Chapter 16. None

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 1843

By NICHOLAS BAKALAR Concussions are not as common in Major League Baseball as they are in professional football, but they happen often enough, with players getting hit by pitches, running into walls or catching a knee in the head sliding into a base. Catchers are particularly at risk — a foul tip off the mask will snap the neck back and give the brain a solid rattle. Collisions at the plate take a toll, too. Now, a study published in the American Journal of Sports Medicine suggests that position players in the majors who sustain concussions do not hit as effectively in their first weeks back after their injury. Under Major League Baseball rules, players can return after a concussion if they pass the concussion protocol — a series of interviews and tests of physical and mental functioning. But the new study found that even after passing the tests and having no apparent symptoms, hitters showed an initial decline when they returned to action. The study identified 66 position players who had concussions between 2007 and 2013, including some who never went on the disabled list. The study then compared their performance in the weeks before and after the injury. The gap was noticeable. In the two weeks before their injuries, the players hit .249 with a .315 on base percentage and a .393 slugging average. For the two weeks after the injury, their line was .227/.287/.347. Baseball instituted a seven-day disabled list in 2011, specifically to let players recover from concussions while allowing the team to maintain a full roster. But there is no set time that a player must stay out after a concussion. If he passes the protocol, he is cleared to play. © 2015 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 20715 - Posted: 03.24.2015

By Brian Handwerk In the U.S., legal hurdles have long hampered research into marijuana. But as more states approve medical and even recreational marijuana, scientific inquiries have spiked, especially studies aimed at finding out what exactly is in today's weed—and what it does to our bodies. In Colorado, which made marijuana legal in November 2012, the latest results show that the pot lining store shelves is much more potent than the weed of 30 years ago. But the boost in power comes at a cost—modern marijuana mostly lacks the components touted as beneficial by medical marijuana advocates, and it is often contaminated with fungi, pesticides and heavy metals. “There's a stereotype, a hippy kind of mentality, that leads people to assume that growers are using natural cultivation methods and growing organically," says Andy LaFrate, founder of Charas Scientific, one of eight Colorado labs certified to test cannabis. "That's not necessarily the case at all." LaFrate presented his results this week at a meeting of the American Chemical Society (ACS) in Denver. LaFrate says he's been surprised at just how strong most of today's marijuana has become. His group has tested more than 600 strains of marijuana from dozens of producers. Potency tests, the only ones Colorado currently requires, looked at tetrahydrocannabinol (THC), the psychoactive compound that produces the plant's famous high. They found that modern weed contains THC levels of 18 to 30 percent—double to triple the levels that were common in buds from the 1980s. That's because growers have cross-bred plants over the years to create more powerful strains, which today tout colorful names like Bruce Banner, Skunkberry and Blue Cookies.

Keyword: Drug Abuse
Link ID: 20712 - Posted: 03.24.2015

By Siri Carpenter “I don’t look like I have a disability, do I?” Jonas Moore asks me. I shake my head. No, I say — he does not. Bundled up in a puffy green coat, Moore, 35 and sandy-haired, doesn’t stand out in the crowd seeking refuge from the winter cold in a drafty Starbucks. His handshake is firm and his blue eyes meet mine as we talk. He comes across as intelligent and thoughtful, if perhaps a bit reserved. His disability — a form of autism — is invisible. That’s part of the problem, Moore says. Like most people with an autism spectrum disorder, he finds relationships challenging. In the past, he has been quick to anger and has had what he calls meltdowns. Those who don’t know he has autism can easily misinterpret his actions. “People think that when I do misbehave I’m somehow intentionally trying to be a jerk,” Moore says. “That’s just not the case.” His difficulty managing emotions has gotten him into some trouble, and he has had a hard time holding onto jobs — an outcome he might have avoided, he says, if his co-workers and bosses had better understood his intentions. Over time, things have gotten better. Moore has held the same job for five years, vacuuming commercial buildings on a night cleaning crew. He attributes his success to getting the right amount of medication and therapy, to time’s maturing him and to the fact that he works mostly alone. Moore is fortunate. His parents help support him financially. He has access to good mental health care where he lives in Wisconsin. And he has found a job that suits him. Many adults with autism are not so lucky.

Keyword: Autism
Link ID: 20711 - Posted: 03.24.2015

|By Susana Martinez-Conde and Stephen L. Macknik All visual art is illusory in that it involves a departure from reality, a filtering through the mind of the artist. This subjectivity applies not only to abstract works but also to representational art, in which the artist translates his or her perception into a physical object capable of inducing a similar perception in the viewer. Painters render the three-dimensional world on a flat surface. These representations are enough to suspend our visual system's disbelief and trigger barrages of neuronal firing that become visions of bathers, bridges and water lilies. It is never about reality but about how the artist sees and wants to portray it. This artistic vision is a mishmash of expectations, memories, assumptions, imagination and intent. It is also, in a sense, a reflection of neural shortcuts and basic visual processes. The picture becomes even more complicated when painters suffer from pathologies of the eyes or brain that force them to see their surroundings in ways that diverge from standard experience. The artwork produced by such artists allows us to participate in their perception—and misperception—of the world. For example, failing vision can translate into an eerie loss of precision and detail in paintings. The pictures of American artist Georgia O'Keeffe became flatter and less intricate as she developed bilateral age-related macular degeneration, a retinal disease that affects central, high-resolution vision. The later works of American painter Mary Cassatt similarly show an uncharacteristic absence of delicacy in faces as she developed cataracts. French impressionist Claude Monet also had cataracts, which rendered his paintings imprecise and muted in color. After he underwent successful cataract surgery, his paintings regained definition and vibrancy. As the examples in this column attest, the effects of vision or brain diseases can sometimes be traced in great works of art. © 2015 Scientific American

Keyword: Vision
Link ID: 20710 - Posted: 03.24.2015

By ANDREW POLLACK An experimental drug for Alzheimer’s disease sharply slowed the decline in mental function in a small clinical trial, researchers reported Friday, reviving hopes for an approach to therapy that until now has experienced repeated failures. The drug, being developed by Biogen Idec, could achieve sales of billions of dollars a year if the results from the small trial are replicated in larger trials that Biogen said it hoped to begin this year. Experts say that there are no really good drugs now to treat Alzheimer’s. Biogen’s stock has risen about 50 percent since early December, when the company first announced that the drug had slowed cognitive decline in the trial, without saying by how much. Analysts and investors had been eagerly awaiting the detailed results, some of them flying to France to hear Biogen researchers present them at a neurology meeting on Friday. The drug, called aducanumab, met and in some cases greatly exceeded Wall Street expectations in terms of how much the highest dose slowed cognitive decline. However, there was a high incidence of a particular side effect that might make it difficult to use the highest dose. Still, the net impression was positive. “Out-of-the-ballpark efficacy, acceptable safety,” Ravi Mehrotra, an analyst at Credit Suisse, wrote on Friday. Shares of Biogen rose $42.33, or 10 percent, to $475.98. Alzheimer’s specialists were impressed, but they cautioned that it was difficult to read much from a small early-stage, or Phase 1, trial that was designed to look at safety, not the effect on cognition. Also, other Alzheimer’s drugs that had looked promising in early studies ended up not working in larger trials. “It’s certainly encouraging,” said Dr. Samuel Gandy, director of the Center for Cognitive Health at Mount Sinai Hospital in New York, who was not involved in the study. He said the effect of the highest dose was “pretty impressive.” © 2015 The New York Times Company

Keyword: Alzheimers
Link ID: 20709 - Posted: 03.21.2015

by Emiko Jozuka Touch, says David J. Linden, is something we take for granted. "It's very hard to imagine it gone," he tells WIRED.co.uk. "You can imagine what it's like to be blind or deaf, or have no sense of smell, but there's no way to turn off touch". Touch might not be an obvious starting point for Linden, who is a professor of neuroscience at the John Hopkins University, studying learning and memory. But according to the professor, "the story of the neuroscience underlying touch has yet to be told". Pointing to the advances made in touch research over the last 20 years, Linden tells us that his own interest in the topic was sparked over lunch by colleagues working in the School of Medicine. Making the complex links between the brain and our sense of touch accessible to a wider audience is no easy feat. Yet in his recent book entitled, Touch: The Science of Hand, Heart, and Mind, Linden offers anecdotal and factual ways in to exploring different aspects of touch, whether that be in the form of pain, itches, hot and cold sensations or caresses. "We think of touch as being a one sense modality, but it's many different sensors in the skin acting in parallel," says Linden. He explains how the information in the form of, for example, an itch, pain or caress relays to the brain, dividing them into either discriminative or emotional forms of touch. The discriminative touch allows a person to understand where the body is being touched, or to understand if an object is textured, smooth or 3D. While emotional touch is what makes pain feel emotionally negative, or an orgasm feel positive, says Linden.

Keyword: Pain & Touch
Link ID: 20708 - Posted: 03.21.2015

By Martin Enserink The Human Brain Project (HBP) has listened to the critics, the reviewers, and the mediators. At a meeting in Paris, the board of directors of the €1 billion project yesterday approved a series of recommendations for reform, proposed by a mediation committee, which will change both HBP’s governance and its research program. Critics of the troubled project welcome the move. “We are absolutely delighted that the board has adopted these recommendations,” says computational neuroscientist Peter Dayan of University College London, one of the hundreds of researchers who signed an open letter last year calling for a major reorganization of HBP. Dayan was a member of the mediation committee charged with finding a way out of the crisis after the publication of the letter. That panel’s report—a summary of which was released on 10 March—roundly acknowledges that the critics were right. The committee “largely supports and emphasizes the critique voiced by parts of the scientific community regarding objectives, scientific approach, governance and management practices,” the report says. The mediation committee said that HBP, now administered by the Swiss Federal Institute of Technology in Lausanne (EPFL), should be run by a new, international entity. “In a first concrete step towards implementing that vision, the board [of directors] has created a governance working group composed of former or current heads of international scientific organisations,” an HBP press release issued today said. (They include CERN, the European Space Agency, and the European Molecular Biology Laboratory.) © 2015 American Association for the Advancement of Science

Keyword: Brain imaging
Link ID: 20704 - Posted: 03.21.2015

Michaeleen Doucleff Malaria is one of the oldest scourges of mankind. Yet it's been a mystery how the deadliest form of the disease kills children. One doctor in Michigan has dedicated her life to figuring that out. Now she and her team report their findings in this week's issue of the New England Journal of Medicine. The key to solving the mystery was looking inside the brain. Most of the time malaria causes a bad fever and body aches. But in rare cases — often in children — the parasite gets stuck in the capillaries of the brain. The child has a seizure, goes into a coma and can die. This all happens in only two or three days, says Dr. Terrie Taylor of Michigan State University. "These are bright, happy children who are suddenly felled by a disease that quickly renders them unconscious. And quickly kills them. It's a catastrophe." The sudden death of a child devastates not just the family but the whole community, Taylor says: "Imagine the ripple effects on their friends and their siblings. Suddenly their friends are gone. Just gone." Since 1986, Taylor has been treating children with severe malaria at Queen Elizabeth Central Hospital in Blantyre, Malawi. Seeing so many families deal with these huge losses, year after year, made Taylor focus her career on one goal: Figuring out why some children die from cerebral malaria but others soon recover. © 2015 NPR

Keyword: Development of the Brain
Link ID: 20702 - Posted: 03.19.2015

|By Erez Ribak and The Conversation UK The human eye is optimised to have good colour vision at day and high sensitivity at night. But until recently it seemed as if the cells in the retina were wired the wrong way round, with light travelling through a mass of neurons before it reaches the light-detecting rod and cone cells. New research presented at a meeting of the American Physical Society has uncovered a remarkable vision-enhancing function for this puzzling structure. About a century ago, the fine structure of the retina was discovered. The retina is the light-sensitive part of the eye, lining the inside of the eyeball. The back of the retina contains cones to sense the colours red, green and blue. Spread among the cones are rods, which are much more light-sensitive than cones, but which are colour-blind. Before arriving at the cones and rods, light must traverse the full thickness of the retina, with its layers of neurons and cell nuclei. These neurons process the image information and transmit it to the brain, but until recently it has not been clear why these cells lie in front of the cones and rods, not behind them. This is a long-standing puzzle, even more so since the same structure, of neurons before light detectors, exists in all vertebrates, showing evolutionary stability. Researchers in Leipzig found that glial cells, which also span the retinal depth and connect to the cones, have an interesting attribute. These cells are essential for metabolism, but they are also denser than other cells in the retina. In the transparent retina, this higher density (and corresponding refractive index) means that glial cells can guide light, just like fibre-optic cables. © 2015 Scientific American

Keyword: Vision; Glia
Link ID: 20701 - Posted: 03.19.2015

By PAM BELLUCK What happens to forgotten memories — old computer passwords, friends’ previous phone numbers? Scientists have long held two different theories. One is that memories do not diminish but simply get overshadowed by new memories. The other is that older memories become weaker, that pulling to mind new passwords or phone numbers degrades old recollections so they do not interfere. The difference could be significant. If old memories stay strong and are merely papered over by new ones, they may be easier to recover. That could be positive for someone trying to remember an acquaintance’s name, but difficult for someone trying to lessen memories of abuse. It could suggest different strategies for easing traumatic memories, evaluating witness testimony about crimes, or helping students study for tests. Now, a study claims to provide evidence of memory’s weakening by showing that people’s ability to remember something and the pattern of brain activity that thing generates both appear to diminish when a competing memory gets stronger. Demonstrating sophisticated use of brain scans in memory research, authors of the study, published Monday in the journal Nature Neuroscience, appear to have identified neural fingerprints of specific memories, distinguishing brain activity patterns produced when viewing a picture of a necklace, say, from a picture of binoculars or other objects. The experiment, conducted by scientists in Birmingham and Cambridge, England, involved several stages with 24 participants first trained to associate words to two unrelated black and white pictures from lists of famous people, ordinary objects or scenes. © 2015 The New York Times Company

Keyword: Learning & Memory
Link ID: 20695 - Posted: 03.17.2015

By RENEE ENGELN ON Tuesday, in the wake of an online petition signed by thousands of people, Facebook announced that it was removing “feeling fat” from its list of status update emoticons. The petition argued that the offending emoticon, with its chubby cheeks and double chin, reinforced negative body images, and Facebook seemed to agree. Is it really such a big deal if you tell everyone how fat you feel? After all, a simple “I’m so fat!” can result in a chorus of empathetic voices, saying, “Me, too!” or “You’re beautiful just the way you are!” And that will help you feel better, and help others feel better, too — right? Wrong. As someone who studies this type of public body self-disparagement, known as “fat talk,” I can say that it probably will make you feel worse. And it may drag down other people with you. Conversational shaming of the body has become practically a ritual of womanhood (though men also engage in it). In a survey that a colleague and I reported in 2011 in the Psychology of Women Quarterly, we found that more than 90 percent of college women reported engaging in fat talk — despite the fact that only 9 percent were actually overweight. In another survey, which we published in December in the Journal of Health Psychology, we canvassed thousands of women ranging in age from 16 to 70. Contrary to the stereotype of fat talk as a young woman’s practice, we found that fat talk was common across all ages and all body sizes. Most important, fat talk is not a harmless social-bonding ritual. According to an analysis of several studies that my colleagues and I published in 2012 in the Psychology of Women Quarterly, fat talk was linked with body shame, body dissatisfaction and eating-disordered behavior. Fat talk does not motivate women to make healthier choices or take care of their bodies; in fact, the feelings of shame it brings about tend to encourage the opposite. © 2015 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 20691 - Posted: 03.17.2015

By Emily Underwood Deep brain stimulation, which now involves surgically inserting electrodes several inches into a person's brain and connecting them to a power source outside the skull, can be an extremely effective treatment for disorders such as Parkinson's disease, obsessive compulsive disorder, and depression. The expensive, invasive procedure doesn't always work, however, and can be risky. Now, a study in mice points to a less invasive way to massage neuronal activity, by injecting metal nanoparticles into the brain and controlling them with magnetic fields. Major technical challenges must be overcome before the approach can be tested in humans, but the technique could eventually provide a wireless, nonsurgical alternative to traditional deep brain stimulation surgery, researchers say. "The approach is very innovative and clever," says Antonio Sastre, a program director in the Division of Applied Science & Technology at the National Institute of Biomedical Imaging and Bioengineering in Bethesda, Maryland. The new work provides "a proof of principle." The inspiration to use magnets to control brain activity in mice first struck materials scientist Polina Anikeeva while working in the lab of neuroscientist-engineer Karl Deisseroth at Stanford University in Palo Alto, California. At the time, Deisseroth and colleagues were refining optogenetics, a tool that can switch specific ensembles of neurons on and off in animals with beams of light. © 2015 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 20690 - Posted: 03.14.2015

By Matthew J.X. Malady One hour and seven minutes into the decidedly hit-or-miss 1996 comedy Black Sheep, the wiseass sidekick character played by David Spade finds himself at an unusually pronounced loss for words. While riding in a car driven by Chris Farley’s character, he glances at a fold-up map and realizes he somehow has become unfamiliar with the name for paved driving surfaces. “Robes? Rouges? Rudes?” Nothing seems right. Even when informed by Farley that the word he’s looking for is roads, Spade’s character continues to struggle: “Rowds. Row-ads.” By this point, he’s become transfixed. “That’s a total weird word,” he says, “isn’t it?” Now, it’s perhaps necessary to mention that, in the context of the film, Spade’s character is high off nitrous oxide that has leaked from the car’s engine boosters. But never mind that. Row-ad-type word wig outs similar to the one portrayed in that movie are things that actually happen, in real life, to people with full and total control over their mental capacities. These wordnesias sneak up on us at odd times when we’re writing or reading text. I was in a full-on wordnesiac state. On one of my spelling attempts, I think I even threw a K into the mix. It was bad. Here’s how they work: Every now and again, for no good or apparent reason, you peer at a standard, uncomplicated word in a section of text and, well, go all row-ads on it. If you’re typing, that means inexplicably blanking on how to spell something easy like cake or design. The reading version of wordnesia occurs when a common, correctly spelled word either seems as though it can’t possibly be spelled correctly, or like it’s some bizarre combination of letters you’ve never before seen—a grouping that, in some cases, you can’t even imagine being the proper way to compose the relevant term. © 2014 The Slate Group LLC.

Keyword: Language
Link ID: 20688 - Posted: 03.14.2015

When it comes to fight or flight for brawling crickets, a chemical in the brain is in charge. Being roughed up in a skirmish can trigger nerve cells in Mediterranean field crickets (Gryllus bimaculatus) to release nitric oxide, making the losing cricket run away, scientists report online March 13 in Science Advances. Watch in this video as two crickets face off. When the loser hits its limit, it flees the fight. In a second bout, the loser then tries to avoid the winner. Nitric oxide prompts this continued submissive behavior, which lasts several hours before a cricket’s will to fight returns. “If you block nitric oxide they recover quickly, and if you give them nitric oxide they don’t,” says Paul Stevenson, a coauthor of the new research and behavioral neurobiologist at Leipzig University in Germany. “It’s a very simple algorithm for controlling a very complicated social situation.” P. Stevenson and J. Rillich. Adding up the odds—Nitric oxide signaling underlies the decision to flee and post-conflict depression of aggression. Science Advances. Published online March 13, 2015.doi: 10.1126/sciadv.1500060. © Society for Science & the Public 2000 - 2015.

Keyword: Aggression
Link ID: 20686 - Posted: 03.14.2015

By Emily Underwood From imaging babies to blasting apart kidney stones, ultrasound has proved to be a versatile tool for physicians. Now, several research teams aim to unleash the technology on some of the most feared brain diseases. The blood-brain barrier, a tightly packed layer of cells that lines the brain's blood vessels, protects it from infections, toxins, and other threats but makes the organ frustratingly hard to treat. A strategy that combines ultrasound with microscopic blood-borne bubbles can briefly open the barrier, in theory giving drugs or the immune system access to the brain. In the clinic and the lab, that promise is being evaluated. This month, in one of the first clinical tests, Todd Mainprize, a neurosurgeon at the University of Toronto in Canada, hopes to use ultrasound to deliver a dose of chemotherapy to a malignant brain tumor. And in some of the most dramatic evidence of the technique's potential, a research team reports this week in Science Translational Medicine that they used it to rid mice of abnormal brain clumps similar to those in Alzheimer's disease, restoring lost memory and cognitive functions. If such findings can be translated from mice to humans, “it will revolutionize the way we treat brain disease,” says biophysicist Kullervo Hynynen of the Sunnybrook Research Institute in Toronto, who originated the ultrasound method. Some scientists stress that rodent findings can be hard to translate to humans and caution that there are safety concerns about zapping the brain with even the low-intensity ultrasound used in the new study, which is similar to that used in diagnostic scans. © 2015 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 20685 - Posted: 03.12.2015

|By Daisy Yuhas The brain is a hotbed of electrical activity. Scientists have long known that brain cells communicate via electrical missives, created by charged atoms and molecules called ions as they travel across the membranes of those cells. But a new study suggests that in the days and weeks that lead up to a brain forming in an embryo or fetus, altering the electrical properties of these cells can dramatically change how the ensuing brain develops. Researchers at Tufts University and the University of Minnesota have investigated how the difference in charge on either side of a resting cell’s membrane—its electrical potential—helps build the brain. In previous work Tufts University developmental biologist Michael Levin found that patterns of electrical potentials in the earliest stages of an embryo’s development can direct how an animal’s body grows, and that manipulating those potentials can cause a creature to sprout extra limbs, tails or functioning eyes. Now, Levin’s group has investigated how these potentials shape the brain. Working with frog embryos the researchers first used dyes to see the patterns of electrical potentials that precede brain development. They noticed that before the development of a normal brain the cells lining the neural tube, a structure that eventually becomes the brain and spinal cord, have extreme differences in ionic charge within and outside the membrane that houses the cells. In other words, these cells are extremely polarized. © 2015 Scientific American

Keyword: Development of the Brain
Link ID: 20684 - Posted: 03.12.2015

Older people could improve or maintain their mental function through heart healthy lifestyle changes, a large randomized trial for dementia prevention shows. Researchers in Finland and Sweden designed a trial to tackle risk factors for Alzheimer's disease. The 1,260 Finns aged 60 to 77 participating in the study were all considered at risk of dementia based on standard test scores. Half were randomly assigned to receive advice from health professionals on maintaining a healthy diet, aerobic and muscle training exercises, brain training exercises and regular checks of blood pressure, height and weight for body mass index and physical exams for two years or regular health advice. Participants in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability or FINGER study had their cognitive function measured in a battery of mental tests. "The main hypothesis was that simultaneous changes in several risk factors (even of smaller magnitude) would lead to a protective effect on cognition," Miia Kivipelto from the Karolinska Institute in Stockholm and her co-authors said in Wednesday's issue of The Lancet. Overall, test scores were 25 per cent in the diet and training group than the control group. There was no effect on memory. ©2015 CBC/Radio-Canada.

Keyword: Alzheimers
Link ID: 20683 - Posted: 03.12.2015

Mutations in the presenilin-1 gene are the most common cause of inherited, early-onset forms of Alzheimer’s disease. In a new study, published in Neuron, scientists replaced the normal mouse presenilin-1 gene with Alzheimer’s-causing forms of the human gene to discover how these genetic changes may lead to the disorder. Their surprising results may transform the way scientists design drugs that target these mutations to treat inherited or familial Alzheimer’s, a rare form of the disease that affects approximately 1 percent of people with the disorder. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For decades, it has been unclear exactly how the presenilin mutations cause Alzheimer’s disease. Presenilin is a component of an important enzyme, gamma secretase, which cuts up amyloid precursor protein into two protein fragments, Abeta40 and Abeta42. Abeta42 is found in plaques, the abnormal accumulations of protein in the brain which are a hallmark of Alzheimer’s. Numerous studies suggested that presenilin-1 mutations increased activity of gamma-secretase. Investigators have developed drugs that block gamma-secretase, but they have so far failed in clinical trials to halt the disease. The study led by Raymond Kelleher, M.D., Ph.D. and Jie Shen, Ph.D., professors of neurology at Harvard Medical School, Boston, provides a plot twist in the association of presenilin-1 mutations and inherited Alzheimer’s disease. Using mice with altered forms of the presenilin gene, Drs. Kelleher and Shen discovered that the mutations may cause the disease by decreasing, rather than increasing, the activity of gamma-secretase.

Keyword: Alzheimers; Genes & Behavior
Link ID: 20682 - Posted: 03.12.2015

By Gretchen Reynolds An easy, two-minute vision test administered on the sidelines after a young athlete has hit his or her head can help to reliably determine whether the athlete has sustained a concussion, according to a new study of student athletes, some as young as 5. The test is so simple and inexpensive that any coach or parent potentially could administer it, the study’s authors believe, and any league afford to provide it as a way to help evaluate and safeguard players. Those of us who coach or care for young athletes know by now that an athlete who falls or collides with something during play or seems dazed, dizzy, loses consciousness or complains of head pain should be tested for a concussion, which occurs when the brain is physically jostled within the skull. But most of us are clueless about how to test young athletes. The most commonly recommended sideline test is the Standardized Assessment of Concussion, a multipart examination during which athletes are asked to name the date, describe how they feel, memorize and recall lists of words, and do jumping jacks and other tests of coordination. Ideally, this assessment should be administered and evaluated by a medical professional. But while the sidelines of college and professional games are crowded with doctors and certified athletic trainers, few high schools and youth leagues have those resources. Most of the time, concussion testing in youth sports falls to volunteer coaches or parents with little if any medical experience. That situation prompted researchers at New York University’s Langone Concussion Center to begin wondering recently whether there might be other, easier diagnostic tools to check young players for concussions. Their thoughts soon turned to vision. “About 50 percent of the brain’s pathways are tied in some to way to vision and visual processing,” said Dr. Steven Galetta, chairman of neurology at N.Y.U. Langone Medical Center and senior author of the study, which was published in The Journal of Neuro-Ophthalmology. © 2015 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 20680 - Posted: 03.12.2015

By Douglas Starr In 1906, Hugo Münsterberg, the chair of the psychology laboratory at Harvard University and the president of the American Psychological Association, wrote in the Times Magazine about a case of false confession. A woman had been found dead in Chicago, garroted with a copper wire and left in a barnyard, and the simpleminded farmer’s son who had discovered her body stood accused. The young man had an alibi, but after questioning by police he admitted to the murder. He did not simply confess, Münsterberg wrote; “he was quite willing to repeat his confession again and again. Each time it became richer in detail.” The young man’s account, he continued, was “absurd and contradictory,” a clear instance of “the involuntary elaboration of a suggestion” from his interrogators. Münsterberg cited the Salem witch trials, in which similarly vulnerable people were coerced into self-incrimination. He shared his opinion in a letter to a Chicago nerve specialist, which made the local press. A week later, the farmer’s son was hanged. Münsterberg was ahead of his time. It would be decades before the legal and psychological communities began to understand how powerfully suggestion can shape memory and, in turn, the course of justice. In the early nineteen-nineties, American society was recuperating from another panic over occult influence; Satanists had replaced witches. One case, the McMartin Preschool trial, hinged on nine young victims’ memories of molestation and ritual abuse—memories that they had supposedly forgotten and then, after being interviewed, recovered. The case fell apart, in 1990, because the prosecution could produce no persuasive evidence of the victims’ claims. A cognitive psychologist named Elizabeth Loftus, who had consulted on the case, wondered whether the children’s memories might have been fabricated—in Münsterberg’s formulation, involuntarily elaborated—rather than actually recovered.

Keyword: Learning & Memory
Link ID: 20679 - Posted: 03.12.2015