Caitlin Stier, video intern The animation, created by Douglas Reedy of Dublin, Ohio, is based on a static illusion developed by Baingio Pinna from the University of Sassari in Italy and Lothar Spillmann from University Hospital Freiberg in Germany. The illusion is created due to the tilt of tiny squares that make up the outline of each circle. When they lean in opposite directions in alternating rings, a spiral is perceived. Tweaking their angle of inclination creates a spiral with a different orientation. The squares in a circle also alternate in colour, which seems to intensify the effect compared to the same pattern in a uniform colour. When the squares are shifted upright, the illusion vanishes. The effect is stronger at the edges of your gaze compared to the center, which gives insight into how it works. Alvin Raj from the Perceptual Science Group at MIT and his team have been investigating the phenomenon by testing a denser version of the illusion with more squares and rings. Raj suggests that the way we size up the image in our peripheral vision causes a calculation error that accounts for the perceived swirl. "Some of the strange things you see might be a by-product of your visual system losing some information and trying to make the best of it," explains collaborator Benjamin Balas of North Dakota State University. © Copyright Reed Business Information Ltd.

Keyword: Vision
Link ID: 16338 - Posted: 02.04.2012

Christof Koch We moderns believe that our momentary, subjective experience is intimately linked to events in the brain. One set of neurons fires, and we perceive an apple's colour, while a different population of cells gives rise to its taste. Yet the self is also stable: turn the brain off, as happens during heart surgery when the body is cooled to frigid temperatures, and on recovery, the patient's character, personality, habits and long-term memories remain intact. It is these stable aspects of the self, rather than the ebb and flow of our thoughts and percepts, that physicist-turned-neuroscientist Sebastian Seung seeks to explain in Connectome. Seung argues intelligently and powerfully that the self lies in the totality of the brain's wiring — the eponymous 'connectome', the word used by neuroscientists to denote all the fibre bundles (the white matter) of the human brain. These insulated nerve axons have a total length of around 150,000 kilometres. Seung hails a new science, 'connectomics', as the key to understanding the brain and its pathologies. This view is grounded in a older doctrine known as connectionism, which postulates that neurons are simple devices and that their connections determine their functions. Cataloguing the links among neurons therefore charts the mind. The heart of Connectome deals with how nervous systems can be reconstructed using electron microscopy. To do this, neural tissue is cut into slices 40–50 nanometres thick, and then imaged to a resolution of a few nanometres. Imaging 1 cubic millimetre of cortex generates 1 petabyte of data, or about a billion photo images from a typical digital camera. © 2012 Nature Publishing Group,

Keyword: Consciousness
Link ID: 16337 - Posted: 02.04.2012

By Diane Mapes The specter of a burned-out Baby Boomer using hard drugs way into middle age may conjure images of addiction, destruction and death. That certainly can be true, but it’s not the complete picture, at least according to a new study from researchers at the University of Alabama at Birmingham, who found that people who occasionally use drugs like cocaine, amphetamines and opiates over the course of their lives are more common than anyone might suspect. “When you think of a drug user, you often think of someone strung-out, using every day, and in deep trouble, but national data shows that that's not the most common thing you see," says Dr. Stefan Kertesz, an associate professor in the UAB Division of Preventive Medicine. “The most common pattern is illicit drug use at lower levels." In other words, these sporadic drug users are “dabblers,” says Kertesz, lead author of the study that followed more than 4,300 people from four cities recruited between the ages of 18 to 30 in 1985 and 1986 -- and then tracked them for almost 20 years. He confirmed what he suspected from his experience in clinical care: that some perfectly functional middle-agers still turn to the drugs of their youth. "I meet people who use harder drugs on an intermittent basis," says Kertesz, who was trying to find ways doctors can better help patients who use drugs recreationally. © 2012 msnbc.com

Keyword: Drug Abuse
Link ID: 16336 - Posted: 02.04.2012

By James Gallagher Health and science reporter, BBC News Abnormalities in the brain may make some people more likely to become drug addicts, according to scientists at the University of Cambridge. They found the same differences in the brains of addicts and their non-addicted brothers and sisters. The study, published in the journal Science, suggested addiction is in part a "disorder of the brain". Other experts said the non-addicted siblings offered hope of new ways of teaching addicts "self-control". It has long been established that the brains of drug addicts have some differences to other people, but explaining that finding has been more difficult. Experts were unsure whether drugs changed the wiring of the brain or if drug addicts' brains were wired differently in the first place. This study, funded by the Medical Research Council, attempted to answer that by comparing the brains of 50 cocaine or crack addicts with the brain of their brother or sister, who had always been clean. Both the addicts and the non-addict siblings had the same abnormalities in the region of the brain which controls behaviour, the fronto-striatal systems. The suggestion is that these brains may be "hard-wired" for addiction in the first place. Lead researcher Dr Karen Ersche said: "It has long been known that not everyone who takes drugs becomes addicted." BBC © 2012

Keyword: Drug Abuse; Brain imaging
Link ID: 16335 - Posted: 02.04.2012

By Gary Stix Concussion, the most common among traumatic brain injuries, which occurs 1.7 million times a year in the U.S., represents a major public-health problem. It occurs when there is a sudden acceleration or deceleration of the head, a process depicted here in this animation. A blow can produce a brief loss of consciousness, headaches and impaired cognition, among other symptoms. Symptoms can last for days or sometimes longer. And a person who experience one risks another and may find recovery takes longer. Scientists continue to learn more about the nefarious consequences of repeated concussions. In the February issue of Scientific American, writer Jeffrey Bartholet details in “The Collision Syndrome evidence for yet another neurodegenerative disorder that can result from concussions. © 2012 Scientific American,

Keyword: Brain Injury/Concussion
Link ID: 16334 - Posted: 02.04.2012

by Jon Cohen As the father-to-son exchange in the old Cat Stevens song advised, "take your time, think a lot, ... think of everything you’ve got." Turns out the mellow ’70s folkie had stumbled upon what may explain a key feature of our brains that sets us apart from our closest relatives: We unhurriedly make synaptic connections through much of our early childhoods, and this plasticity enables us to slowly wire our brains based on our experiences. Given that humans and chimpanzees share 98.8% of the same genes, researchers have long wondered what drives our unique cognitive and social skills. Yes, chimpanzees are smart and cooperative to a degree, but we clearly outshine them when it comes to abstract thinking, self-regulation, assimilation of cultural knowledge, and reasoning abilities. Now a study that looks at postmortem brain samples from humans, chimpanzees, and macaques collected from before birth to up to the end of the life span for each of these species has found a key difference in the expression of genes that control the development and function of synapses, the connections among neurons through which information flows. As researchers describe in a report published online today in Genome Research, they analyzed the expression of some 12,000 genes—part of the so-called transcriptome—from each species. They found 702 genes in the prefrontal cortex (PFC) of humans that had a pattern of expression over time that differed from the two other species. (The PFC plays a central role in social behavior, working toward goals, and reasoning.) By comparison, genes in the chimpanzee PFC at various life stages had only 55 unique expression patterns—12-fold fewer than found in humans. © 2010 American Association for the Advancement of Science.

Keyword: Development of the Brain; Evolution
Link ID: 16333 - Posted: 02.02.2012

By Laura Sanders After surviving a bout of virulent bird flu, mice’s brains show short-term reductions of a key brain chemical and long-lasting signs of infection, a new study finds. The research suggests this type of flu might leave people more vulnerable to brain disorders such as Parkinson’s disease. While most people think of influenza as a disorder of the body, certain kinds of flu also infect the brain. Recent studies have found that the bird flu virus known as H5N1, which kills about half the people it infects, can set up shop in the brain. But exactly what happens next has been a mystery. In the new study, scientists at St. Jude Children’s Research Hospital in Memphis, Tenn., examined the brains of mice that had survived an initial H5N1 infection. As in people, the virus kills about half of mice affected. “The first goal with H5N1 was to characterize the neurological effects,” says study coauthor Richard Smeyne. After being infected with H5N1 isolated from a Vietnamese boy who died from the flu, some mice initially got very sick, but then seemed to recover completely after about 21 days. Yet the story wasn’t so simple in the brain, the team reports in the Feb. 1 Journal of Neuroscience. Nerve cells that make one of the brain’s key messengers — the neurotransmitter dopamine, which helps regulate movement — shut down production about 10 days after infection. These nerve cells, which are the same cells that degenerate in people with Parkinson’s disease, “basically take a time out,” Smeyne says. “All efforts are to survive.” © Society for Science & the Public 2000 - 2012

Keyword: Parkinsons
Link ID: 16332 - Posted: 02.02.2012

By GINA KOLATA Alzheimer’s disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau. The surprising finding answers a longstanding question and has immediate implications for developing treatments, researchers said. And they suspect that other degenerative brain diseases like Parkinson’s may spread in a similar way. Alzheimer’s researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas that involve remembering and reasoning. But for more than a quarter-century, researchers have been unable to decide between two explanations. One is that the spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths that nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and resist the disease longer. The new studies provide an answer. And they indicate it may be possible to bring Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau. © 2012 The New York Times Company

Keyword: Alzheimers
Link ID: 16331 - Posted: 02.02.2012

By The Editors The dangers of life in the National Football League made headlines in 2009, when a study commissioned by the NFL found that retired players were 19 times more likely than other men of similar ages to develop severe memory problems. The obvious culprit: continued play after repeated head injuries. Indeed, head injury can imitate many types of neurodegenerative disease, including Parkinson’s disease and, as journalist Jeffrey Bartholet reports in “The Collision Syndrome,” on page 66, perhaps even amyotrophic lateral sclerosis, commonly referred to as Lou Gehrig’s disease. The problem is not unique to professional sports. About 144,000 people aged 18 and younger are treated every year in U.S. hospital emergency rooms for concussions, according to a December 2010 analysis in the Journal of Pediatrics. Nearly a third of these injuries occur while kids are playing organized sports. Forty percent of pediatric concussions seen in emergency rooms involve high school students. The figure is slightly higher—42 percent—for younger children. Overall, concussions are most common in football and ice hockey, followed by soccer, wrestling and other sports, and slightly more boys than girls suffer concussions. Despite the prevalence of brain injury from kindergarten to high school, relatively little research on the long-term health consequences of concussion has been conducted on child athletes, compared with those in college and in the pros. Scientists have an incomplete understanding of what happens when a child’s brain slams up against the inside of the skull during a blow to the head and how this affects neurological development. As participation in sports continues to grow (1.5 million youngsters now play on football teams in the U.S.), more head injuries are inevitable, making pediatric concussions an emerging public health crisis. © 2012 Scientific American,

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 16330 - Posted: 02.02.2012

by Helen Thomson When you read this sentence to yourself, it's likely that you hear the words in your head. Now, in what amounts to technological telepathy, others are on the verge of being able to hear your inner dialogue too. By peering inside the brain, it is possible to reconstruct speech from the activity that takes place when we hear someone talking. Because this brain activity is thought to be similar whether we hear a sentence or think the same sentence, the discovery brings us a step closer to broadcasting our inner thoughts to the world without speaking. The implications are enormous – people made mute through paralysis or locked-in syndrome could regain their voice. It might even be possible to read someone's mind. Imagine a musician watching a piano being played with no sound, says Brian Pasley at the University of California, Berkeley. "If a pianist were watching a piano being played on TV with the sound off, they would still be able to work out what the music sounded like because they know what key plays what note," Pasley says. His team has done something analogous with brain waves, matching neural areas to their corresponding noises. How the brain converts speech into meaningful information is a bit of a puzzle. The basic idea is that sound activates sensory neurons, which then pass this information to different areas of the brain where various aspects of the sound are extracted and eventually perceived as language. Pasley and colleagues wondered whether they could identify where some of the most vital aspects of speech are extracted by the brain. © Copyright Reed Business Information Ltd

Keyword: Language; Robotics
Link ID: 16329 - Posted: 02.02.2012

By Victoria Gill Science reporter, BBC Nature Gorillas bare their teeth in a playful "grin" to reassure one another during play, scientists have discovered. This "flash of teeth" seems to let their playmate know that they do not intend to harm them. The researchers, from the University of Portsmouth, study the facial expressions of primates to uncover the evolutionary origins of human smiling and laughter. They published their findings in the American Journal of Primatology. Lead researcher Dr Bridget Waller explained that non-human primates have two expressions "that shed light on our smiling". Their "playface", she explained, appears to be a foundation of human laughter. Dr Waller told BBC Nature: "[During play, gorillas] open their mouths and cover their teeth as if to say, 'I could bite you but I'm not going to'." Another expression the primates use, where they reveal both rows of "sparkly white teeth" is believed to show one of the origins of human smiling. Smiling signal This is not a playful expression, Dr Waller said. "It's a greeting; a subordinate display." BBC © 2012

Keyword: Emotions; Evolution
Link ID: 16328 - Posted: 02.02.2012

By Sandra G. Boodman, “Men in Black” was flickering on the screen, and Laura Cossolotto and her husband were enjoying a rare night at the movies in their home town of Centerville, Iowa, when her brother-in-law rushed into the darkened theater. The couple’s third child, 6-month-old Michaela, had just suffered a serious seizure and was at a nearby hospital. As Cossolotto raced to be with the baby, she immediately remembered that Michaela had been running a fever after receiving a vaccine against diphtheria, pertussis and tetanus (DPT) three days earlier. “I thought the shot must have something to do with it,” Cossolotto recalled. “I had three kids, and nothing like this had ever happened, so what else could it have been?” At the hospital, doctors reassured her that Michaela had suffered a febrile seizure, a frightening and usually harmless event they said was unlikely to recur. As a precaution, the baby was admitted for observation. Hours later, after doctors had trouble controlling a second, more severe seizure, the infant was whisked by helicopter to a larger hospital in Des Moines, 100 miles north. That night in July 1997 marked the beginning of a 101 / 2-year ordeal, as more than a dozen specialists in four states tried without success to find an underlying cause for Michaela’s frequent, in­trac­table seizures — and a treatment that would control them before they caused irreparable brain damage or death. © 1996-2012 The Washington Post

Keyword: Epilepsy; Genes & Behavior
Link ID: 16327 - Posted: 01.31.2012

Brian Switek The largest mammals to walk Earth evolved from shrew-like creatures that proliferated after the dinosaurs died out, 65 million years ago. But the change from pipsqueak to behemoth took a while: 24 million generations. Researchers led by Alistair Evans, an evolutionary biologist at Monash University in Clayton, Australia, investigated how maximum body mass increased among 28 orders of mammals on multiple continents during the past 70 million years. By comparing the sizes of the largest members of mammal groups at different points in time, and using modern mammals to estimate the length of a generation for each group, Evans and colleagues tracked the speed at which mammals expanded. Their work is published online in the Proceedings of the National Academy of Sciences1 today. The top speed of mammal inflation was slower than had been thought. Previous estimates of the time it takes for a mouse-sized mammal to grow to the size of an elephant — a 100,000-fold size increase — had been based on observations of much smaller, 'microevolutionary' changes in mice, and ranged from 200,0002 to 2 million generations. “This tells us how much slower so-called macroevolution is compared to microevolution,” says Evans, explaining that small size changes can occur quickly, but larger-scale alterations require more time. To put this into perspective, “if we wiped out everything above the size of a rabbit, it would take at least 5 million generations to get to elephant-sized animals”, a 1,000-fold increase. That translates to about 20 million years. Bucking the trend But not all groups followed the same rule. Whales, the largest mammals ever, grew much more quickly than land-dwelling mammals, needing only about 3 million generations for a 1,000-fold size increase. Evans says that the difference was probably the result of different evolutionary constraints of life in the sea, such as the need to retain body heat, which is easier with a larger body mass. © 2012 Nature Publishing Group

Keyword: Evolution
Link ID: 16326 - Posted: 01.31.2012

By ABIGAIL ZUGER, M.D. Science generally succeeds in bringing some order to human existence — except when it does just the reverse, imposing a structure that never quite fits properly no matter how much it is tweaked. Then it just accentuates the underlying chaos. The much-disputed, oft-revised manual of psychiatric diagnosis might serve as one illustration of this phenomenon; given that it runs to almost 1,000 pages, Hanne Blank gets a pat on the back for dispatching the equally murky entity of heterosexuality in fewer than 200, plus back matter. One can almost hear a chorus of experts in the many sciences of sex and gender muttering that her amusing, readable synthesis is a featherweight effort, simplistic and derivative. But for those not in the field but still in the game, as it were — readers never previously moved to reason from first principles exactly what it means to be a heterosexual or act like one — Ms. Blank darts from one intriguing, thought-provoking point to another. She is a self-described “independent scholar” in Baltimore with several volumes of erotica and a well-received history of the virgin to her credit. Is Ms. Blank herself a heterosexual? That question prompts the first of her looping mind games. She has had romantic relationships with women in the past — so, no, right? Now, though, she is in a stable, long-term romantic partnership with a man (so, yes, right?). But her partner has a complicated genome, with some ordinary male XY cells and some that have an XXY pattern, giving him a softer, more stereotypically feminine aspect than usual, despite standard-issue male genitalia. And suddenly that word, “heterosexual,” becomes less than the helpful, scientifically precise term one might wish for. © 2012 The New York Times Company

Keyword: Sexual Behavior
Link ID: 16325 - Posted: 01.31.2012

By NATALIE ANGIER Meet the African crested rat, or Lophiomys imhausi, a creature so large, flamboyantly furred and thickly helmeted it hardly seems a member of the international rat consortium. Yet it is indeed a rat, a deadly dirty rat, its superspecialized pelt permeated with potent toxins harvested from trees. As a recent report in the journal Proceedings of the Royal Society B makes clear, the crested rat offers one of the most extreme cases of a survival strategy rare among mammals: deterring predators with chemical weapons. Venoms and repellents are hardly rare in nature: Many insects, frogs, snakes, jellyfish and other phyletic characters use them with abandon. But mammals generally rely, for defense or offense, on teeth, claws, muscles, keen senses or quick wits. Every so often, however, a mammalian lineage discovers the wonders of chemistry, of nature’s burbling beakers and tubes. And somewhere in the distance a mad cackle sounds. Skunks and zorilles mimic the sulfurous, anoxic stink of a swamp. The male duck-billed platypus infuses its heel spurs with a cobralike poison. The hedgehog declares: Don’t quite get the point of my spines? Allow me to sharpen their sting with a daub of venom I just chewed off the back of a Bufo toad. © 2012 The New York Times Company

Keyword: Evolution; Chemical Senses (Smell & Taste)
Link ID: 16324 - Posted: 01.31.2012

By James Gallagher Health and science reporter, BBC News Skin cells have been converted directly into cells which develop into the main components of the brain, by researchers studying mice in California. The experiment, reported in Proceedings of the National Academy of Sciences, skipped the middle "stem cell" stage in the process. The researchers said they were "thrilled" at the potential medical uses. Far more tests are needed before the technique could be used on human skin. Stem cells, which can become any other specialist type of cell from brain to bone, are thought to have huge promise in a range of treatments. Many trials are taking place, such as in stroke patients or specific forms of blindness. One of the big questions for the field is where to get the cells from. There are ethical concerns around embryonic stem cells and patients would need to take immunosuppressant drugs as any stem cell tissue would not match their own. An alternative method has been to take skin cells and reprogram them into "induced" stem cells. These could be made from a patient's own cells and then turned into the cell type required, however, the process results in cancer-causing genes being activated. The research group, at the Stanford University School of Medicine in California, is looking at another option - converting a person's own skin cells into specialist cells, without creating "induced" stem cells. It has already transformed skin cells directly into neurons. BBC © 2012

Keyword: Stem Cells
Link ID: 16323 - Posted: 01.31.2012

by Jessica Hamzelou YOU'RE running late for work and you can't find your keys. What's really annoying is that in your frantic search, you pick up and move them without realising. This may be because the brain systems involved in the task are working at different speeds, with the system responsible for perception unable to keep pace. So says Grayden Solman and his colleagues at the University of Waterloo in Ontario, Canada. To investigate how we search, Solman's team created a simple computer-based task that involved searching through a pile of coloured shapes on a computer screen. Volunteers were instructed to find a specific shape in a stack as quickly as possible, while the computer monitored their actions. "Between 10 and 20 per cent of the time, they would miss the object," says Solman, even though they picked it up. "We thought that was remarkably often." To find out why, the team developed a number of further experiments. To check whether volunteers were just forgetting their target, they gave a new group a list of items to memorise before the search task, which they had to recall afterwards. The idea was to fill each volunteer's "memory load", so that they were unable to hold any other information in their short-term memory. Although this was expected to have a negative effect on their performance at the search task, the extra load made no difference to the percentage of mistakes volunteers made. © Copyright Reed Business Information Ltd.

Keyword: Attention; Learning & Memory
Link ID: 16322 - Posted: 01.31.2012

By Andrea Anderson Mood disorders such as depression are known to increase drug abuse risk. Yet mounting evidence suggests that substance abuse also makes people more vulnerable to depression and the negative effects of stress, according to Eric J. Nestler, chair of neuroscience at the Mount Sinai School of Medicine. He and his team reported new details about the link between depression and drug abuse in Neuron in August. The team found that mice given cocaine daily for a week—a simulation of chronic drug abuse in humans—were more likely than their drug-free counter­parts to display behaviors reminiscent of depression after being subjected to socially stressful situations involving an aggressive and intimidating mouse. The drug-treated mice became lethar­gic and reluctant to interact with other mice following a shorter-than-usual bout of this “social defeat” stress, which is commonly used to study depression in mice. Most striking, the researchers found that the cocaine use led to the same molecular changes in the nucleus accumbens, a reward region, as are found in mice prone to stress and depression. The mice had lower levels of a molecule that polices the activity of certain genes and keeps at least one signaling circuit in check. When the researchers artificially dialed down or up the levels of this regulatory molecule in the nucleus accumbens, they were able to produce or protect against depression in mice. This effect suggests that shifts in that brain region can cause—and are not just a side effect of—depression. © 2012 Scientific American,

Keyword: Drug Abuse; Stress
Link ID: 16321 - Posted: 01.31.2012

By Ferris Jabr At a meeting of the Icelandic Medical Association last week, Yale University child psychologist Fred Volkmar gave a presentation on how the American Psychiatric Association (APA) is changing the definition of autism. In his talk, Volkmar came to a startling conclusion: more than half of the people who meet the existing criteria for autism would not meet the APA’s new definition of autism and, therefore, may not receive state educational and medical services. The APA defines autism in a reference guide for clinicians called the Diagnostic and Statistical Manual for Mental Disorders (DSM). The newest version of the manual, the DSM-5, is slated for publication in May 2013. In Iceland, Volkmar presented data from an unpublished preliminary analysis of 372 high-functioning autistic children and adults with IQs above 70. He plans to publish a broader analysis later this year. On a key PowerPoint slide that Volkmar shared with Scientific American, he notes that there are 2,688 ways to get a diagnosis of autistic disorder in DSM-IV, but only six ways to get a diagnosis of autism spectrum disorder in DSM-5. Although intriguing at first glance, it turns out that both these numbers are slightly wrong—and that they are pretty much useless when comparing the DSM-IV and DSM-5. You cannot reduce autism to a math problem. Scientific American wanted to explore this gaping discrepancy further, so we asked astronomer and Hubble Fellow Joshua Peek of Columbia University to code a computer program that would calculate the total possible ways to get a diagnosis of autistic disorder in DSM-IV and the total possible ways to get a diagnosis of autism spectrum disorder in DSM-5. You can do the math by hand, too, if you like: It all comes down to factorials. The DSM-IV criteria are a set of 12 items in three groups from which you must choose 6, with at least two items from group one and at least one item each from groups two and three. © 2012 Scientific American

Keyword: Autism
Link ID: 16320 - Posted: 01.31.2012

By Ferris Jabr People have been arguing about autism for a long time—about what causes it, how to treat it and whether it qualifies as a mental disorder. The controversial idea that childhood vaccines trigger autism also persists, despite the fact that study after study has failed to find any evidence of such a link. Now, psychiatrists and members of the autistic community are embroiled in a more legitimate kerfuffle that centers on the definition of autism and how clinicians diagnose the disorder. The debate is not pointless semantics. In many cases, the type and number of symptoms clinicians look for when diagnosing autism determines how easy or difficult it is for autistic people to access medical, social and educational services. The controversy remains front and center because the American Psychiatric Association (APA) has almost finished redefining autism, along with all other mental disorders, in an overhaul of a hefty tome dubbed the Diagnostic and Statistical Manual of Mental Disorders (DSM)—the essential reference guide that clinicians use when evaluating their patients. The newest edition of the manual, the DSM-5, is slated for publication in May 2013. Psychiatrists and parents have voiced concerns that the new definition of autism in the DSM-5 will exclude many people from both a diagnosis and state services that depend on a diagnosis. The devilish confusion is in the details. When the APA publishes the DSM-5, people who have already met the criteria for autism in the current DSM-IV will not suddenly lose their current diagnosis as some parents have feared, nor will they lose state services. But several studies recently published in child psychiatry journals suggest that it will be more difficult for new generations of high-functioning autistic people to receive a diagnosis because the DSM-5 criteria are too strict. Together, the studies conclude that the major changes to the definition of autism in the DSM-5 are well grounded in research and that the new criteria are more accurate than the current DSM-IV criteria. © 2012 Scientific American

Keyword: Autism
Link ID: 16319 - Posted: 01.31.2012