By Susan Milius Hey evolution, thanks for nothing. When a mammal embryo develops, its middle ear appears to form in a pop-and-patch way that seals one end with substandard, infection-prone tissue. “The way evolution works doesn’t always create the most perfect, engineered structure,” says Abigail Tucker, a developmental biologist at King’s College London. “Definitely, it’s made an ear that’s slightly imperfect.” The mammalian middle ear catches sound and transfers it, using three tiny bones that jiggle against the eardrum, to the inner ear chamber. Those three bones — the hammer, anvil and stirrup — are a distinctive trait that distinguishes the group from other evolutionary lineages. Research in mouse embryos finds that the middle ear begins as a pouch of tissue. Then its lining ruptures at one end and the break lets in a different kind of tissue, which forms the tiny bones of the middle ear. This intruding tissue originates from what’s called the embryo’s neural crest, a population of cells that gives rise to bone and muscle. Neural crest tissue has never been known before to create a barrier in the body. Yet as the mouse middle ear forms, this tissue creates a swath of lining that patches the rupture, Tucker and colleague Hannah Thompson, report in the March 22 Science. © Society for Science & the Public 2000 - 2013

Keyword: Hearing; Development of the Brain
Link ID: 17947 - Posted: 03.25.2013

By JANE E. BRODY Noise, not age is the leading cause of hearing loss. Unless you take steps now to protect to your ears, sooner or later many of you — and your children — will have difficulty understanding even ordinary speech. Tens of millions of Americans, including 12 percent to 15 percent of school-age children, already have permanent hearing loss caused by the everyday noise that we take for granted as a fact of life. “The sad truth is that many of us are responsible for our own hearing loss,” writes Katherine Bouton in her new book, “Shouting Won’t Help: Why I — and 50 Million Other Americans — Can’t Hear You.” The cause, she explains, is “the noise we blithely subject ourselves to day after day.” While there are myriad regulations to protect people who work in noisy environments, there are relatively few governing repeated exposure to noise outside the workplace, from portable music devices, rock concerts, hair dryers, sirens, lawn mowers, leaf blowers, vacuum cleaners, car alarms and countless other sources. We live in a noisy world, and every year it seems to get noisier. Ms. Bouton notes that the noise level inside Allen Fieldhouse at the University of Kansas often exceeds that of a chain saw. After poor service, noise is the second leading complaint about restaurants. Proprietors believe that people spend more on food and drink in bustling eateries, and many have created new venues or retrofitted old ones to maximize sound levels. Copyright 2013 The New York Times Company

Keyword: Hearing
Link ID: 17946 - Posted: 03.25.2013

A lack of a protein in Down's syndrome brains could be the cause of learning and memory problems, says a US study. Writing in Nature Medicine, Californian researchers found that the extra copy of chromosome 21 in people with the condition triggered the protein loss. Their study found restoring the protein in Down's syndrome mice improved cognitive function and behaviour. The Down's Syndrome Association said the study was interesting but the causes of Down's were very complex. Prof Huaxi Xu, senior author of the study from the Sanford-Burnham Medical Research Institute, said that in experiments on mice they discovered that the SNX27 protein was important for brain function and memory formation. Mice with less SNX27 had fewer active glutamate receptors and therefore had impaired learning and memory. The SNX27-deficient mice shared some characteristics with Down's syndrome, so the researchers looked at human brains with the condition. This confirmed their findings in the lab - that people with Down's syndrome also have significantly lower levels of SNX27. BBC © 2013

Keyword: Development of the Brain; Genes & Behavior
Link ID: 17945 - Posted: 03.25.2013

Two years after New Brunswick decided to help multiple sclerosis patients pay for an unproven treatment that's only offered outside the country, the number of patients who have sought the so-called liberation treatment has fallen short of expectations. A leading authority on MS says he's not surprised the numbers are falling off. The Finance Department says since April 1, 2011, 82 people who wanted the treatment that widens constricted veins in the neck have been approved for payments of $2,500 each. Applicants get the government funding if a community group raises matching funds. The provincial government budgeted $400,000 for the program in its first two years of operation — or enough to help 160 people seek the treatment. The government approved 25 applications in the first four months the money was available, but interest has tapered off and there have been no applications in the last two months. “It's getting fewer and fewer because every month a negative study is coming out," said Dr. Jock Murray, a neurologist at Dalhousie University in Halifax. Italian vascular specialist Paolo Zamboni reported dramatic improvements in his patients after he pioneered the procedure, but Murray said none of the subsequent studies done around the world have had the same results. “Every study has tended to be negative," he said. © CBC 2013

Keyword: Multiple Sclerosis
Link ID: 17944 - Posted: 03.25.2013

By John Horgan Does anyone still remember “The Decade of the Brain“? Youngsters don’t, but perhaps some of my fellow creaky, cranky science-lovers do. In 1990, the brash, fast-growing Society for Neuroscience convinced Congress to name the ’90s the Decade of the Brain. The goal, as President George Bush put it, was to boost public awareness of and support for research on the “three-pound mass of interwoven nerve cells” that serves as “the seat of human intelligence, interpreter of senses and controller of movement.” One opponent of this public-relations stunt was Torsten Wiesel, who won a Nobel Prize in 1981 for work on the neural basis of vision. When I interviewed him in 1998 for my book The Undiscovered Mind, he grumbled that the Decade of the Brain was “foolish.” Scientists “need at least a century, maybe even a millennium,” to understand the brain, Wiesel said. “We are at the very beginning of brain science.” I recalled Wiesel’s irritable comments as I read about big new neuroscience initiatives in the U.S. and Europe. In January, the European Union announced it would sink more than $1 billion over the next decade into the Human Brain Project, an attempt to construct a massive computer simulation of the brain. The project, according to The New York Times, involves more than 150 institutions. Meanwhile, President Barack Obama is reportedly planning to commit more than $3 billion to a similar project, called the Brain Activity Map. © 2013 Scientific American

Keyword: Brain imaging
Link ID: 17943 - Posted: 03.25.2013

By Brian Palmer, As a columnist who tries to explain scientific and other puzzles, I get asked a lot of strange questions. Here’s one that has been bugging me for some time: Are there visually impaired animals? Are there nearsighted deer that could use glasses or farsighted elephants that could benefit from an enormous set of contacts? How about astigmatic alligators? It seems like an animal question, but, at its core, it’s motivated by an astute comparison with humans. We’re undeniably visual creatures, yet many of us have trouble seeing well. According to some estimates, up to 42 percent of Americans are myopic, or nearsighted. Isn’t this a failure of natural selection? Shouldn’t our blurry-sighted ancestors have starved to death or been consumed by predators because of their visual handicaps? Does nature allow other animals to have such poor vision? These questions turn out to be surprisingly complicated. Let’s start out with the non-human animals and work back to our own visual shortcomings. Ophthalmologists can’t ask lions to read an eye chart or put glasses on a whale. Instead, they shine a light into the animal’s eye to see how it refracts and focuses on the retina. And with a trainable animal, such as a hawk or a horse, researchers can teach it to respond to a visual cue, then determine how well the animal picks up the cue when it is far away, very close or somehow obscured. © 1996-2013 The Washington Post

Keyword: Vision
Link ID: 17942 - Posted: 03.25.2013

Michael Corballis, professor of cognitive neuroscience and psychology at the University of Auckland in New Zealand, responds: Although teaching people to become ambidextrous has been popular for centuries, this practice does not appear to improve brain function, and it may even harm our neural development. Calls for ambidexterity were especially prominent in the late 19th and early 20th centuries. For instance, in the early 20th century English propagandist John Jackson established the Ambidextral Culture Society in pursuit of universal ambidexterity and “two-brainedness” for the betterment of society. This hype died down in the mid-20th century as benefits of being ambidextrous failed to materialize. Given that handedness is apparent early in life and the vast majority of people are right-handed, we are almost certainly dextral by nature. Recent evidence even associated being ambidextrous from birth with developmental problems, including reading disability and stuttering. A study of 11-year-olds in England showed that those who are naturally ambidextrous are slightly more prone to academic difficulties than either left- or right-handers. Research in Sweden found ambidextrous children to be at a greater risk for developmental conditions such as attention-deficit hyperactivity disorder. Another study, which my colleagues and I conducted, revealed that ambidextrous children and adults both performed worse than left- or right-handers on a range of skills, especially in math, memory retrieval and logical reasoning. © 2013 Scientific American

Keyword: Laterality; Learning & Memory
Link ID: 17941 - Posted: 03.25.2013

Philip Ball No one with even a passing interest in scientific trends will have failed to notice that the brain is the next big thing. It has been said for at least a decade, but now it’s getting serious — with, for example, the recent award by the European Commission of €500 million (US$646 million) to the Human Brain Project to build a new “infrastructure for future neuroscience” and a $1-billion initiative endorsed by President Obama. Having failed to ‘find ourselves’ in our genome, we’re starting a search in the grey matter. It’s a reasonable objective, but only if we have a clear idea of what we hope and expect to find. Some neuroscientists have grand visions, such as that adduced by Semir Zeki of University College London: “It is only by understanding the neural laws that dictate human activity in all spheres — in law, morality, religion and even economics and politics, no less than in art — that we can ever hope to achieve a more proper understanding of the nature of man.” Zeki heads the UCL Institute of Neuroesthetics. This is one of many fields that attaches ‘neuro’ to some human trait with the implication that the techniques of neuroscience, such as functional magnetic resonance imaging, will explain it. We have neurotheology, neuroethics, neurocriminology and so on. Meanwhile, in popular media, a rash of books and articles proclaim (in a profoundly ugly trope) that “this is your brain on drugs/music/religion/sport”. It seems unlikely that studies of the brain will ever be able to wholly explain how we respond to art. © 2013 Nature Publishing Group

Keyword: Emotions; Vision
Link ID: 17940 - Posted: 03.23.2013

By Felicity Muth This move from my old site to the Scientific American network has also coincided with my own physical move from the UK to the USA to start some new research. Given this is the closing of a chapter of my life (or rather, my PhD thesis, which will now no doubt sit on a dusty shelf somewhere until a grad student picks it up in 10 years time to use as a door stop), I felt now might be an appropriate time to write a little bit about what I have been doing for the past three years. In the past I have only written about other people’s research, but given that I am now a few months beyond the shock (I will resist using the word ‘trauma’ here) of it ‘all being over’, I feel like it might be time now to share a bit of what I did over my PhD. In one of my first meetings with my PhD supervisor, she said to me, ‘The way that I see it, you can either spend three months reading the limited amount of literature in your subject area, or you can go to Africa and get some data for yourself.’ This may have been the point where I realised I had chosen a good topic to study. Not only did not having much ‘literature’ to read due to the dearth of previous work done on this topic mean that I could kid myself that I was an ‘expert’ in the field after a few weeks, it was also liberating to know that most experiments that I carried out would be finding out new things. So, even before moving my books into my new PhD office, I was on a plane to Botswana to collect data on the nest building behaviour of the Southern masked weaverbird. When I tell people that the aim of my research is to work out how birds learn how to build nests, I usually get one of two responses. The first is, ‘they don’t learn anything of course, nest building in birds is innate.’ The other response is ‘surely that’s been done already?’ But actually, both of these (perfectly reasonable) assumptions are incorrect. © 2013 Scientific American,

Keyword: Learning & Memory
Link ID: 17939 - Posted: 03.23.2013

By Gary Stix A little shuteye refreshes. Right, but what does that really mean? Not talking here about leaping out of bed ready for a five-mile run upon awakening, but rather about what’s happening at the level of individual brain cells deep inside your head. A new study by R. Douglas Fields, a pioneer in researching out-of-the-mainstream brain areas and neural activity, holds one promising suggestion. Fields’s team at the National Institutes of Child Health and Development in Bethesda, Maryland, built on an earlier observation that during sleep (or even when just chilling out), neural signals travel the “wrong way” in cells of a critical region of the hippocampus, the brain structure involved with forming some types of new memories. The new study by Fields demonstrates, in a lab dish, that this reverse trafficking functions as a form of “editing,” a physical paring back of inessential parts of a brain cell to ensure that you don’t forget what you learned the previous day. Specifically, electrical signals in the CA1 area of the hippocampus reverse direction like the opposite flow of cars during the evening rush hour. The spiking electrical pulses move up instead of down the long extensions of nerve cells known as axons. The train of spikes pass through the cell body where the nucleus resides before reaching the ends of thousands of tiny branching tendrils called dendrites. © 2013 Scientific American

Keyword: Sleep
Link ID: 17938 - Posted: 03.23.2013

Arran Frood Two studies have decoded the structure of two of the brain's serotonin receptors. Here shown is a receptor known as 1B with the migraine drug ergotamine (pink) locked into one of its binding pockets. Researchers have deciphered the molecular structures of two of the brain's crucial lock-and-key mechanisms. The two molecules are receptors for the natural neurotransmitter serotonin — which regulates activities such as sleep, appetite and mood — and could provide targets for future drugs to combat depression, migraines or obesity. “This is huge,” says Bryan Roth, a neuropharmacologist at the University of North Carolina Chapel Hill Medical School, and a co-author of the two studies published in Science today1, 2. “Before this there was no crystal structure for any serotonin receptor. A lot of what was theoretical is now known with a great degree of certainty,” he says. Scientists have been trying to decipher serotonin receptors for years. Armed with information on the atomic level, they might now be able to make breakthroughs in drug discovery and in understanding how the physical structures of the brain produce consciousness, says Roth. Christoph Anacker, a neuropharmacologist at King's College London, agrees that the findings are important for drug discovery. “These receptors are involved in so many conditions, especially depression, and knowing the molecular structures will help to develop more specific drugs and avoid the expression of undesired side effects.” © 2013 Nature Publishing Group,

Keyword: Depression
Link ID: 17937 - Posted: 03.23.2013

Joshua P. Johansen Anxiety does not arise from a single neural circuit. An interplay between neighbouring, yet opposing, circuits produces anxiety, and outputs from these circuits regulate specific anxiety responses. We all know anxiety. We might have experienced it while waiting to hear about a promotion at work, or on our way to see the doctor because she wants to talk about test results in person. A diffuse uneasiness, sometimes accompanied by perspiration and subtle changes in breathing, anxiety ebbs and flows depending on life's circumstances, and can even occur for no apparent reason. The condition can be healthy and adaptive, but research in the United States1 shows that, for roughly one-third of people, anxiety is a debilitating disorder at some point in their lives. Nevertheless, answers to important questions — such as how different neuronal populations represent anxiety, and how the various components of the anxious state are constructed and represented in neural circuits — remain elusive. In two papers published on Nature's website today, Jennings et al.2 and Kim et al.3 address these questions using optogenetics to manipulate distinct neuronal subpopulations in mice and so dissect out the contribution of intermixed but functionally distinct cell groups. Both teams analysed a large, diffuse brain region called the bed nucleus of the stria terminalis (BNST). Previous studies4, 5, 6, 7 have found that lesions of the BNST reduce anxiety and fear of specific environments. Other work has discovered8, 9 distinct subregions and subpopulations of BNST neurons, and has found that the region has connections with several other brain areas that are involved in motivated behaviour and stress responses. However, the functions of the various BNST subpopulations and subregions, as well as the significance of these connections, have remained unclear. © 2013 Nature Publishing Group,

Keyword: Emotions; OCD - Obsessive Compulsive Disorder
Link ID: 17936 - Posted: 03.23.2013

by Emily Underwood Hallucinations and paranoia aren't the only symptoms that make life difficult for people with schizophrenia. Problems with memory and other cognitive functions also interfere with daily tasks, such as remembering the way to the office or balancing a checkbook. Now, by dampening the activity of a small group of neurons deep within the mouse brain, researchers have produced cognitive deficits similar to those found in those with schizophrenia, a discovery that they say could potentially lead to new treatments for the disorder, which affects roughly 24 million people worldwide. There's an ongoing debate over how much mice can mirror human psychiatric diseases, ranging from autism to depression. Still, neuroscientists often turn to rodents to study specific features of these human conditions. One abnormality that researchers have observed in functional magnetic resonance imaging scans of the brains of people with schizophrenia is an unusually low level of activity from a specific group of neurons near the brain stem. Called the mediodorsal thalamus (MD), the region appears to work with the prefrontal cortex—an area associated with planning and decision-making—to carry out tasks that require us to remember and process multiple pieces of information at once. (Going to the kitchen to fetch something, while remembering what it was you needed, for example.) In the past, scientists have studied the effects of low brain activity in the MD by cutting it out in mice—an extreme measure that didn't accurately mimic the "mild" reduction in activity seen in schizophrenia, says Columbia University psychiatrist Joshua Gordon. To create a more realistic mouse model of low MD activity, the team devised a new method that uses a virus to embed into the surface of MD neurons receptors that block cellular activity in the presence of a compound called clozapine-N-oxide. The beauty of this approach is its "exquisite specificity," Gordon says—it targets only neurons in the MD, and you can control how many neurons get shut down. © 2010 American Association for the Advancement of Science

Keyword: Schizophrenia
Link ID: 17935 - Posted: 03.23.2013

By Tina Hesman Saey Like many women with parents of the Mad Men generation, Susan Murphy grew up in a household full of cigarette smoke. Both dad and mom smoked heavily, even while Murphy was still in her mother’s womb. “That explains a lot,” Murphy quips, poking fun at herself. But Murphy isn’t worried about her own health. She’s fine. Her children aren’t, though. One boy died of cancer as a toddler. Another has autism. And her daughter has attention deficit disorder. Murphy knows the scientific evidence isn’t in yet, but she still can’t help wondering whether their fates might have been affected by her exposure to tobacco smoke before she was born. Murphy, a researcher at Duke University, studies links between a mother’s diet and chemical exposures during pregnancy with the child’s later health. She and others have established that the womb is the antithesis of Las Vegas; what happens there not only doesn’t stay there, it can influence a child’s health for life. Now, animal studies and a smattering of human data suggest such prenatal effects could reach farther down the family tree: The vices, virtues, inadvertent actions and accidental exposures of a pregnant mother may pose health consequences for her grandchildren and great-grandchildren, and perhaps even their offspring. Scientists have long known that radiation or certain chemicals can cause typos in a developing fetus’s genome — his or her genetic instruction book. Such mutations can get passed along to future generations in the DNA of sperm or egg cells. While exposure to sex hormones or a high-fat diet in the womb doesn’t directly change or damage DNA, those sorts of exposures can induce scribblings in the genome’s margins that can also be passed down. © Society for Science & the Public 2000 - 2013

Keyword: Epigenetics; Genes & Behavior
Link ID: 17934 - Posted: 03.23.2013

By Smitha Mundasad Health reporter, BBC News The risk of developing autism may be passed on through - and not just to - future generations, researchers say. The international study suggests older fathers are more likely to have grandchildren with autism than their younger counterparts. The mechanism is unclear but it is thought they may transmit "silent mutations" to their grandchildren. But experts have urged caution, stressing autism is the result of many different factors. The study, looking at almost 6,000 people with the condition, is published in the journal Jama Psychiatry. According to the National Autistic Society, more than one in every 100 people in the UK have the condition. Previous studies suggested older fathers may be at greater risk of having children with autism than younger dads. But the team of UK, Swedish and Australian researchers say this is one of the first pieces of evidence to show the risk can be passed on through - rather than just straight to - future generations. The "silent mutations" - changes in genetic material - are likely to have no obvious impact on older fathers' own children, but they may build up through subsequent generations, or interact with other genes and environmental factors, to increase the chance of their grandchildren developing the condition, the researchers say. BBC © 2013

Keyword: Autism; Epigenetics
Link ID: 17933 - Posted: 03.23.2013

by Peter Aldhous Women abused in childhood are more likely to have children with autism, a new epidemiological study suggests. The finding adds a disturbing new dimension to the heated debate over the condition's underlying causes. Andrea Roberts of the Harvard School of Public Health suspected that there might be a link between childhood abuse and having an autistic child: women abused early in life are more likely to smoke, suffer from gestational diabetes and have premature babies – all factors that may affect fetal brain development. To investigate, Roberts and her colleagues turned to the Nurses' Health Study II, which includes almost 55,000 women who had indicated if they had a child with autism spectrum disorder and also answered a questionnaire about their experience of abuse as a child. This allowed the researchers to develop a scale rating all the women for the intensity of abuse in their childhood. There was a clear link between the "dose" of abuse received and the risk of having an autistic child. "The associations get stronger as the level of abuse increases," Roberts says. After accounting for demographic factors such as age and socioeconomic status, the 2 per cent of women who reported the most serious childhood abuse – who were frequently hit and also sexually abused – were about 3.5 times as likely to have a child with autism as those who reported no abuse at all. "I think it's a really interesting, innovative and well-conducted study," says Hannah Gardener at the University of Miami in Florida. "There aren't a lot of risk factors with that magnitude." © Copyright Reed Business Information Ltd.

Keyword: Autism; Epigenetics
Link ID: 17932 - Posted: 03.23.2013

At 7 months of age, children who are later diagnosed with autism take a split second longer to shift their gaze during a task measuring eye movements and visual attention than do typically developing infants of the same age, according to researchers supported by the National Institutes of Health. The difference between the groups’ test results was 25 to 50 milliseconds on average, the researchers found, too brief to be detected in social interactions with an infant. However, they showed that this measurable delay could be accounted for by differences in the structure and organization of actively developing neurological circuits of a child’s brain. Image of brain structure known as the splenium of the corpus callosum When they were infants, children who were later diagnosed with autism took longer to shift their gaze during a measure of eye movements than did infants who were not diagnosed with autism. The researchers believe that brain circuits involved with a brain structure known as the splenium of the corpus callosum (shown in this scan) may account for the differences in gaze shifting between the two groups. Image courtesy of Jason Wolff, Ph.D., University of North Carolina at Chapel Hill. Efficiently shifting attention early in infancy is thought to be important for later social and cognitive development. Split-second delays, the researchers suggested, could be a precursor to such well known symptoms of autism as difficulty making eye contact or following a parent’s pointing finger, problems that generally emerge after a child turns 1. Typically, autism spectrum disorder (ASD) is not diagnosed until after 3 or 4 years of age. The study appears in the American Journal of Psychiatry.

Keyword: Autism; Vision
Link ID: 17931 - Posted: 03.23.2013

By Bruce Bower Malnutrition in the first year life, even when followed by a good diet and restored physical health, predisposes people to a troubled personality at age 40, new research suggests. The study of 77 formerly malnourished people represents the first evidence linking malnutrition shortly after birth to adult personality traits. The traits in some cases may foretell psychiatric problems, says a team led by psychiatrist Janina Galler of Harvard Medical School in Boston and psychologist Paul Costa of Duke University Medical Center in Durham. Compared with peers who were well-fed throughout their lives, formerly malnourished men and women reported markedly more anxiety, vulnerability to stress, hostility, mistrust of others, anger and depression, Galler’s team reports March 12 in the Journal of Child Psychology and Psychiatry. Survivors of early malnutrition also cited relatively little intellectual curiosity, social warmth, cooperativeness and willingness to try new experiences and to work hard at achieving goals. Previous studies of people exposed prenatally to famine have reported increased rates of certain personality disorders and schizophrenia. Another investigation found that malnutrition at age 3 predisposed youngsters on the Indian Ocean island of Mauritius to delinquent and aggressive behavior at ages 8, 11 and 17. As is true in the new study, distrust of others, anxiety and depression often accompany high levels of anger, says psychologist Adrian Raine of the University of Pennsylvania in Philadelphia, who directed the Mauritius research. “Poor nutrition early in life seems to predispose individuals to a suspicious personality, which may then fuel a hostile attitude toward others,” Raine proposes. © Society for Science & the Public 2000 - 2013

Keyword: Development of the Brain; Emotions
Link ID: 17930 - Posted: 03.23.2013

By Meghan Rosen Shushing neural chitchat in mouse brains can spark schizophrenia-like symptoms, a new study suggests. The findings are the first to demonstrate — at least in mice — that curbing communication among neurons in certain parts of the brain can cause some of the cognitive problems associated with schizophrenia. By muzzling neurons in the mediodorsal thalamus, or MD — a cell cluster that sends signals to the brain’s outer layer — researchers hindered mouse memory and learning in much the same way that schizophrenia seems to do in humans, scientists report March 20 in Neuron. Cognitive problems in schizophrenia have long been a mystery to scientists and a troubling symptom for people with the condition. The findings suggest that the problems stem from the thalamus, says neuropsychologist Neil Woodward of Vanderbilt University in Nashville, who was not involved with the new work. People with schizophrenia suffer from a range of debilitating symptoms: hallucinations, delusions and social disorders, says study coauthor Christoph Kellendonk of Columbia University. Patients also have problems with short-term memory and learning. Unlike other symptoms, these cognitive problems have been nearly impossible to treat. Brain imaging of people with schizophrenia had previously linked cognitive defects to changes in the MD — part of a walnut-sized chunk of gray matter snuggled above the brain stem. Normally, the MD relays information to and from the prefrontal cortex, the brain region behind the forehead that controls complex thought. In people with schizophrenia, the imaging showed, the MD is unusually quiet. © Society for Science & the Public 2000 - 2013

Keyword: Schizophrenia; Brain imaging
Link ID: 17929 - Posted: 03.23.2013

by Sara Reardon When she returned from serving in the Gulf conflict in 1991, US Air Force nurse Denise Nichols experienced sudden aches, fatigue and cognitive problems, but had no idea 'what was causing them. They grew worse: even helping her daughter with multiplication tables became difficult, she says, and eventually she had to quit her job. Nichols wasn't alone. About a third of Gulf war veterans – possibly as many as 250,000 – returned with a similar set of symptoms. Now an imaging study has found that these veterans have what appear to be unique structural changes in the wiring of their brains. This fits with the scientific consensus that Gulf War syndrome (GWS) is a physical condition rather than a psychosomatic one, and should be treated with painkilling drugs instead of counselling. The military in various countries has in the past consistently denied that there is a physical basis to GWS. Although the US Department of Veterans Affairs (VA) now officially accepts that the disorder is physical, the issue has been mired in controversy. Earlier this month, Steven Coughlin, a former senior epidemiologist at the VA, testified to a Congressional panel that the VA had suppressed and manipulated research data so as to suggest that the disorder was psychosomatic. © Copyright Reed Business Information Ltd.

Keyword: Stress; Brain imaging
Link ID: 17928 - Posted: 03.23.2013