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By MAGGIE KOERTH-BAKER More than a decade ago, a 43-year-old woman went to a surgeon for a hysterectomy. She was put under, and everything seemed to be going according to plan, until, for a horrible interval, her anesthesia stopped working. She couldn’t open her eyes or move her fingers. She tried to breathe, but even that most basic reflex didn’t seem to work; a tube was lodged in her throat. She was awake and aware on the operating table, but frozen and unable to tell anyone what was happening. Studies of anesthesia awareness are full of such horror stories, because administering anesthesia is a tightrope walk. Too much can kill. But too little can leave a patient aware of the procedure and unable to communicate that awareness. For every 1,000 people who undergo general anesthesia, there will be one or two who are not as unconscious as they seem — people who remember their doctors talking, and who are aware of the surgeon’s knife, even while their bodies remain catatonic and passive. For the unlucky 0.13 percent for whom anesthesia goes awry, there’s not really a good preventive. That’s because successful anesthetization requires complete unconsciousness, and consciousness isn’t something we can measure. There are tools that anesthesiologists use to get a pretty good idea of how well their drugs are working, but these systems are imperfect. For most patients receiving inhaled anesthesia, they’re no better at spotting awareness than dosing metrics developed half a century ago, says George Mashour, a professor of anesthesiology at the University of Michigan Medical School. There are two intertwined mysteries at work, Mashour told me: First, we don’t totally understand how anesthetics work, at least not on a neurological basis. Second, we really don’t understand consciousness — how the brain creates it, or even what, exactly, it is. © 2013 The New York Times Company
By Graham Lawton Patricia Churchland, a neurophilosopher at the University of California at San Diego, says our hopes, loves and very existence are just elaborate functions of a complicated mass of grey tissue. Accepting that can be hard, but what we know should inspire us, not scare us. Her most recent book is Touching a Nerve: The Self as Brain. Graham Lawton: You compare revelations in neuroscience with the discoveries that the Earth goes around the sun and that the heart is a pump. What do you think these ideas have in common? Patricia Churchland: They challenge a whole framework of assumptions about the way things are. For Christians, it was very important that the Earth was at the center of the universe. Similarly, many people believed that the heart was somehow what made us human. And it turned out it was just a pump made of meat. I think the same is true about realizing that when we're conscious, when we make decisions, when we go to sleep, when we get angry, when we're fearful, these are just functions of the physical brain. Coming to terms with the neural basis of who we are can be very unnerving. It has been called "neuroexistentialism," which really captures the essence of it. We're not in the habit of thinking about ourselves that way. GL: Why is it so difficult for us to see the reality of what we actually are? PC: Part of the answer has to do with the evolution of nervous systems. Is there any reason for a brain to know about itself? We can get along without knowing, just as we can get along without knowing that the liver is in there filtering out toxins. The wonderful thing, of course, is that science allows us to know. © 2013 The Slate Group, LLC.
Link ID: 19024 - Posted: 12.11.2013
by Chelsea Whyte For chameleons, war paint isn't just an accessory, it is a battle flag. The brightness of the colours these lizards display and how rapidly they change are good indicators of which animal will win in a fight. Chameleons are famous for changing colour to hide from predators by blending into their surroundings, but they also use colour for social communication. One of the most diversely coloured species is the veiled chameleon (Chamaeleo calyptratus), which lives in parts of Saudi Arabia and Yemen. "At their brightest, they have vertical yellow stripes, blue-green bellies, black speckles that provide contrast and make their stripes stand out, and orange around the corner of their mouths," says Russell Ligon, a behavioural ecologist at Arizona State University in Tempe. To see if individual variations in these colours and patterns influenced the outcome of a fight, Ligon and his colleague Kevin McGraw staged a round-robin tournament in which 10 male veiled chameleons were pitted against each other. Using a high-speed camera, they were able to capture the brightness and colour changes from 28 points on each animal, taking into account how the colours would look to a chameleon's eye – which sees both visible and ultraviolet light. They found that males with the brightest side stripes were more likely to instigate a fight, whereas those with brighter heads that changed colour most rapidly were more likely to win. This suggests that different colours and patterns may signal different aspects of competitive behaviour – how motivated the chameleon is versus its strength. © Copyright Reed Business Information Ltd.
By Ben Thomas 2013’s Nobel prize in Physiology or Medicine honors three researchers in particular – but what it really honors is thirty-plus years of work not only from them, but also from their labs, their graduate students and their collaborators. Winners James Rothman, Randy Schekman and Thomas Südhof all helped assemble our current picture of the cellular machinery that enables neurotransmitter chemicals to travel from one nerve cell to the next. And as all three of these researchers agree, that process of understanding didn’t catalyze until the right lines of research, powered by the right tools, happened to converge at the right time. Long before that convergence, though, these three scientists began by seeking the answers to three different questions – none of which seemed to have anything to do with the others. When James Rothman started out as a researcher at Harvard in 1978, his goal was to find out exactly how vesicle transmission worked. Vesicles – Latin for “little vessels” – are the microscopic capsules that carry neurotransmitter molecules like serotonin and dopamine from one brain cell to another. By the late 1960s, the old-guard biochemist George Palade, along with other researchers, had already deduced that synaptic vesicles are necessary for neurotransmission – but the questions of which proteins guided these tiny vessels on their journey, and how they docked with receiving neurons, remained mysterious. Yale University's James Rothman set out to break down the process of vesicle transmission, chemical-by-chemical, reaction-by-reaction. Courtesy of Yale University. In other words, although researchers had established the existence of this vesicle transmission process, no one knew exactly what made it work, or how. © 2013 Scientific American
Link ID: 19022 - Posted: 12.11.2013
by Bethany Brookshire When neurons throughout the brain and body send messages, they release chemical signals. These chemicals, neurotransmitters, pass into the spaces between neurons, or synapses, binding to receptors to send a signal along. When they are not in use, neurotransmitters are stored within the cell in tiny bubbles called vesicles. During signaling, these vesicles head to the membrane of the neuron, where they dump neurotransmitter into the synapse. And after delivering their cargo, most vesicles disappear. But more vesicles keep forming, filling with neurotransmitters so neurons can keep sending signals. What goes up must come down. When vesicles go out, they must come back. But how fast to the vesicles re-appear? Must faster, it turns out, than we first thought. Neurotransmission happens fast. An electrical signal comes down a neuron in your brain and triggers vesicles to move to the cell membrane. When the vesicles merge into the membrane and release their chemical cargo, the neurotransmitters float across the open synapse to the next neuron. This happens every time the neuron “fires.” This needs to happen very quickly, as neurons often fire at 100 hertz, or 100 times per second. Some neurons perform a “kiss-and-run,” opening up a temporary pore in the membrane, releasing a little bit of neurotransmitter and darting away again. Other vesicles need to merge with the synapse entirely. With the assistance of docking proteins, these vesicles fuse with the membrane of the neuron to release the neurotransmitters, a process called exocytosis. © Society for Science & the Public 2000 - 2013.
Link ID: 19021 - Posted: 12.11.2013
By Jeanene Swanson Depression strikes some 35 million people worldwide, according to the World Health Organization, contributing to lowered quality of life as well as an increased risk of heart disease and suicide. Treatments typically include psychotherapy, support groups and education as well as psychiatric medications. SSRIs, or selective serotonin reuptake inhibitors, currently are the most commonly prescribed category of antidepressant drugs in the U.S., and have become a household name in treating depression. The action of these compounds is fairly familiar. SSRIs increase available levels of serotonin, sometimes referred to as the feel-good neurotransmitter, in our brains. Neurons communicate via neurotransmitters, chemicals which pass from one nerve cell to another. A transporter molecule recycles unused transmitter and carries it back to the pre-synaptic cell. For serotonin, that shuttle is called SERT (short for “serotonin transporter”). An SSRI binds to SERT and blocks its activity, allowing more serotonin to remain in the spaces between neurons. Yet, exactly how this biochemistry then works against depression remains a scientific mystery. In fact, SSRIs fail to work for mild cases of depression, suggesting that regulating serotonin might be an indirect treatment only. “There’s really no evidence that depression is a serotonin-deficiency syndrome,” says Alan Gelenberg, a depression and psychiatric researcher at The Pennsylvania State University. “It’s like saying that a headache is an aspirin-deficiency syndrome.” SSRIs work insofar as they reduce the symptoms of depression, but “they’re pretty nonspecific,” he adds. © 2013 Scientific American
Link ID: 19020 - Posted: 12.11.2013
Taking some heartburn medications for more than two years is linked to a higher risk of vitamin B12 deficiency in adults, a U.S. study suggests. Left untreated, vitamin B12 deficiency can lead to dementia, neurological damage, anemia, and other complications. Knowing that stomach acid aids in vitamin B12 absorption, researchers set out to test whether suppressing the acids can lead to vitamin deficiency. The drugs in question are known as proton pump inhibitors and they include such well known brands as Losec, Nexium, Prabacid and Pariet. Doses of more than 1.5 pills per day were more strongly associated with vitamin D deficiency than doses of less than 0.75 pills per day, Dr. Douglas Corley, a gastroenterologist and research scientist with the Kaiser Permanente Division of Research in Broadway, Calif. and his co-authors said in Wednesday's issue of the Journal of the American Medical Association. "This research raises the question of whether people who are taking acid-depressing medications long term should be screened for vitamin B12 deficiency," Corley said in a release. "It's a relatively simple blood test, and vitamin supplements are an effective way of managing the vitamin deficiency, if it is found." For the study, researchers looked at electronic health records of 25,956 adults diagnosed with vitamin B12 deficiency in Northern California between January 1997 and June 2011, and compared them with 184,199 patients without B12 deficiency during the same time period. Among the 25,956 patients who had vitamin B12 deficiency, 12 per cent used proton pump inhibitors for at least two years, compared with 7.2 per cent of those in the control group. © CBC 2013
By Ingfei Chen The way doctors diagnose Alzheimer's disease may be starting to change. Traditionally clinicians have relied on tests of memory and reasoning skills and reports of social withdrawal to identify patients with Alzheimer's. Such assessments can, in expert hands, be fairly conclusive—but they are not infallible. Around one in five people who are told they have the neurodegenerative disorder actually have other forms of dementia or, sometimes, another problem altogether, such as depression. To know for certain that someone has Alzheimer's, doctors must remove small pieces of the brain, examine the cells under a microscope and count the number of protein clumps called amyloid plaques. An unusually high number of plaques is a key indicator of Alzheimer's. Because such a procedure risks further impairing a patient's mental abilities, it is almost always performed posthumously. In the past 10 years, however, scientists have developed sophisticated brain scans that can estimate the amount of plaque in the brain while people are still alive. In the laboratory, these scans have been very useful in studying the earliest stages of Alzheimer's, before overt symptoms appear. The results are reliable enough that last year the Food and Drug Administration approved one such test called Amyvid to help evaluate patients with memory deficits or other cognitive difficulties. Despite the FDA's approval, lingering doubts about the exact role of amyloid in Alzheimer's and ambivalence about the practical value of information provided by the scan have fueled debate about when to order an Amyvid test. Not everyone who has an excessive amount of amyloid plaque develops Alzheimer's, and at the moment, there is generally no way to predict whom the unlucky ones will be. Recent studies have shown that roughly one third of older citizens in good mental health have moderate to high levels of plaque, with no noticeable ill effects. And raising the specter of the disorder in the absence of symptoms may upset more people than it helps because no effective treatments exist—at least not yet. © 2013 Scientific American
By Dan Hurley Darwin and Freud walk into a bar. Two alcoholic mice — a mother and her son — sit on two bar stools, lapping gin from two thimbles. The mother mouse looks up and says, “Hey, geniuses, tell me how my son got into this sorry state.” “Bad inheritance,” says Darwin. “Bad mothering,” says Freud. For over a hundred years, those two views — nature or nurture, biology or psychology — offered opposing explanations for how behaviors develop and persist, not only within a single individual but across generations. And then, in 1992, two young scientists following in Freud’s and Darwin’s footsteps actually did walk into a bar. And by the time they walked out, a few beers later, they had begun to forge a revolutionary new synthesis of how life experiences could directly affect your genes — and not only your own life experiences, but those of your mother’s, grandmother’s and beyond. The bar was in Madrid, where the Cajal Institute, Spain’s oldest academic center for the study of neurobiology, was holding an international meeting. Moshe Szyf, a molecular biologist and geneticist at McGill University in Montreal, had never studied psychology or neurology, but he had been talked into attending by a colleague who thought his work might have some application. Likewise, Michael Meaney, a McGill neurobiologist, had been talked into attending by the same colleague, who thought Meaney’s research into animal models of maternal neglect might benefit from Szyf’s perspective.
Link ID: 19017 - Posted: 12.11.2013
Three lawsuits filed last week that attempted to achieve “legal personhood” for four chimpanzees living in New York have been struck down. The suits, brought by the animal rights group the Nonhuman Rights Project (NhRP), targeted two chimps on private property and two in a research lab at Stony Brook University in New York. They were the first step in a nationwide campaign to grant legal rights to a variety of animals. NhRP had spent 5 years honing its legal strategy. It picked what it thought would be the most favorable jurisdictions and petitioned the judges with a writ of habeas corpus, which allows a person being held captive to have a say in court. Suffolk County Supreme Court Justice W. Gerard Asher denied the writ for the Stony Brook chimpanzees, writing in a brief decision that the animals did not qualify for habeas corpus because they were not “persons.” Both chimps are used in locomotion research at the university in work that is attempting to shed light on the origin of bipedalism in humans. Asher did not meet with NhRP lawyers; he issued his decision via a court clerk. The other judges were more accommodating. Fulton County Supreme Court Justice Joseph Sise and Niagara County Supreme Court Justice Ralph Boniello both allowed NhRP lawyers to make oral arguments in the courtroom. “As an animal lover, I appreciate your work,” said Sise, who handled the case of a chimpanzee named Tommy living in cage on his owner’s property in Gloversville, according to an NhRP press release. The group made “a very strong argument,” Sise said, according to the release, but he did not agree that habeas corpus applied to chimpanzees. Boniello, who oversaw the case of a chimp named Kiko living on his owner’s property in Niagara Falls, said he did not want to be the first “to make that leap of faith” equating chimpanzees with human beings. © 2013 American Association for the Advancement of Science.
Keyword: Animal Rights
Link ID: 19016 - Posted: 12.11.2013
Someday, a smart phone app that asks what you’re feeling 10 times a day may be able to tell you if you’re edging closer to depression—and recommend that you seek preventive therapy or drugs. Scientists have discovered that how quickly someone bounces back from negative feelings, over hours or days, can predict whether that person is at risk of an episode of major depressive disorder. “The holy grail of depression epidemiology is that we want to intervene early to prevent people from having depressive episodes,” says social scientist Stephen Gilman of Harvard University, who was not involved in the study. “Where this work is headed is making an advance in that direction, toward early detection and therefore early intervention.” Researchers asked more than 600 people—some healthy and some with a diagnosis of depression—to track their emotions for 5 or 6 days. Ten times a day, at random intervals, a watch would beep and the subjects would record how strongly they identified with each of four emotions: cheerful, content, sad, and anxious. Six to 8 weeks later, participants filled out a more detailed questionnaire that rated their levels of clinical depression. By the end of the follow-up period, about 13% of the subjects had experienced a shift toward being more depressed, a number consistent with what would be expected in the general population. Trends in the daily mood records, the team discovered, could predict whether a previously healthy person would make that shift toward depression. © 2013 American Association for the Advancement of Science
Link ID: 19015 - Posted: 12.10.2013
By JAMES GORMAN Sometimes the scientists who study animal behavior solve puzzles and other times they uncover new ones. The war between mockingbirds and cowbirds is a case in point. Cowbirds are brood parasites, meaning they lay their eggs in the nests of other bird species, thus unloading the messy and demanding business of chick-rearing. They also peck holes in the eggs of the host birds, destroying as many as they can. Mockingbirds are a favorite target of this plan, and it seems to make perfect sense for them to viciously attack cowbirds when they catch them in the nest. But when Ros Gloag, then a doctoral student at Oxford, and her colleagues in Argentina looked closely at the war between chalk-browed mockingbirds and shiny cowbirds, they found something unexpected, as they reported in the November issue of Animal Behaviour. They stationed small video cameras near the nests of 40 pairs of chalk-browed mockingbirds. Over two breeding seasons they recorded more than 200 attacks on intruding cowbirds. They were surprised to find that these attacks, which their videos show to be quite vicious, did not stop the cowbirds from laying eggs. The cowbirds would hunker down and let the much large mockingbirds deliver hammer blows to the head, but in matter of seconds they would lay an egg and flee. How could such a failed strategy persist in evolution? © 2013 The New York Times Company
Brian Owens Fruitflies know exactly how much alcohol will be good for their young. Larvae living on a food source with the right concentration of ethanol will grow into heavy, healthy adults and will be protected against parasites — which explains why the insects are attracted to rotting fruit or the crate of empty beer bottles in your kitchen but not to the vodka or gin. Now researchers have uncovered the neural mechanism that allows the fruitfly Drosophila melanogaster to choose the best place to lay its eggs. The work is published today in Proceedings of the National Academy of Sciences1. A team led by Ulrike Heberlein, a molecular biologist at the Howard Hughes Medical Institute’s Janelia Farm Research Campus in Ashburn, Virginia, found that clusters of neurons, working in opposition to each other, help the flies to choose the place with the most beneficial concentration of ethanol in which to lay their eggs. The neurons all release the neurotransmitter dopamine, a key player in the brain's reward circuitry. Neurons of the PAM and PPM3 clusters encourage the flies to seek out ethanol, whereas PPL1 neurons apply the brakes, preventing the flies from laying their eggs on food containing high levels of ethanol that could harm the larvae. “They can discriminate among ethanol concentrations that are very similar — 3% versus 5% — so the system evolved to have great sensitivity,” says Heberlein. Their favourite booze strength is 5%, similar to that of a typical beer. Heberlein's team also traced the neurons involved in ethanol preference to specific brain regions. Both the pro-ethanol PAM and anti-ethanol PPL1 neurons were active in the mushroom body, whereas the pro-ethanol PPM3 ones were active in the ellipsoid body. Both of these brain structures are involved in decision-making and memory, and mushroom body neurons also play a part in ethanol-reward memory. © 2013 Nature Publishing Group,
Keyword: Chemical Senses (Smell & Taste)
Link ID: 19013 - Posted: 12.10.2013
Researchers striving to understand the origins of dementia are building the case against a possible culprit: lead exposure early in life. A study spanning 23 years has now revealed that monkeys who drank a lead-rich formula as infants later developed tangles of a key brain protein, called tau, linked to Alzheimer's disease. Though neuroscientists say more work is needed to confirm the connection, the research suggests that people exposed to lead as children—as many in America used to be before it was eliminated from paint, car emissions, water, and soil—could have an increased risk of the common, late-onset form of Alzheimer’s disease. Even in small doses, lead can wreak havoc on the heart, intestines, kidneys, and nervous system. Children are especially prone to its pernicious effects, as it curbs brain development. Many studies have linked early lead exposure with lower IQs. Researchers estimate that one in 38 children in the United States still have harmful levels of the metal in their systems, but evidence linking this exposure to dementia later in life has been tenuous. A team led by toxicologist Nasser Zawia, however, has vigorously pursued the lead hypothesis. In one early study, from 2008, the group showed that plaques, insoluble globs of a protein called β-amyloid, marred the brains of five macaques that had consumed a lead-enriched formula as infants. The researchers had compared the preserved brain tissues from those macaques, sacrificed in 2003 at age 23 in a National Institutes of Health lab, with four similarly aged monkeys who had had lead-free formula. The amyloid plaques closely resembled those in the brains of adults with Alzheimer's disease that are thought to contribute to the dementia. © 2013 American Association for the Advancement of Science.
By Sandra Steingard, What does it mean that the man who killed 12 people at the Washington Naval Yard had told people that he was “hearing voices”? I have spent 30 years as a psychiatrist treating people who are psychotic. Almost every day I meet with individuals who hear voices that no one else hears, are sure the TV or radio is talking to them or have such confused thinking that it is hard to understand what they are trying to tell me. Sometimes these patients lead quiet lives. But not uncommonly these voices get them into trouble. I’ve had patients who call the police repeatedly, demanding that they stop bugging their phone. And others who stay up all night talking back at the voices. Some accuse family members of being involved in the torment. In many cases, this is a frightening experience — for the people I see and those who love them. And the labels we use — “schizophrenia,” “bipolar disorder,” “psychosis” — only crudely capture these experiences. About 60 years ago, a group of drugs was discovered that appeared to quiet the voices, improve the clarity of thought and lessen the preoccupation with delusion beliefs. Originally called major tranquilizers and later renamed antipsychotic drugs, these have been considered essential for the treatment of people with schizophrenia. Once it was clear that these drugs were helpful in the short term, questions arose over how long people should remain on them. Studies done in the 1970s and 1980s looked at people who were stabilized after being treated with antipsychotic drugs for several months and then followed them for up to two years. Some continued on the drugs, while others stopped taking them. The relapse rate was much higher in the group that stopped the medications. Based on these studies, treatment guidelines now state that people should stay on anti-psychotics indefinitely. The problem with “indefinitely” is that antipsychotic drugs have many troubling side effects. © 1996-2013 The Washington Post
Link ID: 19011 - Posted: 12.10.2013
There is more than meets the eye following even a mild traumatic brain injury. While the brain may appear to be intact, new findings reported in Nature suggest that the brain’s protective coverings may feel the brunt of the impact. Using a newly developed mouse trauma model, senior author Dorian McGavern, Ph.D., scientist at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, watched specific cells mount an immune response to the injury and try to prevent more widespread damage. Notably, additional findings suggest a similar immune response may occur in patients with mild head injury. In this study, researchers also discovered that certain molecules, when applied directly to the mouse skull, can bypass the brain’s protective barriers and enter the brain. The findings suggested that, in the mouse trauma model, one of those molecules may reduce effects of brain injury. Although concussions are common, not much is known about the effects of this type of damage. As part of this study, Lawrence Latour, Ph.D., a scientist from NINDS and the Center for Neuroscience and Regenerative Medicine, examined individuals who had recently suffered a concussion but whose initial scans did not reveal any physical damage to brain tissue. After administering a commonly used dye during MRI scans, Latour and his colleagues saw it leaking into the meninges, the outer covers of the brain, in 49 percent of 142 patients with concussion. To determine what happens following this mild type of injury, researchers in Dr. McGavern’s lab developed a new model of brain trauma in mice.
Keyword: Brain Injury/Concussion
Link ID: 19010 - Posted: 12.10.2013
Many physicians and parents report that their autistic children have unusually severe gastrointestinal problems, such as chronic constipation or diarrhea. These observations have led some researchers to speculate that an ailing gut contributes to the disorder in some cases, but scientific data has been lacking. Now, a provocative study claims that a probiotic treatment for gastrointestinal issues can reduce autismlike symptoms in mice and suggests that this treatment could work for humans, too. The reported incidence of gut maladies in people with autism varies wildly between published studies—from zero to more than 80%—making it difficult to establish just how commonly the two conditions go together, says principal investigator Sarkis Mazmanian, a microbiologist at the California Institute of Technology (Caltech) in Pasadena. Overall, however, the evidence seems to point toward a connection. Last year, for example, a Centers for Disease Control and Prevention study of thousands of children with developmental disabilities found that kids with autism were twice as likely as children with other types of disorders to have frequent diarrhea or colitis, an inflammation of the large intestine. For many years, Mazmanian and his and colleagues have been studying the effects of a nontoxic strain of the bacterium Bacteroides fragilis on diseases such as Crohn's disease, which causes intestinal inflammation and allows potentially harmful substances that should pass out of the body to leak through junctions between cells that are normally tight. Although the researchers don’t understand the mechanism, the bacterium appears to restore the damaged gut, possibly by helping close these gaps. © 2013 American Association for the Advancement of Science.
Link ID: 19009 - Posted: 12.06.2013
By Dana Smith Daniel Tammet has memorized Pi to the 22,514th digit. He speaks ten different languages, including one of his own invention, and he can multiply enormous sums in his head within a matter of seconds. However, he is unable to hold down a standard 9-to-5 job, in part due to his obsessive adherence to ritual, down to the precise times he has his tea every day. Daniel is a savant. He is also autistic. And he is a synesthete. Daniel experiences numbers as having color, as well as shape and texture. This helps him perform amazing mathematical feats seemingly without effort, the answer simply materializing to him rather than having to calculate it out. In an interview he gave with The Guardian, Daniel explained, “When I multiply numbers together, I see two shapes. The image starts to change and evolve, and a third shape emerges. That’s the answer. It’s mental imagery. It’s like maths without having to think.” Clearly this man has an extraordinary brain. However, Daniel is perhaps not entirely unique, and it appears that the link between autism and synesthesia is more common than originally thought. This suggests that there is a potential common mechanism between these two conditions, which may even help to explain some of Daniel’s special savant abilities. A new study published in the journal Molecular Autism from a team of researchers at the University of Cambridge now empirically shows that there is an almost three-fold higher occurrence of synesthesia in individuals with autism (18.9%), compared with that of the general population (7.2%). This increased prevalence implies that there is indeed a significant link between autism and synesthesia. © 2013 Scientific American
Link ID: 19008 - Posted: 12.06.2013
Helen Shen Dyslexia may be caused by impaired connections between auditory and speech centres of the brain, according to a study published today in Science1. The research could help to resolve conflicting theories about the root causes of the disorder, and lead to targeted interventions. When people learn to read, their brains make connections between written symbols and components of spoken words. But people with dyslexia seem to have difficulty identifying and manipulating the speech sounds to be linked to written symbols. Researchers have long debated whether the underlying representations of these sounds are disrupted in the dyslexic brain, or whether they are intact but language-processing centres are simply unable to access them properly. A team led by Bart Boets, a clinical psychologist at the Catholic University of Leuven in Belgium, analysed brain scans and found that phonetic representations of language remain intact in adults with dyslexia, but may be less accessible than in controls because of deficits in brain connectivity. "The authors took a really inventive and thoughtful approach," says John Gabrieli, a neuroscientist at the Massachusetts Institute of Technology in Cambridge, Massachusetts. "They got a pretty clear answer." Communication channels Boets and his team used a technique called multivoxel pattern analysis to study fine-scale brain signals as people listened to a battery of linguistic fragments such as 'ba' and 'da'. To the researchers' surprise, neural activity in the primary and secondary auditory cortices of participants with dyslexia showed consistently distinct signals for different sounds. © 2013 Nature Publishing Group
by Bob Holmes Perseverance in the face of adversity is an admirable character trait – now it turns out you can conjure it up with a quick zap to a tiny spot in the brain. The discovery in two people with epilepsy was accidental but it is the first to show that simple brain stimulation can create rich, complex alterations of consciousness. Josef Parvizi, a neurologist at Stanford University in California, and his colleagues had implanted electrodes in the brains of two people with epilepsy to help identify the source of their seizures. In the course of their work, they noticed that an odd thing happened when they stimulated a region in the anterior midcingulate cortex – a part of the limbic system involved in emotion, processing, learning and memory. Both patients reported feeling a sense of foreboding, coupled with a determination to overcome whatever challenge they were about to face. During the stimulation, one patient reported feeling "worried that something bad is going to happen" but also noted that "it made me stronger". The other said he felt as if he were figuring out how to get through something. He likened it to driving your car when one of the tires bursts. You're only halfway to your destination and you have no option but to keep going forward. "You're like… am I gonna get through this?" he said (see video). He also reported a sense of urgency: "It was more of a positive thing like… push harder, push harder, push harder to try and get through this." One singular sensation In contrast, when the researchers applied a sham stimulation – going through exactly the same procedure, but with the current set to zero – neither volunteer reported feeling any specific sensations. Stimulation of other nearby regions of the brain less than 5 millimetres away also failed to produce the feelings of either foreboding or perseverance. © Copyright Reed Business Information Ltd.