Posts tagged science

ScienceDaily (June 6, 2012) — New pictures from the University of Iowa show what it looks like when a person runs out of patience and loses self-control.

Brain activity when people exert self-control. (Credit: Image courtesy of University of Iowa)

A study by University of Iowa neuroscientist and neuro-marketing expert William Hedgcock confirms previous studies that show self-control is a finite commodity that is depleted by use. Once the pool has dried up, we’re less likely to keep our cool the next time we’re faced with a situation that requires self-control.

But Hedgcock’s study is the first to actually show it happening in the brain using fMRI images that scan people as they perform self-control tasks. The images show the anterior cingulate cortex (ACC) — the part of the brain that recognizes a situation in which self-control is needed and says, “Heads up, there are multiple responses to this situation and some might not be good” — fires with equal intensity throughout the task.

However, the dorsolateral prefrontal cortex (DLPFC) — the part of the brain that manages self-control and says, “I really want to do the dumb thing, but I should overcome that impulse and do the smart thing” — fires with less intensity after prior exertion of self-control.

He said that loss of activity in the DLPFC might be the person’s self-control draining away. The stable activity in the ACC suggests people have no problem recognizing a temptation. Although they keep fighting, they have a harder and harder time not giving in.

Which would explain why someone who works very hard not to take seconds of lasagna at dinner winds up taking two pieces of cake at desert. The study could also modify previous thinking that considered self-control to be like a muscle. Hedgcock says his images seem to suggest that it’s like a pool that can be drained by use then replenished through time in a lower conflict environment, away from temptations that require its use.

The researchers gathered their images by placing subjects in an MRI scanner and then had them perform two self-control tasks — the first involved ignoring words that flashed on a computer screen, while the second involved choosing preferred options. The study found the subjects had a harder time exerting self-control on the second task, a phenomenon called “regulatory depletion.” Hedgcock says that the subjects’ DLPFCs were less active during the second self-control task, suggesting it was harder for the subjects to overcome their initial response.

Hedgcock says the study is an important step in trying to determine a clearer definition of self-control and to figure out why people do things they know aren’t good for them. One possible implication is crafting better programs to help people who are trying to break addictions to things like food, shopping, drugs, or alcohol. Some therapies now help people break addictions by focusing at the conflict recognition stage and encouraging the person to avoid situations where that conflict arises. For instance, an alcoholic should stay away from places where alcohol is served.

But Hedgcock says his study suggests new therapies might be designed by focusing on the implementation stage instead. For instance, he says dieters sometimes offer to pay a friend if they fail to implement control by eating too much food, or the wrong kind of food. That penalty adds a real consequence to their failure to implement control and increases their odds of choosing a healthier alternative.

The study might also help people who suffer from a loss of self-control due to birth defect or brain injury.

"If we know why people are losing self-control, it helps us design better interventions to help them maintain control," says Hedgcock, an assistant professor in the Tippie College of Business marketing department and the UI Graduate College’s Interdisciplinary Graduate Program in Neuroscience.

Source: Science Daily

June 6, 2012 by Chris Barncard

Stress may affect brain development in children — altering growth of a specific piece of the brain and abilities associated with it — according to researchers at the University of Wisconsin–Madison.

"There has been a lot of work in animals linking both acute and chronic stress to changes in a part of the brain called the prefrontal cortex, which is involved in complex cognitive abilities like holding on to important information for quick recall and use,” says Jamie Hanson, a UW–Madison psychology graduate student. “We have now found similar associations in humans, and found that more exposure to stress is related to more issues with certain kinds of cognitive processes.”

Children who had experienced more intense and lasting stressful events in their lives posted lower scores on tests of what the researchers refer to as spatial working memory. They had more trouble navigating tests of short-term memory such as finding a token in a series of boxes, according to the study, which will be published in the June 6 issue of the Journal of Neuroscience.

Brain scans revealed that the anterior cingulate, a portion of the prefrontal cortex believed to play key roles in spatial working memory, takes up less space in children with greater exposure to very stressful situations.

"These are subtle differences, but differences related to important cognitive abilities" Hanson says.

But they maybe not irreversible differences.

"We’re not trying to argue that stress permanently scars your brain. We don’t know if and how it is that stress affects the brain," Hanson says. "We only have a snapshot — one MRI scan of each subject — and at this point we don’t understand whether this is just a delay in development or a lasting difference. It could be that, because the brains is very plastic, very able to change, that children who have experienced a great deal of stress catch up in these areas."

The researchers determined stress levels through interviews with children ages 9 to 14 and their parents. The research team, which included UW–Madison psychology professors Richard Davidson and Seth Pollak and their labs, collected expansive biographies of stressful events from slight to severe.

"Instead of focusing in on one specific type of stress, we tried to look at a range of stressors," Hanson says. "We wanted to know as much as we could, and then use all this information to later to get an idea of how challenging and chronic and intense each experience was for the child."

Interestingly, there was little correlation between cumulative life stress and age. That is, children who had several more years of life in which to experience stressful episodes were no more likely than their younger peers to have accumulated a length stress resume. Puberty, on the other hand, typically went hand-in-hand with heavier doses of stress.

The researchers, whose work was funded by the National Institutes of Health, also took note of changes in brain tissue known as white matter and gray matter. In the important brain areas that varied in volume with stress, the white and gray matter volumes were lower in tandem.

White matter, Hanson explained, is like the long-distance wiring of the brain. It connects separated parts of the brain so that they can share information. Gray matter “does the math,” Hanson says. “It takes care of the processing, using the information that gets shared along the white matter connections.”

Gray matter early in development appears to enable flexibility; children can play and excel at many different activities. But as kids age and specialize, gray matter thins. It begins to be “pruned” after puberty, while the amount of white matter grows into adulthood.

"For both gray and white matter, we actually see smaller volumes associated with high stress," Hanson says. "Those kinds of effects across different kinds of tissue, those are the things we would like to study over longer periods of time. Understanding how these areas change can give you a better picture of whether this is just a delay in development or more lasting."

More study could also show the researchers how to help children who have experienced an inordinate amount of stress.

"There are groups around the country doing working memory interventions to try to train or retrain people on this particular cognitive ability and improve performance," Hanson says. "Understanding if and how stress affects these processes could help us know whether there may be similar interventions that could aid children living in stressful conditions, and how this may affect the brain.”

Provided by University of Wisconsin-Madison

Source: medicalxpress.com

June 6, 2012

New research by scientists at the University of North Carolina School of Medicine may have pinpointed an underlying cause of the seizures that affect 90 percent of people with Angelman syndrome (AS), a neurodevelopmental disorder.

This image shows inhibitory neurons (red) and cell bodies (blue) in the cerebral cortex of an Angelman syndrome model mouse. Credit: Philpot Lab, UNC School of Medicine

Published online Thursday June 7, 2012 in the journal Neuron, researchers led by Benjamin D. Philpot, PhD, professor of cell and molecular physiology at UNC, describe how seizures in individuals with AS could be linked to an imbalance in the activity of specific types of brain cells.

"Our study indicates that a common abnormality that may apply to many neurodevelopmental disorders is an imbalance between neuronal excitation and inhibition," Philpot said. This imbalance has been observed in several genetic disorders including Fragile X and Rett syndromes, both of these, like AS, can be associated with autism.

Angelman syndrome occurs in one in 15,000 live births. The syndrome often is misdiagnosed as cerebral palsy or autism. Its characteristics, along with seizures, include cognitive delay, severe intellectual disability, lack of speech (minimal or no use of words), sleep disturbance, hand flapping and motor and balance disorders.

The most common genetic defect of the syndrome is the lack of expression of the maternally inherited allele of gene UBE3A on chromosome 15.

This loss of gene function in AS animal models has been linked to decreased release of an excitatory neurotransmitter which increases the activity of other neurons. But that seems at odds with the high seizure activity observed in AS patients. The new study may clarify this issue.

In his lab in UNC’s Neuroscience Research Center, Philpot and graduate student Michael L. Wallace, the study’s first author, explored the neurocircuitry of an Angelman syndrome mouse model. These mice show behavioral features similar to humans with AS, including seizures.

The researchers used electrophysiological methods to record excitatory and inhibitory activity from individual neurons. These involved highly precise recording electrodes, microscopic tips attached to individual neurons. “In this way you can record from precise neuron types and tell which neuron you’re recording from and what its activity is,” explained Philpot.

"You can stimulate it to drive other neurons and also record the activity on other neurons onto it."

The researchers found that neurotransmitters sent from inhibitory neurons and carrying chemical messages meant to stop excitatory neurons from increasing their activity were defective.

In addition, they found that AS model mice have a defect in their inhibitory neurons which decreases their ability to recover from high levels of activity. “One of the reasons why inhibition is so important is that it’s needed to ensure that brain activity is regulated,” Philpot said. “Inhibition plays an important role in timing of information transfer between neurons, and if the timing is messed up, as you might observe if you had a decrease in inhibition, then a lot of information is lost in that transfer.”

"We found a disproportionately large decrease in inhibition to excitation," Wallace said. "We think that the circuit we investigated is in a hyperexcitable state and may be underlying some of the epileptic problems observed in the AS animal model. This improperly regulated brain activity might also underlie cognitive impairments in AS.”

Philpot says one of their goals is to understand exactly how these changes in the connections between neurons underlie seizures in AS. “A very long term goal is to try to get better treatments for these individuals because their epilepsy is very hard to treat.”

Provided by University of North Carolina Health Care

Source: medicalxpress.com

ScienceDaily (June 6, 2012) — Cutting the amount we drink to just over half a unit a day could save 4,600 lives a year in England, according to a modelling study by Oxford University researchers published in the journal BMJ Open.

Half a unit of alcohol is as little as a quarter of a glass of wine, or a quarter of a pint. (Credit: © G.G. Lattek / Fotolia)

Scientists have carried out a complex analysis in an attempt to determine the “optimal” level of alcohol consumption that is associated with the lowest rates of chronic disease in the UK. They conclude that the intake of about one-half of a typical drink per day would result in the healthiest outcomes, and the authors conclude that the recommended alcohol intake for the UK should be reduced from the current advised level of drinking.

Half a unit of alcohol is as little as a quarter of a glass of wine, or a quarter of a pint. That’s much lower than current government recommendations of between 3 to 4 units a day for men and 2-3 units for women.

The researchers set out to find the optimum daily amount of alcohol that would see fewest deaths across England from a whole range of diseases connected to drink. Previous studies have often looked at the separate effects of alcohol on heart disease, liver disease or cancers in isolation.

'Although there is good evidence that moderate alcohol consumption protects against heart disease, when all of the chronic disease risks are balanced against each other, the optimal consumption level is much lower than many people believe,' says lead author Dr Melanie Nichols of the BHF Health Promotion Research Group in the Department of Public Health at Oxford University.

The team used a mathematical model to assess what impact changing average alcohol consumption would have on deaths from 11 conditions known to be at least partially linked to drink.

These included coronary heart disease, stroke, high blood pressure, diabetes, cirrhosis of the liver, epilepsy, and five cancers. Over 170,000 people in England died from these 11 conditions in 2006, and ill health linked to alcohol is estimated to cost the NHS in England £3.3 billion every year.

The researchers used information from the 2006 General Household Survey on levels of alcohol consumption among adults in England. They combined this with the disease risks for differing levels of alcohol consumption as established in large analyses of published research.

They found that just over half a unit of alcohol a day was the optimal level of consumption among current drinkers.

They calculate this level of drinking would prevent around 4,579 premature deaths, or around 3% of all deaths from the 11 conditions.

The number of deaths from heart disease would increase by 843, but this would be more than offset by around 2,600 fewer cancer deaths and almost 3,000 fewer liver cirrhosis deaths.

'Moderating your alcohol consumption overall, and avoiding heavy-drinking episodes, is one of several things, alongside a healthy diet and regular physical activity, that you can do to reduce your risk of dying early of chronic diseases,' says Dr Nichols.

She adds: ‘We are not telling people what to do, we are just giving them the best balanced information about the different health effects of alcohol consumption, so that they can make an informed decision about how much to drink.

'People who justify their drinking with the idea that it is good for heart disease should also consider how alcohol is increasing their risk of other chronic diseases. A couple of pints or a couple of glasses of wine per day is not a healthy option.'

Although this study in BMJ Open did not look at patterns of drinking, Dr Nichols says: ‘Regardless of your average intake, if you want to have the best possible health, it is also very important to avoid episodes of heavy drinking (“binge drinking”) as there is very clear evidence that this will increase your risks of many diseases, as well as your risk of injuries.’

Source: Science Daily

June 6, 2012

A genetically-modified version of the rabies virus is helping scientists at Harvard to trace neural pathways in the brain, a research effort that could one day lead to treatments for Parkinson’s disease and addiction.

As described in a paper published on June 7 in the journal Neuron, a team of researchers led by Associate Professor of Molecular and Cellular Biology Naoshige Uchida used the virus to create the first-ever comprehensive list of inputs that connect directly to dopamine neurons in two regions of the brain, the ventral tegmental area (VTA), known for processing reward, and the substantia nigra (SNc), known for motor control.

"You may be familiar with the term connectome," Uchida explained. "The basic idea is we want to understand the brain in terms of connectivity and the various cell types. In this case, we’re examining long-range connections; that is, how other parts of the brain connect directly to dopamine neurons.

Dopamine neurons are thought to be important for processing reward and regulating motor output.

"By understanding their inputs, we might be able to better understand how the function of dopamine neurons is regulated, and, in turn, how addiction happens, and how Parkinson’s disease and other motor-control disorders are affected by problems with dopamine neurons,” Uchida continued. “And because this application provides us with very quantitative data, it’s possible that this is a technique that might be useful in attacking the causes of those diseases.”

Creating that connectivity diagram, however, is anything but easy.

While both the VTA and SNc are known to have high concentrations of dopamine neurons, Uchida chose to examine both areas because the cells in the two regions fire differently.

"We wanted to know what the difference was, generally," Uchida said. "That’s why we compared the inputs to both structures. Based on how other neurons are connected there, we can start to explain why these two regions of the brain do different things."

The challenge, however, is that dopamine neurons are packed into relatively small regions with several other cell types. To ensure they were only observing dopamine neurons, researchers turned to an organism more typically known for damaging neurons – the rabies virus.

Before they infect genetically-engineered mice with the rabies virus, however, they first inject the animals with a pair of “helper” viruses. The first causes dopamine neurons to produce a receptor protein, meaning the rabies virus can only infect dopamine neurons, while the second restores the virus’ ability to “hop” from one neuron to another.

The mice are then infected with a version of the rabies virus that has been genetically-modified to produce a fluorescent protein, allowing researchers to track the virus as it binds with dopamine neurons, and then jumps to the cells that link directly to those neurons.

The results, as depicted in images of a mouse’s brain showing the wealth of connections to dopamine neurons, show that a number of brain regions – including some previously unknown areas – are connected to dopamine neurons.

"We found some new connections, and we found some that we suspected were there, but that were not well understood," Uchida said. "For example, we found that there are connection between the motor cortex and the SNc, which may be related to SNc dopamine neurons’ role in motor control.

"Other connections, though, were more intriguing," he continued. "We found that the subthalmic nucleus preferentially connects to SNc neurons – that’s particularly important because that region is a popular target for deep brain stimulation as a treatment for Parkinson’s."

Often used as a treatment for Parkinson’s and a variety of other disorders, deep brain stimulation involves implanting a device, called a brain pacemaker, into a patient’s brain. The device then electrically stimulates specific regions of the brain, helping to mitigate symptoms of the disease.

"The mechanism for why deep brain stimulation works is not completely understood," Uchida said. "There was speculation that it might have been inhibiting neurons in the subthalmic nucleus, but our findings suggest, because there is a direct connection between those neurons and dopamine neurons in the SNc, that it is actually activating those neurons. I don’t think this explains the entire mechanism for why deep brain stimulation works, but this may be part of it.”

"This work also offers us a roadmap for other areas we might investigate, so now we can target those areas and record from them," Uchida added. "This is a critical step for future investigations."

Provided by Harvard University

Source: medicalxpress.com

June 6, 2012

Ask the average person the street how the brain develops, and they’ll likely tell you that the brain’s wiring is built as newborns first begin to experience the world. With more experience, those connections are strengthened, and new branches are built as they learn and grow.

A new study conducted in a Harvard lab, however, suggests that just the opposite is true.

As reported on June 7 in the journal Neuron, a team of researchers led by Jeff Lichtman, the Jeremy R. Knowles Professor of Molecular and Cellular Biology, has found that just days before birth mice undergo an explosion of neuromuscular branching. At birth, the research showed, some muscle fibers are contacted by as many as 10 nerve cells. Within days, however, all but one of those connections had been pruned away.

"By the time mammals – and humans would certainly be included – are first coming into the world, when they can do almost nothing, the brain is probably very wired up," Lichtman said. "Through experience, the brain works to select, out of this mass of possible circuits, a very small subset…and everything else that could have been there is gone.

"I don’t think anyone suspected that this was taking place – I certainly didn’t," he continued. "In some simple muscles, every nerve cell branches out and contacts every muscle fiber. That is, the wiring diagram is as diffuse as possible. But by the end, only two weeks later, every muscle fiber is the lifelong partner of a single nerve cell, and 90 percent of the wires have disappeared."

Though researchers, including Lichtman, had shown as early as the 1970’s that mice undergo an early developmental period in which target cells including muscle fibers and some neurons are contacted by multiple nerve cells before being reduced to a single connection, those early studies and his current work were hampered by the same problem – technological challenges make it difficult to identify individual nerve cells in earlier and earlier stages of life.

And though the use of mice that have been genetically-engineered to express fluorescent protein molecules in nerve cells has made it easier for researchers to identify nerve cells, it remains challenging to study early stages of development because the fluorescent labeling in the finest nerve cell wires often becomes so weak as to be invisible.

Read more …

ScienceDaily (June 6, 2012) — One of the top suspects behind killer vascular diseases is the victim of mistaken identity, according to researchers from the University of California, Berkeley, who used genetic tracing to help hunt down the real culprit.

Within the walls of blood vessels are smooth muscle cells and newly discovered vascular stem cells. The stem cells are multipotent and are not only able to differentiate into smooth muscle cells, but also into fat, cartilage and bone cells. UC Berkeley researchers provide evidence that the stem cells are contributing to clogged and hardened arteries. (Credit: Song Li illustration)

The guilty party is not the smooth muscle cells within blood vessel walls, which for decades was thought to combine with cholesterol and fat that can clog arteries. Blocked vessels can eventually lead to heart attacks and strokes, which account for one in three deaths in the United States.

Instead, a previously unknown type of stem cell — a multipotent vascular stem cell — is to blame, and it should now be the focus in the search for new treatments, the scientists report in a new study appearing June 6 in the journal Nature Communications.

"For the first time, we are showing evidence that vascular diseases are actually a kind of stem cell disease," said principal investigator Song Li, professor of bioengineering and a researcher at the Berkeley Stem Cell Center. "This work should revolutionize therapies for vascular diseases because we now know that stem cells rather than smooth muscle cells are the correct therapeutic target."

The finding that a stem cell population contributes to artery-hardening diseases, such as atherosclerosis, provides a promising new direction for future research, the study authors said.

"This is groundbreaking and provocative work, as it challenges existing dogma," said Dr. Deepak Srivastava, who directs cardiovascular and stem cell research at the Gladstone Institutes in San Francisco, and who provided some of the mouse vascular tissues used by the researchers. "Targeting the vascular stem cells rather than the existing smooth muscle in the vessel wall might be much more effective in treating vascular disease."

Read more …

ScienceDaily (June 6, 2012) — Swiss researchers have succeeded in generating detailed three-dimensional images of the spatial distribution of amyloid plaques in the brains of mice afflicted with Alzheimer’s disease. These plaques are accumulations of small pieces of protein in the brain and are a typical characteristic of Alzheimer’s. The new technique used in the investigations provides an extremely precise research tool for a better understanding of the disease. In the future, scientists hope that it will also provide the basis for a new and reliable diagnosis method.

Virtual cut. (Credit: Image courtesy of Paul Scherrer Institut (PSI))

The results were achieved within a joint project of two teams of researchers — one from the Paul Scherrer Institute (PSI) and ETH Zurich, the other from the École Polytechnique Fédérale de Lausanne (EPFL). They have been published in the journal Neuroimage.

Alzheimer’s disease is responsible for about 60% to 80% of all cases of dementia. This disease affects people differently, but the most common initial symptom is the difficulty in remembering new information, because the disease first affects brain regions involved in the formation of new memories. Alzheimer’s dementia is characterized by typical brain lesions that spread to other brain regions as the disease progresses. One of these lesions, the so-called amyloid plaque, is composed of the accumulation of extracellular protein aggregates. These lesions appear early in the course of the disease and there is a high interest in detecting them in patients to diagnose or evaluate the progression of the disease. Recently, medical imaging methods have been developed and validated for this purpose. These allow regional amount of amyloid deposits to be measured, but individual plaques cannot be quantified.

The latest results obtained by researchers from the Paul Scherrer Institute (PSI), ETH Zurich and the École Polytechnique Fédérale de Lausanne (EPFL) show that imaging single plaques is feasible under certain conditions. “This achievement could help to advance the development and evaluation of new imaging diagnostic markers for ultimately improving the diagnosis of Alzheimer’s disease,” explains Matthias Cacquevel, one of the authors at EPFL.

Precise plaque distribution in 3D

Using a method known as Phase Contrast Imaging, the researchers were able, within a short time, to make visible the exact three-dimensional distribution of amyloid plaques in the brains of mice with Alzheimer’s. Before this achievement, the only possibility of studying the distribution of amyloid plaques at the single-plaque level was to perform time-consuming studies. “Until now, for such an investigation, the brain had to be cut into slices and the slices coloured so that the plaques became visible,” explains Bernd Pinzer, from the Paul Scherrer Institute, who carried out the investigations. “This process is the gold standard amongst such investigations. It is, however, very time-consuming, as everything has to be done by hand. At the same time, it provides much less information than our new method. Naturally, we compared the results from our new method with those obtained using this traditional method, and they showed excellent agreement.”

As a first concrete result, the researchers determined the distribution of plaques in the brains of a number of mice with different stages of the disease. For each brain, the scientists obtained a three-dimensional image of the overall plaque distribution so that the development of the disease could be followed in detail. With conventional processes, it would hardly have been possible to gather such comprehensive information.

Developments for reliable diagnostic techniques

"One goal is to use the phase contrast technique to help improve imaging methods which make visible the plaques in the brain of a living patient, and thereby allow a reliable diagnosis of Alzheimer’s disease to be made," explains Pinzer. "These methods are under constant development and it is important to compare their results with those achieved using a known and reliable method. Now it will be possible to directly compare the two sets of 3D images of a mouse brain produced both by a diagnostic method and by our phase contrast technique. One of the diagnostic methods available is Positron Emission Tomography (PET), in which special molecules are attached to the plaques and, after some time, emit gamma radiation, which can be ascertained externally."

Although the deposited radiation dose required — which is high, in order to generate the necessary high resolution — prevents measurements being made on living animals at the moment, the method is already an outstanding research tool, which will lead to a better understanding of Alzheimer’s disease. “This tool will allow much more precise studies on how amyloid plaques are distributed,” explains Matthias Cacquevel, one of the authors at EPFL. “The relationship between plaques and the symptoms of the disease are still unclear, and information on how these plaques spread throughout the brain is also missing.”

Comprehensive information from changes in the light

These investigations were carried out at the Swiss Light Source (SLS) at PSI. The SLS generates synchrotron light — X-rays that are very intensive and well focused. The investigation is similar to a conventional X-ray examination — the scientists pass the X-rays through the object under investigation and determine how they have changed on their way. A normal X-ray picture, however, only shows how strongly the light is attenuated by the object; in a sense, it shows the shadow of the object. The problem is that various kinds of soft tissue attenuate X-rays in approximately the same way, which makes it difficult to distinguish between them.

"With the phase contrast method that we are using here, we also take into consideration the fact that different tissues deviate the light slightly from its original direction by a different amount. In physics, this effect is known to generate a so-called X-ray phase shift," explains Marco Stampanoni, Professor of X-Ray Microscopy at the Institute of Biomedical Technology at the ETH Zürich and Project Manager at PSI. The team he is leading built up the measuring station and designed the experiment. "Our instrument is able to measure such subtle shifts very precisely and transform this information into understandable images."

Phase Contrast Imaging for various medical applications

"While we cannot carry out an investigation on patients using the phase contrast method to detect Alzheimer’s disease, we are close to developing diagnostic tools for other diseases," emphasises Stampanoni. "We have already shown, in a pilot study on the imaging of tumours in the female breast, how useful the additional information can be. A first step in the direction of the hospital is the development of a mammography facility, the first prototype of which can be used in a doctor’s practice."

Source: Science Daily

June 6, 2012

A 25-year follow-up study reveals that 68% of patients with juvenile myoclonic epilepsy (JME) became seizure-free, with nearly 30% no longer needing antiepileptic drug (AED) treatment. Findings published today in Epilepsia, a journal of the International League Against Epilepsy (ILAE), report that the occurrence of generalized tonic-clonic seizures preceded by bilateral myoclonic seizures, and AED polytherapy significantly predicted poor long-term seizure outcome.

Patients with JME experience “jerking” of the arms, shoulders, and sometimes the legs. Previous evidence suggests that JME is a common type of epilepsy (in up to 11% of people with epilepsy), occurring more frequently in females than in males, and with onset typically in adolescence.. There is still much debate among experts over the long-term outcome of JME, and about which factors predict seizure outcome.

To further investigate JME outcomes and predictive factors, Dr. Felix Schneider and colleagues from the Epilepsy Center at the University of Greifswald in Germany studied data from 12 male and 19 female patients with JME. All participants had a minimum of 25 years follow-up which included review of medical records, and telephone or in-person interviews.

Sixty-eight percent of the 31 JME patients became free of seizures, and 28% discontinued AED treatment due to seizure-freedom. Significant predictors of poor long-term seizure outcome included: occurrence of generalized tonic-clonic seizures (GTCS - formerly known as grand mal seizures) that affect the entire brain and which are preceded by bilateral myoclonic seizures (abnormal movements on both sides of the body and a regimen of AED polytherapy.

Researchers also determined that remission of GTCS using AED therapy significantly increased the possibility of complete seizure-freedom. However, once AED therapy is discontinued, the occurrence of photoparoxysmal responses (brain discharges in response to brief flashes of light) significantly predicted an increased risk of seizure recurrence.

"Our findings confirm the feasibility of personalized treatment of the individual JME patient," concludes Dr. Schneider. "Life-long AED therapy is not necessarily required in many patients to maintain seizure freedom. Understanding the predictors for successful long-term seizure outcome will aid clinicians in their treatment options for those with JME.”

Provided by Wiley

Source: medicalxpress.com

ScienceDaily (June 5, 2012) — In a discovery that could help in the identification and treatment of anxiety disorders, Michigan State University scientists say the brains of anxious girls work much harder than those of boys.

This electrode cap was worn by participants in an MSU experiment that measured how people responded to mistakes. Female subjects who identified themselves as big worriers recorded the highest brain activity. (Credit: G.L. Kohuth)

The finding stems from an experiment in which college students performed a relatively simple task while their brain activity was measured by an electrode cap. Only girls who identified themselves as particularly anxious or big worriers recorded high brain activity when they made mistakes during the task.

Jason Moser, lead investigator on the project, said the findings may ultimately help mental health professionals determine which girls may be prone to anxiety problems such as obsessive compulsive disorder or generalized anxiety disorder.

"This may help predict the development of anxiety issues later in life for girls," said Moser, assistant professor of psychology. "It’s one more piece of the puzzle for us to figure out why women in general have more anxiety disorders."

The study, reported in the International Journal of Psychophysiology, is the first to measure the correlation between worrying and error-related brain responses in the sexes using a scientifically viable sample (79 female students, 70 males).

Participants were asked to identify the middle letter in a series of five-letter groups on a computer screen. Sometimes the middle letter was the same as the other four (“FFFFF”) while sometimes it was different (“EEFEE”). Afterward they filled out questionnaires about how much they worry.

Although the worrisome female subjects performed about the same as the males on simple portions of the task, their brains had to work harder at it. Then, as the test became more difficult, the anxious females performed worse, suggesting worrying got in the way of completing the task, Moser said.

"Anxious girls’ brains have to work harder to perform tasks because they have distracting thoughts and worries," Moser said. "As a result their brains are being kind of burned out by thinking so much, which might set them up for difficulties in school. We already know that anxious kids — and especially anxious girls — have a harder time in some academic subjects such as math."

Currently Moser and other MSU researchers are investigating whether estrogen, a hormone more common in women, may be responsible for the increased brain response. Estrogen is known to affect the release of dopamine, a neurotransmitter that plays a key role in learning and processing mistakes in the front part of the brain.

"This may end up reflecting hormone differences between men and women," Moser said.

In addition to traditional therapies for anxiety, Moser said other ways to potentially reduce worry and improve focus include journaling — or “writing your worries down in a journal rather than letting them stick in your head” — and doing “brain games” designed to improve memory and concentration.

Source: Science Daily