By JAMES GORMAN TRONDHEIM, Norway — In 1988, two determined psychology students sat in the office of an internationally renowned neuroscientist in Oslo and explained to him why they had to study with him. Unfortunately, the researcher, Per Oskar Andersen, was hesitant, May-Britt Moser said as she and her husband, Edvard I. Moser, now themselves internationally recognized neuroscientists, recalled the conversation recently. He was researching physiology and they were interested in the intersection of behavior and physiology. But, she said, they wouldn’t take no for an answer. “We sat there for hours. He really couldn’t get us out of his office,” Dr. May-Britt Moser said. “Both of us come from nonacademic families and nonacademic places,” Edvard said. “The places where we grew up, there was no one with any university education, no one to ask. There was no recipe on how to do these things.” “And how to act politely,” May-Britt interjected. “It was just a way to get to the point where we wanted to be. But seen now, when I know the way people normally do it,” he said, smiling at the memory of his younger self, “I’m quite impressed.” So, apparently, was Dr. Andersen. In the end, he yielded to the Mosers’ combination of furious curiosity and unwavering determination and took them on as graduate students. They have impressed more than a few people since. In 2005, they and their colleagues reported the discovery of cells in rats’ brains that function as a kind of built-in navigation system that is at the very heart of how animals know where they are, where they are going and where they have been. They called them grid cells. © 2013 The New York Times Company

Keyword: Attention
Link ID: 18099 - Posted: 04.30.2013

By ABIGAIL ZUGER, M.D. Addiction swallows lives whole, and not only with overdose, illness and concentric cycles of rehab and relapse. A less onerous but still tenacious kind of post-traumatic stress disorder may develop as well, with recovered addicts and their families compulsively reliving the past in private — or, like David Sheff and his son Nic, in public. In the last five years the two have written a small library of memoirs centered on Nic’s battle with substance use, with two by Nic (now 31, and sober) and the 2008 best seller by his father, “Beautiful Boy.” Now comes “Clean,” less memoir than guide for those just entering the terrain Mr. Sheff knows so well. If the book represents a certain redundancy of subject, its likely audience — those who must watch as friends and family spiral away — cannot hear too many sympathetic reiterations of the same truths. In “Clean,” Mr. Sheff changes perspective, writing as advocate and journalist rather than distraught father. Still, his story line recreates that of “Beautiful Boy,” tracing the trajectory of addiction from cradle to rehab and beyond with the same question in mind: How does a promising cleareyed kid from a good family wind up in an inconceivable sea of trouble? His answer, bludgeoned home with the repetitive eloquence of the missionary, is entirely straightforward: The child is ill. Addiction must be considered a disease, as devoid of moral overtones as diabetes or coronary artery disease, just as amenable as they are to scientific analysis, and just as treatable with data-supported interventions, not hope, prayer or hocus-pocus. © 2013 The New York Times Company

Keyword: Drug Abuse
Link ID: 18098 - Posted: 04.30.2013

By Cheryl Knepper Substance abuse and dependence rarely occur in a vacuum. Today’s addict is faced with a multitude of issues that may co-exist and compromise recovery. Co-existing addictions/compulsive behaviors such as drugs and alcohol, pathological gambling, sex, food, work, internet and gaming can become chronic and progressive if left unidentified and untreated. Many of these addictions don’t only coexist, but interact, reinforce and fuse together becoming part of a package known as Addiction Interaction. The term “Addiction Interaction Disorder” was introduced by Patrick Carnes PhD in 2011. Caron Treatment Centers conducted a research study among adult patients with drug and alcohol addictions to determine what percentage may be at risk for sex and love addiction. The 485 participants were given the SAST-R (Sexual Addiction Screening Tool-Revised a 45 item forced choice (Yes/No) instrument): Carnes, Green & Carnes, 2010. The findings of this study indicated that 21 percent of individuals being treated for primary substance dependence scored at risk. Another interesting finding from the study showed a higher percentage of cannabis, cocaine and amphetamine abuse or dependence diagnosis in the individuals that scored at-risk for sexual addiction. In addition, at-risk individuals had higher percentages of mood disorder, PTSD and eating disorder diagnoses. © 2013 Scientific American

Keyword: Drug Abuse
Link ID: 18097 - Posted: 04.30.2013

By Sophie Moura The year I was in fifth grade, I saw a television commercial for tampons. Like most 10-year-olds, I'd never heard of a tampon. But when I asked my mom what one was, she started crying. How do you tell your daughter that she's never going to need tampons? That she won't get her period or have babies, and that those things are the least of what sets her apart? From the outside, there was no sign that the little kid watching TV in a suburb of Pittsburgh was so different. I've always been girly — obsessed with dresses, sparkles, and the color pink, donning felt poodle skirts for Halloween and loving makeup. What isn't obvious is that I have a rare condition called androgen insensitivity syndrome, or AIS. I was born with XY chromosomes, the combination found in boys. With AIS, an XY embryo doesn't respond to the crucial hormones that tell the penis and scrotum to form. At the earliest stage of life, my body missed those signals, and I developed as a girl, with a clitoris and vulva. But what's inside me doesn't match. My parents learned this when I was 6. That year, I collapsed in the shower with a painful lump in my groin. Convinced I had a hernia, my parents, both doctors, rushed me to the hospital. But when surgeons operated (a hernia is tough to X-ray and needs to be fixed surgically), there was no twisted loop of intestine behind that bump. It was a testicle that had started descending. Across my abdomen, they found another one. The upper portion of my vagina, and my cervix, uterus, and fallopian tubes were missing. ©2013 Hearst Communication, Inc.

Keyword: Sexual Behavior
Link ID: 18096 - Posted: 04.30.2013

By Ferris Jabr On any given day, millions of conversations reverberate through New York City. Poke your head out a window overlooking a busy street and you will hear them: all those overlapping sentences, only half-intelligible, forming a dense acoustic mesh through which escapes an exclamation, a buoyant laugh, a child’s shrill cry now and then. Every spoken consonant and vowel begins as an internal impulse. Electrical signals crackle along branching neurons in brain regions specialized for language and movement; further pulses spread across facial nerves, surge toward the throat and chest and zip down the spine. The diaphragm contracts—pulling air into the lungs—and relaxes, pushing air into that birdcage of calcium and cartilage—the larynx—within which wings of tissue draw near one another and hum. As this vibrating air enters the mouth, the tongue guides its flow and the lips give each breath a final shape and sound. Liberated syllables travel between one person and another in waves of colliding air molecules. All these conversations are matched in number and complexity by much more elusive discourses. The human brain loves soliloquy. Even when speaking with others—and especially when alone—we continually talk to ourselves in our heads. Such speech does not require the bellows in the chest, quivering flaps of tissue in the throat or a nimble tongue; it does not need to disturb even one hair cell in our ears, nor a single particle of air. We can speak to ourselves without making a sound. Stick your head out that same window above the crowded street and you will hear nothing of what people are saying to themselves privately. All that inner dialogue remains submerged beneath the ocean of human speech, like a novel written in invisible ink behind the text of another book. © 2013 Scientific American,

Keyword: Consciousness
Link ID: 18095 - Posted: 04.30.2013

By Meghan Rosen A child who is good at learning math may literally have a head for numbers. Kids’ brain structures and wiring are associated with how much their math skills improve after tutoring, researchers report April 29 in the Proceedings of the National Academy of Sciences. Certain measures of brain anatomy were even better at judging learning potential than traditional measures of ability such as IQ and standardized test results, says study author Kaustubh Supekar of Stanford University. These signatures include the size of the hippocampus — a string bean–shaped structure involved in making memories — and how connected the area was with other parts of the brain. The findings suggest that kids struggling with their math homework aren’t necessarily slacking off, says cognitive scientist David Geary of the University of Missouri in Columbia. “They just may not have as much brain region devoted to memory formation as other kids.” The study could give scientists clues about where to look for sources of learning disabilities, he says. Scientists have spent years studying brain regions related to math performance in adults, but how kids learn is still “a huge question,” says Supekar. He and colleagues tested IQ and math and reading performance in 24 8- and 9-year-olds, then scanned their brains in an MRI machine. The scans measured the sizes of different brain structures and the connections among them. “It’s like creating a circuit diagram,” says study leader Vinod Menon, also of Stanford. © Society for Science & the Public 2000 - 2013

Keyword: Learning & Memory
Link ID: 18094 - Posted: 04.30.2013

By TARA PARKER-POPE Are doctors nicer to patients who aren’t fat? A provocative new study suggests that they are — that thin patients are treated with more warmth and empathy than those who are overweight or obese. For the study, published in the medical journal Obesity, researchers at Johns Hopkins obtained permission to record discussions between 39 primary care doctors and more than 200 patients who had high blood pressure. Although patients were there to talk about blood pressure, not weight, most fell into the overweight or obese category. Only 28 were of normal weight, meaning they had a body mass index below 25. Of the remaining patients, 120 were obese (B.M.I. of 30 or greater) and 60 were classified as overweight (index of 25 to 30). For the most part, all of the patients were treated about the same; there were no meaningful differences in the amount of time doctors spent with them or the topics discussed. But when researchers analyzed transcripts of the visits, there was one striking difference. Doctors seemed just a bit nicer to their normal-weight patients, showing more empathy and warmth in their conversations. Although the study was relatively small, the findings are statistically significant. “It’s not like the physicians were being overtly negative or harsh,” said the lead author, Dr. Kimberly A. Gudzune, an assistant professor of general internal medicine at the Johns Hopkins School of Medicine. “They were just not engaging patients in that rapport-building or making that emotional connection with the patient.” Copyright 2013 The New York Times Company

Keyword: Obesity; Emotions
Link ID: 18093 - Posted: 04.30.2013

By Stephani Sutherland Itching is not the only sensation to arise from unique neurons. A team at the California Institute of Technology has identified neurons that transmit the pleasurable sensations of massage, at least in mice. The cells responded to gentle rubbing but not to pinching or poking. Activation of the cells requires “a pressure component,” says lead investigator David Anderson, a neuroscientist at Caltech, “much like you would apply if you were stroking your cat.” The team first identified the mysterious cells several years ago by an unusual protein on their surface called MrgprB4—closely related to the receptor expressed by the newly identified itch cells. The rare sensory cells make up only about 2 percent of the body's peripheral neurons that respond to external stimuli, but they seem to cover about half the skin's surface with large, branching nerve endings. Whereas sensory neurons that transmit pain have been intensely studied, this is the first demonstration in live animals of a sensory cell that gives pleasure. After the scientists activated those neurons with a designer drug, the mice came to favor the place where they received the drug, according to the paper published January 31 in Nature. © 2013 Scientific American

Keyword: Pain & Touch
Link ID: 18092 - Posted: 04.30.2013

By Christie Wilcox What does your voice say about you? Our voices communicate information far beyond what we say with our words. Like most animals, the sounds we produce have the potential to convey how healthy we are, what mood we’re in, even our general size. Some of these traits are important cues for potential mates, so much so that the sound of your voice can actually affect how good looking you appear to others. Which, really, brings up one darn good question: what makes a voice sound sexy? To find out, a team spearheaded by University College London researcher Xi Yu created synthetic male and female voices and altered their pitch, vocal quality and formant spacing (an acoustics term related to the frequencies of sound), the last of which is related to body size. They also adjusted the voices to be normal (relaxed), breathy, or pressed (tense). Through several listening experiments, they asked participants of the opposite gender to say which voice was the most attractive and which sounded the friendliest or happiest. The happiest-sounding voices were those with higher pitch, whether male or female, while the angriest were those with dense formants, indicating large body size. As for attractiveness, the men preferred a female voice that is high-pitched, breathy and had wide formant spacing, which indicates a small body size. The women, on the other hand, preferred a male voice with low pitch and dense formant spacing, indicative of larger size. But what really surprised the scientists is that women also preferred their male voices breathy. “The breathiness in the male voice attractiveness rating is intriguing,” explain the authors, “as it could be a way of neutralizing the aggressiveness associated with a large body size.”

Keyword: Language; Sexual Behavior
Link ID: 18091 - Posted: 04.30.2013

By YUDHIJIT BHATTACHARJEE One summer night in 2011, a tall, 40-something professor named Diederik Stapel stepped out of his elegant brick house in the Dutch city of Tilburg to visit a friend around the corner. It was close to midnight, but his colleague Marcel Zeelenberg had called and texted Stapel that evening to say that he wanted to see him about an urgent matter. The two had known each other since the early ’90s, when they were Ph.D. students at the University of Amsterdam; now both were psychologists at Tilburg University. In 2010, Stapel became dean of the university’s School of Social and Behavioral Sciences and Zeelenberg head of the social psychology department. Stapel and his wife, Marcelle, had supported Zeelenberg through a difficult divorce a few years earlier. As he approached Zeelenberg’s door, Stapel wondered if his colleague was having problems with his new girlfriend. Zeelenberg, a stocky man with a shaved head, led Stapel into his living room. “What’s up?” Stapel asked, settling onto a couch. Two graduate students had made an accusation, Zeelenberg explained. His eyes began to fill with tears. “They suspect you have been committing research fraud.” Stapel was an academic star in the Netherlands and abroad, the author of several well-regarded studies on human attitudes and behavior. That spring, he published a widely publicized study in Science about an experiment done at the Utrecht train station showing that a trash-filled environment tended to bring out racist tendencies in individuals. And just days earlier, he received more media attention for a study indicating that eating meat made people selfish and less social. © 2013 The New York Times Company

Keyword: Attention
Link ID: 18090 - Posted: 04.29.2013

By Scicurious Say you are out on a camping trip with some friends. You’re in the woods, the tents are up, the beer is out, the sun is down, the campfire is starting up. As you sit there, you hear the campfire crackling loudly. To most people, the crackling of the campfire is just that: a campfire. Nothing threatening at all. But for someone with a severe anxiety disorder such as post-traumatic stress disorder (PTSD), the crackling of the campfire may be associated with terrible memories, a huge conflagration during house to house fighting or a house fire that destroyed all they loved, causing them horrible distress and terrible anxiety. A campfire during a camping trip and the horrible things they endured are entirely dissimilar things, but in severe anxiety disorders, that makes no difference at all. No, this post is not about whether or not anxiety disorders are being over diagnosed. Rather, it’s about how over-generalization within the brain might influence the development of anxiety disorders. What is the difference between a house fire and a campfire? How does your brain know? It’s the idea of pattern separation, an idea that the authors of this review believe could be incredibly important in treating some types of anxiety disorders. Pattern separation is one of the many actions of the hippocampus, the large, curved area in the interior of the brain which is thought to play a role in things like memory and in disorders such as anxiety and depression. Pattern separation was originally observed related to memory, but the authors of this review propose that it may also relate to things like anxiety. © 2013 Scientific American

Keyword: Stress
Link ID: 18089 - Posted: 04.29.2013

By Nathan Seppa The tobacco and fruit mixture smoked in public hookah bars might be considerably more dangerous than its pleasant scent would suggest. An analysis of people who smoked from water pipes three times a day finds that the pipes deliver more carbon monoxide and benzene, a carcinogen, than does smoking half a pack of cigarettes daily. In an upcoming issue of Cancer Epidemiology, Biomarkers & Prevention, researchers document those and several other cancer-causing compounds that showed up in urine tests of the water-pipe smokers. The research calls into question a common assumption: that hookahs are safe. “This is a great addition to the literature,” says Thomas Eissenberg, a psychologist at Virginia Commonwealth University in Richmond. He and his colleagues had previously found toxic substances in hookah smoke. The new paper extends his findings by detecting carcinogens and other bad actors in water-pipe smokers themselves, he says. Hookah smoking goes back hundreds of years in India, the Middle East and North Africa, but it is newer in parts of Europe and North America. The substances heated in a hookah vary. In the study, researchers used pastes chosen by the participants that were 5 to 10 percent tobacco combined with honey, molasses and bits of fruit. This paste goes in the bowl of the pipe, which is covered with a perforated piece of aluminum foil and topped with a burning piece of charcoal, says study coauthor Peyton Jacob III, a research chemist at the University of California, San Francisco. © Society for Science & the Public 2000 - 2013

Keyword: Drug Abuse
Link ID: 18088 - Posted: 04.29.2013

The Brain: Our Food-Traffic Controller By KATHLEEN A. PAGE and ROBERT S. SHERWIN IMAGINE that, instead of this article, you were staring at a plate of freshly baked chocolate chip cookies. The mere sight and smell of them would likely make your mouth water. The first bite would be enough to wake up brain areas that control reward, pleasure and emotion — and perhaps trigger memories of when you tasted cookies like these as a child. That first bite would also stimulate hormones signaling your brain that fuel was available. The brain would integrate these diverse messages with information from your surroundings and make a decision as to what to do next: keep on chewing, gobble down the cookie and grab another, or walk away. Studying the complex brain response to such sweet temptations has offered clues as to how we might one day control a profound health problem in the country: the obesity epidemic. The answer may partly lie in a primitive brain region called the hypothalamus. The hypothalamus, which monitors the body’s available energy supply, is at the center of the brain’s snack-food signal processing. It keeps track of how much long-term energy is stored in fat by detecting levels of the fat-derived hormone leptin — and it also monitors the body’s levels of blood glucose, minute-to-minute, along with other metabolic fuels and hormones that influence satiety. When you eat a cookie, the hypothalamus sends out signals that make you less hungry. Conversely, when food is restricted, the hypothalamus sends signals that increase your desire to ingest high-calorie foods. The hypothalamus is also wired to other brain areas that control taste, reward, memory, emotion and higher-level decision making. These brain regions form an integrated circuit that was designed to control the drive to eat. © 2013 The New York Times Company

Keyword: Obesity; Attention
Link ID: 18087 - Posted: 04.28.2013

By VATSAL G. THAKKAR IN the spring of 2010, a new patient came to see me to find out if he had attention-deficit hyperactivity disorder. He had all the classic symptoms: procrastination, forgetfulness, a propensity to lose things and, of course, the inability to pay attention consistently. But one thing was unusual. His symptoms had started only two years earlier, when he was 31. Though I treat a lot of adults for attention-deficit hyperactivity disorder, the presentation of this case was a violation of an important diagnostic criterion: symptoms must date back to childhood. It turned out he first started having these problems the month he began his most recent job, one that required him to rise at 5 a.m., despite the fact that he was a night owl. The patient didn’t have A.D.H.D., I realized, but a chronic sleep deficit. I suggested some techniques to help him fall asleep at night, like relaxing for 90 minutes before getting in bed at 10 p.m. If necessary, he could take a small amount of melatonin. When he returned to see me two weeks later, his symptoms were almost gone. I suggested he call if they recurred. I never heard from him again. Many theories are thrown around to explain the rise in the diagnosis and treatment of A.D.H.D. in children and adults. According to the Centers for Disease Control and Prevention, 11 percent of school-age children have now received a diagnosis of the condition. I don’t doubt that many people do, in fact, have A.D.H.D.; I regularly diagnose and treat it in adults. But what if a substantial proportion of cases are really sleep disorders in disguise? © 2013 The New York Times Company

Keyword: Sleep; ADHD
Link ID: 18086 - Posted: 04.28.2013

By LINDA LOGAN The last time I saw my old self, I was 27 years old and living in Boston. I was doing well in graduate school, had a tight circle of friends and was a prolific creative writer. Married to my high-school sweetheart, I had just had my first child. Back then, my best times were twirling my baby girl under the gloaming sky on a Florida beach and flopping on the bed with my husband — feet propped against the wall — and talking. The future seemed wide open. I don’t think there is a particular point at which I can say I became depressed. My illness was insidious, gradual and inexorable. I had a preview of depression in high school, when I spent a couple of years wearing all black, rimming my eyes in kohl and sliding against the walls in the hallways, hoping that no one would notice me. But back then I didn’t think it was a very serious problem. The hormonal chaos of having three children in five years, the pressure of working on a Ph.D. dissertation and a genetic predisposition for a mood disorder took me to a place of darkness I hadn’t experienced before. Of course, I didn’t recognize that right away. Denial is a gauze; willful denial, an opiate. Everyone seemed in league with my delusion. I was just overwhelmed, my family would say. I should get more help with the kids, put off my Ph.D. When I told other young mothers about my bone-wearying fatigue, they rolled their eyes knowingly and mumbled, “Right.” But what they didn’t realize was that I could scarcely push the stroller to the park, barely summon the breath to ask the store clerk, “Where are the Pampers?” I went from doctor to doctor, looking for the cause. Lab tests for anemia, low blood sugar and hypothyroidism were all negative. © 2013 The New York Times Company

Keyword: Schizophrenia
Link ID: 18085 - Posted: 04.28.2013

By Russell Foster "Making teens start school in the morning is ‘cruel,’ brain doctor claims." So declared a British newspaper headline in 2007 after a talk I gave at an academic conference. One disbelieving reader responded: "This man sounds brain-dead." That was a typical reaction to work I was reporting at the time on teenage sleep patterns and their effect on performance at school. Six years on, there is growing acceptance that the structure of the academic day needs to take account of adolescent sleep patterns. The latest school to adopt a later start time is the UCL Academy in London; others are considering following suit. So what are the facts about teenage slumber, and how should society adjust to these needs? The biology of human sleep timing, like that of other mammals, changes as we age. This has been shown in many studies. As puberty begins, bedtimes and waking times get later. This trend continues until 19.5 years in women and 21 in men. Then it reverses. At 55 we wake at about the time we woke prior to puberty. On average this is two hours earlier than adolescents. This means that for a teenager, a 7 a.m. alarm call is the equivalent of a 5 a.m. start for people in their 50s. Precisely why this is so is unclear, but the shifts correlate with hormonal changes at puberty and the decline in those hormones as we age. However, biology is only part of the problem. Additional factors include a more relaxed attitude to bedtimes by parents, a general disregard for the importance of sleep, and access to TVs, DVDs, PCs, gaming devices, cellphones, and so on, all of which promote alertness and eat into time available for sleep. © 2013 The Slate Group, LLC.

Keyword: Sleep; Development of the Brain
Link ID: 18084 - Posted: 04.27.2013

By David Levine Sleep deprivation is a quick and efficient way to treat depression. It works 60 to 70 percent of the time—far better than existing drugs—but the mood boost usually lasts only until the patient falls asleep. As an ongoing treatment, sleep deprivation is impractical, but researchers have been studying the phenomenon in an effort to uncover the cellular mechanisms behind depression and remission. Now a team at Tufts University has pinpointed glia as the key players. The researchers previously found that astrocytes, a star-shaped type of glial cell, regulate the brain chemicals involved in sleepiness. During our waking hours, astrocytes continuously release the neurotransmitter adenosine, which builds up in the brain and causes “sleep pressure,” the feeling of sleepiness and its related memory and attention impairments. The neurotransmitter causes this pressure by binding to adenosine receptors on the outside of neurons like a key fitting into a lock. As more adenosine builds up, more receptors are triggered, and the urge to sleep gets stronger. In the new study, published online January 15 in the journal Translational Psychiatry, the scientists investigated whether this process is responsible for the antidepressant effects of sleep deprivation. Mice with depressivelike symptoms were administered three doses of a compound that triggers adenosine receptors, thus mimicking sleep deprivation. Although the mice continued to sleep normally, after 12 hours they showed a rapid improvement in mood and behavior, which lasted for 48 hours. © 2013 Scientific American

Keyword: Depression; Sleep
Link ID: 18083 - Posted: 04.27.2013

by Emily Underwood In the cartoon series named after them, Pinky and the Brain, two laboratory mice genetically enhanced to increase their intelligence plot to take over the world—and fail each time. Perhaps their creators hadn't tweaked the correct gene. Researchers have now found a genetic mutation that causes mammalian neural tissue to expand and fold. The discovery may help explain why humans evolved more elaborate brains than mice, and it could suggest ways to treat disorders such as autism and epilepsy that arise from abnormal neural development. In mice and humans alike, the cerebral cortex—the outermost layer of brain tissue associated with high-level functions such as memory and decision-making—starts out as a spherical sheet of tissue made up of only neural stem cells. As these stem cells divide, the cortex increases its surface area, expanding like an inflating balloon, says neuroscientist Victor Borrell of the Institute of Neurosciences of Alicante in Spain. Unlike the small, smooth mouse brain, however, the uppermost layers of tissue in the human brain cram millions of neurons into specialized folds and furrows responsible for complex tasks such as language and thought. Because the human cerebral cortex is generally considered "special," some scientists have hypothesized that the genes that govern its development of cortical folds and furrows are also unique to humans, Borrell says. In studies of neural development in mice, Stahl found that TRNP1 produces a protein that determines whether neural stem cells self-replicate, leading to a balloonlike expansion of cortical surface area, or whether they differentiate into a plethora of intermediate stem cell types and neurons, thickening the cortex and forming more complex brain structures. Based on that discovery, the team hypothesized that varying levels of the gene's expression in mice and humans might account for the varying levels of cortical thickness and different shapes between the two species. © 2010 American Association for the Advancement of Science

Keyword: Development of the Brain; Genes & Behavior
Link ID: 18082 - Posted: 04.27.2013

by Dr. Claire McCarthy April is Autism Awareness Month--and if there's anything that we need when it comes to autism, it's awareness. We need people to be aware of this condition that affects a staggering 1 in 50 children, so that we can understand what causes it, and find ways to prevent it. And we need people to be aware of the signs of autism--because getting help early can make a real difference. Many children aren't diagnosed with autism until they get to preschool, or sometimes even later--and that means important time is lost. The signs of autism can be present in toddlers--and when we find it then, we can get help to those children and their families right away. The trick is in asking the right questions--and acting on the answers. In the practice where I work, as in many other practices, we ask parents to fill out questionnaires about the behavior and development of their children. At the 18 month and 24 month visits, we ask parents to fill out one called the MCHAT (Modified Checklist for Autism in Toddlers)--that's the tool we've chosen to help us look for autism. It's a list of questions that parents answer yes or no to, questions about how their child acts, plays and interacts with other people. While all the questions on the MCHAT are important, there are six that are most important: Does your child take an interest in other children? Does your child ever use his finger to point at or ask for something? Does your child ever bring objects over to you to show you something? Does your child imitate you? Does your child respond to his name when you call? If you point at a toy across the room, does your child look at it? © 2013 NY Times Co.

Keyword: Autism
Link ID: 18081 - Posted: 04.27.2013

By Karen Rowan and MyHealthNewsDaily Children at an increased risk of autism may have abnormal structures in the placenta that can be detected at birth, a new study finds. The findings suggest behavioral interventions aimed at social and motor skill development in these children could be started right away, the researchers said. Studies have shown that such interventions are more effective in children with autism when they are started earlier. It's much too early to say that an examination of the placenta could be used as a definitive test for autism at birth, said study researcher Dr. Harvey Kliman, director of Reproductive and Placental Research at the Yale University School of Medicine. Autism spectrum disorders are typically diagnosed when children are ages 3 or 4, or even older. However, if these structures were found upon a child's birth and interventions were started, the child might benefit greatly if they did turn out to have autism, while there would be little downside if a child turned out not to have autism -- it's unlikely they would be harmed by the effort, Kliman said. In the study, Kliman and his colleagues collected samples of placenta tissue from 117 children born to families who already had a child with autism, and compared them with placentas from 100 babies born into families in which no older children had autism. The researchers, who didn't know which placentas had come from each group of children, examined samples of the placentas under microscopes. © 2013 Scientific American

Keyword: Autism; Development of the Brain
Link ID: 18080 - Posted: 04.27.2013