percent on optimism that its drug, which failed to meet pre-defined efficacy goals in studies, may still be approved to address an estimated $1.5 billion market.

Depomed’s Sefelsa was effective in reducing the frequency and severity of hot flashes related to menopause after four weeks of treatment in studies, but results varied after 12 weeks of treatment, FDA staff observed in a report posted online on Thursday. (r.reuters.com/jyx36t)

Japanese drugmaker Hisamitsu’s paroxetine mesylate capsules was shown to be more consistent at reducing the incidence of the condition than at reducing the severity of flashes. (r.reuters.com/fab46t)

Both drugs are vying to become the first approved, non-hormonal drug to treat menopausal hot flashes.

Most women going through menopause experience these flashes, a complex set of feelings that start with warmth and redness, accompanied by sweating, palpitations and anxiety that typically lasts several minutes.

About 13 million of nearly 32 million women who experience hot flashes during menopause seek treatment in the United States, according to Depomed.

The only approved and most effective treatment for the condition is traditional hormone replacement therapy, but it has shown to increase the risks of breast cancer and heart stroke.

This prompted off-label use of paroxetine mesylate and gabapentin, the chemical name of Sefelsa, which are both widely available generics and shown to be moderately effective in treating hot flashes in some studies.

Depomed already sells gabapentin as Gralise to treat shingles-related pain and the drug added about $7.6 million to the company’s total sales in the October-December period. Paroxetine mesylate is sold as Paxil and Pexeva, among other trade names, to treat depression and anxiety.

The FDA staff’s comments on the marketing applications of the two drugs will be used by an advisory panel to the U.S. Food and Drug Administration, when it meets to review the drugs on Monday.

The FDA will take the panel’s analysis of the drugs into account when it delivers a final decision on Sefelsa by May 31 and on Hisamitsu’s paroxetine mesylate by June 28.

Analyst Jim Molloy of Janney Capital Markets said he continues to recommend buying Depomed stock as he estimates that the FDA panel will vote in favor of Sefelsa.

The staff noted on Thursday that suicidal risks persisted with both drugs.

In late-stage studies, Sefelsa did not show consistent and meaningful reduction in the frequency and severity of hot flashes, but Depomed still submitted a marketing application last July, saying it believed the data warranted a review by the regulator.

Depomed shares have gained about 13 percent since then. The stock, which rose as much as 8 percent to $6.65, was trading at $6.48 Thursday afternoon on the Nasdaq.

(Reporting by Zeba Siddiqui in Bangalore; Editing by Anthony Kurian)

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No clear benefits for kids’ blood pressure checks

By Genevra Pittman

NEW YORK | Thu Feb 28, 2013 2:56pm EST

NEW YORK (Reuters Health) – There’s no evidence that checking kids’ and teens’ blood pressure – and treating them if it’s high – can reduce their heart risks in adulthood, according to a new analysis.

What’s more, researchers found blood pressure tests may not always be accurate among young people, or consistent from one reading to the next.

“At this point, the jury is out. We just don’t know if this is worth doing or not,” said Dr. Matthew Thompson, who led the new research at Oxford University in the UK.

“We desperately need research on how to diagnose kids with high blood pressure, which kids should be treated and what are the most effective treatments.”

Thompson said although most U.S. children have their blood pressure measured at routine checkups, those readings are never taken on healthy kids in the UK.

His team reviewed the latest evidence on childhood blood pressure tests for the government-backed U.S. Preventive Services Task Force.

Thompson and his colleagues analyzed 34 studies covering diagnosis, treatment and long-term effects of high blood pressure in kids and teens. None of those answered the researchers’ central question – whether screening can help prevent or delay cardiovascular disease in adults.

Accuracy of blood pressure readings from one measurement to the next was “modest at best,” according to Thompson.

“The false positive rate… means that most children who screen positive won’t actually have high blood pressure,” he told Reuters Health.

Among studies that tracked children and teens over time, researchers found anywhere from 19 to 65 percent of youth with high blood pressure also had hypertension as adults.

Seven studies tested seven different drugs for kids with hypertension and found they typically weren’t any better at lowering blood pressure than a drug-free placebo pill. But those studies lasted only a few weeks – and children with hypertension would likely take the drugs for years.

“That’s really not good enough evidence to know if they’re effective and safe for decades,” Thompson said.

Programs aiming to change young people’s lifestyle, such as by encouraging them to be more active or eat less salt, also didn’t have a clear effect, the researchers wrote this week in Pediatrics.

‘PART OF STANDARD CARE’

Based on the findings, the Task Force concluded in a draft recommendation that there isn’t enough evidence to balance the benefits and harms of screening young people to prevent future disease.

The draft is available online for public comment for the next month here: bit.ly/uRZqMF.

The U.S. National Heart, Lung, and Blood Institute recommends all children routinely get their blood pressure measured. But another recent review also concluded there isn’t enough evidence to support blood pressure checks for kids, further stoking controversy on the issue (see Reuters Health story of Jan 7, 2013 here: reut.rs/V5FY63.)

Dr. Bonita Falkner, a pediatrician at Thomas Jefferson University in Philadelphia who has studied hypertension, said she doesn’t think the findings should change practice.

“It remains unknown how much hypertension in childhood contributes to (adult high blood pressure), but there is evidence it begins in childhood,” Falkner, who wasn’t involved in the review, told Reuters Health.

The researchers agreed there’s a need for more studies to address the information gaps related to childhood blood pressure checks.

“It’s been recommended for some time now that pediatricians measure blood pressure in children, starting at age three, as part of routine health assessments,” she said. “It’s pretty much become part of standard care.”

Thompson said until more research is done, it’s unclear what the right answer is on blood pressure checks for youth.

“To me, the evidence shows that it’s not clear that screening or not screening is good or bad,” he said.

SOURCE: bit.ly/WtBzqF Pediatrics, online February 25, 2013.

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Imaging Suggests Wide Window for Alzheimer’s Tx

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Alzheimer’s Disease

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By Charles Bankhead, Staff Writer, MedPage Today

Published: February 27, 2013

Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania

Action Points

  • This study used serial amyloid PET imaging to model rates of beta-amyloid accumulation.
  • Low rates of accumulation were observed in those with the lowest and highest baseline amyloid burden, whereas amyloid accumulation was highest in those with mid-range baseline amyloid levels.

The biological path to Alzheimer’s disease might continue for more than a decade, suggesting a broad window of opportunity for intervention, according to a study of amyloid plaque accumulation.

Longitudinal measurement by PET imaging showed that plaque buildup reached a plateau at 2.7 times baseline values, a process that required about 15 years.

The results not only suggest ample opportunity for secondary prevention but imply that therapies with the potential to block plaque accumulation would be less effective when the plateau has been reached, investigators reported in the March 5 issue of Neurology.

“Given that the time course of the disease evaluable by currently available biomarkers may span 30 or more years, it will take decades to collect such an idealized dataset,” Clifford Jack, MD, of the Mayo Clinic in Rochester, Minn., and colleagues noted in their discussion of the findings. “An alternative, however, is to piece together shorter time-interval data in many participants to create plausible long-term disease models.”

“We believe that indexing individual participants by amyloid PET standardized uptake value ratio (SUVR) provides a valid solution to this problem in the current context where we are evaluating an amyloid biomarker,” they added.

The most established biomarkers of Alzheimer’s disease fall into two categories: 1) measures of neuronal injury and degeneration and 2) measures of beta-amyloid accumulation in the brain, including cerebrospinal fluid.

Jack and colleagues have proposed a model of the evolution of Alzheimer’s disease biomarkers. They hypothesized that amyloid accumulation follows an inverted-U (sigmoid) trajectory over time, initially accelerating and then decelerating (Lancet Neurol 2010; 9: 119-128).

The authors conducted a study to test the hypothesis that PET-derived amyloid load versus time can be modeled by a sigmoid function.

The study involved 260 participants in Mayo studies of aging and Alzheimer’s research. The participants had an age range of 70 to 92 at enrollment, and all of them underwent two or more PET studies of brain amyloid.

The study population consisted of 205 participants with normal cognitive function, 47 with mild cognitive impairment, and eight with Alzheimer’s disease.

For each participant, investigators measured baseline amyloid SUVR and estimated the slope of annual rate of amyloid accumulation. They also developed regression models to predict the annual rate of amyloid accumulation on the basis of baseline amyloid SUVR and evaluated age, sex, cognition classification, and apolipoprotein E4 genotype as covariates.

Lastly, investigators integrated the association between amyloid accumulation rate and baseline amyloid SUVR into an amyloid PET-SUVR-versus-time association.

The participants’ PET scans occurred over an average of 1.3 years. Low baseline amyloid SUVR was associated with low rates of amyloid accumulation. The accumulation rates increased with SUVR to a baseline maximum of about 2.0. Thereafter, the rate of accumulation declined and reached 0 at a baseline SUVR of about 2.7.

The rate of amyloid accumulation as a function of baseline SUVR resulted in an inverted U-shaped curve. The estimated time span from an SUVR of 1.5 to 2.5 was about 15 years.

“This roughly 15-year interval where the slope of the amyloid SUVR versus time curve is greatest and roughly linear represents a large therapeutic window for secondary preventive interventions,” the authors concluded.

The study “breaks new ground in providing insight into the nature of amyloid accumulation,” Jeffrey M. Burns, MD, and Russell H. Swerdlow, MD, said in an accompanying editorial. However, application of the results remains limited by an imprecise understanding of amyloid’s clinical relevance to Alzheimer’s disease.

“The study does not examine how amyloid burden or the apparent kinetics of amyloid accumulation … relates to clinical outcomes,” said Burns and Swerdlow, of the University of Kansas in Kansas City. “In fact, the rate of accumulation was not clearly different between impaired and cognitively normal groups, and many individuals with the highest levels of amyloid were cognitively normal.”

The incongruity between amyloid burden and cognitive impairment is consistent with autopsy studies suggesting that amyloid burden has at best a loose association with dementia.

“If the amyloid cascade hypothesis is correct, pharmacologically targeting amyloid accumulation after the amyloid accumulation process burns itself out is probably too little too late,” Burns and Swerdlow added. “Because the period of accelerated amyloid deposition frequently occurs before clinical symptoms manifest, this view supports the assumption that robust disease modification will only be accomplished when initiated very early in the course of the disease.

“It is also important to consider, however, that if amyloid turns out to be only a secondary biomarker of the disease, as opposed to its cause, then targeting its accumulation at any stage will have, at most, a limited effect on clinical outcomes.”

The study was supported by the National Institutes of Health, the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Foundation, the Robert H. and Clarice Smith Alzheimer’s Disease Research Program of the Mayo Foundation, and General Electric.

Jack disclosed relationships with Janssen, Bristol-Myers Squibb, General Electric, Johnson & Johnson, Allon, and Baxter. Co-authors disclosed relationships with Lilly Pharmaceuticals, Janssen, Bayer Schering, GE Healthcare, Siemens Molecular Imaging, MN Partnership for Biotechnology, Medical Genomics, Pfizer, Elan Pharmaceuticals, Cephalon, and the Mangurian Foundation. One or more authors disclosed royalty interests related to book publication.

Burns disclosed relationships with PRA International, Janssen, Wyeth, Danone, and Baxter. Swerdlow disclosed a relationship with PhotoThera.

Primary source: Neurology
Source reference:
Jack CR Jr, et al “Brain ß-amyloid load approaches a plateau” Neurology 2013; 80: 890-896.

Additional source: Neurology
Source reference:
Burns JM, Swerdlow RH “Backwaters and rapids on the amyloid river” Neurology 2013; 80: 878-879.

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Fatal MI More Likely After Sibling Dies

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By Crystal Phend, Senior Staff Writer, MedPage Today

Published: February 27, 2013

Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania

Action Points

  • Because the death of sibling is a stressful life event, this study looked at the association between loss of an adult sibling and mortality from myocardial infarction up to 18 years since bereavement.
  • The study provided found evidence for mortality from myocardial infarction associated with the death of a sibling at adult age.

The death of an adult brother or sister may boost one’s own risk of dying from a heart attack in the following years, a population-based study showed.

The fatal heart attack risk was 25% higher for women and 15% higher for men who had experienced death of an adult sibling, Mikael Rostila, PhD, of Stockholm University and the Karolinska Institutet in Stockholm, and colleagues found.

The impact wasn’t seen in the first months of bereavement but was in the roughly 1 to 3 years afterward, the group reported online in the Journal of the American Heart Association.

Shared risk factors may have been partly to blame; but whatever the mechanism, physicians need to keep an eye on their patient’s heart after a loss, Rostila and colleagues recommended.

“It is important for healthcare workers to follow bereaved siblings after the death of a sibling and recognize signs of acute or chronic psychosocial stress mechanisms that could lead to risk of myocardial infarction,” they suggested.

“Triggered cardiovascular events might be prevented with traditional cardiovascular medications (aspirin, beta-blockers, statins) and by stress management.”

Given well-known risks from loss of a spouse, parent, or child, Rostila’s group looked to see if the same would hold for siblings.

Their study included all 130,920 Swedes ages 40 to 69 years who lost a sibling between 1981 and 2002, based on national registry data, along with a 10% sample of nonbereaved adults.

The raw myocardial infarction (MI) mortality rate was roughly doubled among those who had an adult sibling die during that period, at 0.85 versus 0.45 per 1,000 person-years for men and 0.24 versus 0.11 per 1,000 person-years for women.

After controlling for number of siblings and other factors, the rate ratio for death from MI was 1.25 among bereaved women (95% confidence interval 1.02 to 1.28) and 1.15 among bereaved men (95% CI 1.03 to 1.28) compared with controls.

The risk of death from MI afterward appeared to have peaks around year 1 and year 3 for men, with about a 30% higher risk over those years, albeit not statistically significant compared with controls.

The risk spiked among women in years 2 and 3 after their sibling’s death to about twice that of controls.

Neither gender group showed an immediate or late impact after their sibling’s death.

Differences between men and women are plausible, based on prior studies suggesting that the risk period after bereavement is more prolonged for women, perhaps due to their greater emphasis on social relationships with the family, the researchers noted.

Mechanisms might include changes to the sympathetic nervous system that induce inflammation as well as negative coping responses, such as smoking, drinking more, and poor diet and exercise habits after bereavement, they wrote.

However, shared genetic and environmental exposure earlier in life may play a role too.

At least part of the association between loss of an adult brother or sister and death from MI appeared to be due to confounding from shared predisposition.

For men, the risk of fatal MI was elevated much more in the setting of bereavement if the sibling had also died from MI than if the sibling had died from any other cause. The rate ratio was 1.98 versus 0.84 in the setting of sibling death from an accident or other external cause, and 1.05 for non-MI deaths.

Women also showed a higher risk of MI death if their sibling died from the same cause, with a rate ratio of 1.62 versus nonbereaved persons.

Both sexes likewise showed a relatively strong link between death from MI and death of a sibling from other cardiovascular causes (rate ratio 1.74 for men and 1.50 for women, albeit not significant among the latter).

But women still showed an impact of bereavement of a sibling on MI mortality even when the brother or sister had died from an external cause, especially if it wasn’t suicide (rate ratios 1.54 and 1.86, respectively).

Limitations of the study included lack of data on comorbidities, severity of bereavement, or psychiatric screening; and inability to look at nonfatal MI.

Rostila reported receiving funding from the Swedish Council for Working Life and Social Research and the Swedish Research Council.

The researchers reported having no conflicts of interest to disclose.

Primary source: Journal of the American Heart Association
Source reference:
Rostila M, et al “Mortality from myocardial infarction after the death of a sibling: A nationwide follow-up study from Sweden” JAMA 2013.

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Poison probe nurse is suspended

27 February 2013 Last updated at 08:26 ET

Breaking news

A nurse cleared of poisoning patients at a hospital has been suspended for three months after admitting taking drugs from the site.

The decision came after a three-day disciplinary hearing for Rebecca Leighton, 29, who worked at Stepping Hill Hospital in Stockport.

She has been suspended from nursing by the Nursing and Midwifery Council.

Ms Leighton spent six weeks in jail but was freed as there was not enough evidence against her.


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Exam error prompts doctor job recall

27 February 2013 Last updated at 11:04 ET

Junior doctorMedical students are having to wait to find out the location of their first job

Thousands of medical students face having their first hospital job offer withdrawn due to marking errors in their exams.

On Monday more than 7,000 final year students were told the region they were assigned to as junior doctors.

However, a day later the examining body, the UK Foundation Programme Office (UKFPO), withdrew all offers due to flaws in the scoring system.

The British Medical Association says the situation is “unacceptable”.

The UKFPO announced on Tuesday that it had discovered “a potential error in the scanning process of the situational judgement test” and promised to manually re-mark all the affected sheets within a week. The test is a multiple-choice exam used to test judgement in clinical scenarios.

Combined with other exams, this test helps determine the geographical region students will work in for the duration of their foundation programme – a two-year training course which forms the bridge between medical school and training for a specialism. They then choose their preferred hospitals in this region.

A large number of medical students have contacted the BBC saying their initial elation of being offered their preferred job location has turned to anxiety.

‘Extremely distressing’

Jonathan Ford, a final year medical student at Leicester, said: “My dad cried when I told him I had got my first choice – he was so proud. But now I don’t know what will happen.

“It is extremely distressing and stressful – and couldn’t come at a worst time – many of us are facing our final exams in the next two weeks.”

Alice Rutter, the co-chair of the BMA medical students committee, said: “This is totally unacceptable. We view this problem very seriously indeed and will be taking action to ensure students who are affected are kept updated and supported.”

Dr Katie Petty-Saphon, executive director of the Medical Schools Council, who commissioned the suppliers who introduced the errors apologised. She said: “I do understand how upsetting and frustrating it must be to be told you have a particular position one day and then to be warned the next that this might not be the case.

“We shall provide the results as soon as we are completely confident that we have done all we can to ensure their accuracy.”


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