Chapter 19. Language and Hemispheric Asymmetry
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Abdul-Kareem Ahmed In the world of recreational and professional sports, many athletes—particularly in contact sports—suffer concussions. These mild traumatic brain injuries cause headaches, memory problems and confusion, but usually resolve on their own with rest. Some players, however, especially after repeated concussions, continue to experience symptoms for many months—a phenomenon termed post-concussion syndrome. A few of these players will eventually develop chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease that causes dementia symptoms similar to Alzheimer’s disease. CTE can lead to personality changes, movement problems and, sometimes, mortality. CTE is diagnosed after death because it requires postmortem examination of a player’s brain. Post-concussion syndrome, in contrast, is diagnosed based on patient symptoms. To date, doctors do not have any objective tests to determine syndrome severity or relate it to the risk of developing CTE. Now, a group of researchers from Sweden and the U.K. say they have developed such a test, reporting their findings last week in JAMA Neurology. The test measures biomarkers in the cerebrospinal fluid—the colorless liquid that supports and suspends the brain and spinal cord—that appear to provide a measure of concussion severity and CTE risk. The researchers collected cerebrospinal fluid via spinal taps from 16 professional Swedish ice hockey players and a similar number of healthy individuals. The hockey players had all experienced post-concussion syndrome, causing nine of them to retire from the game. © 2016 Scientific American,
By KEN BELSON One of the frustrations of researchers who study chronic traumatic encephalopathy, the degenerative brain disease linked to repeated head hits, is that it can be detected only in autopsies, and not in the living. Researchers, though, have been trying to solve this problem in two primary ways: by identifying biomarkers linked to the disease that show up on imaging tests in certain locations in the brain, and by trying to locate in the blood the protein that is the hallmark of the disease. On Monday, two groups of researchers said they had made what they considered small steps in developing both methods. The announcements are small parts of much larger studies that will take years to bear fruit, if they ever do. Both methods have been questioned by detractors, some of whom say the hype is getting ahead of the science. Scientists, these critics note, have spent decades trying to find ways to accurately diagnose Alzheimer’s disease, which has some of the same characteristics as C.T.E. Still, at a medical conference in Boston on Monday, Robert Stern, a professor of neurology at Boston University, said technology developed by the company Quanterix (paid for in part with a grant from the N.F.L.) had identified elevated levels of tau proteins in blood samples of 96 former football players between 40 and 69 years old, compared with only 25 people of the same age in a control group. The results, which are part of a seven-year study and are under review for publication, are preliminary because they identify only the total amount of tau in the blood, not the amount of the specific tau linked to C.T.E. Additional tests are being done in Sweden to determine the amount of the C.T.E.-related tau in the blood samples, Stern said. Even so, Stern said, the blood samples from the 96 former players suggest that absorbing repeated head hits earlier in life can lead to higher concentrations of tau in the blood later. © 2016 The New York Times Company
Jon Hamilton There's growing evidence that a physical injury to the brain can make people susceptible to post-traumatic stress disorder. Studies of troops deployed to Iraq and Afghanistan have found that service members who suffer a concussion or mild traumatic brain injury are far more likely to develop PTSD, a condition that can cause flashbacks, nightmares and severe anxiety for years after a traumatic event. And research on both people and animals suggest the reason is that a brain injury can disrupt circuits that normally dampen the response to a frightening event. The result is like "driving a car and the brake's not fully functioning," says Minxiong Huang, a biomedical physicist at the University of California, San Diego. Scientists have suspected a link between traumatic brain injury (TBI) and PTSD for many years. But the evidence was murky until researchers began studying troops returning from Iraq and Afghanistan. What they found was a lot of service members like Charles Mayer, an Army sniper from San Diego who developed PTSD after finishing a deployment in Iraq. In 2010, Mayer was on patrol in an Army Humvee near Baghdad when a roadside bomb went off. "I was unconscious for several minutes," he says. So he found out what happened from the people who dragged him out. The blast fractured Mayer's spine. It also affected his memory and thinking. That became painfully clear when Mayer got out of the Army in 2012. © 2016 npr
By Virginia Morell There will never be a horse like Mr. Ed, the talking equine TV star. But scientists have discovered that the animals can learn to use another human tool for communicating: pointing to symbols. They join a short list of other species, including some primates, dolphins, and pigeons, with this talent. Scientists taught 23 riding horses of various breeds to look at a display board with three icons, representing wearing or not wearing a blanket. Horses could choose between a “no change” symbol or symbols for “blanket on” or “blanket off.” Previously, their owners made this decision for them. Horses are adept at learning and following signals people give them, and it took these equines an average of 10 days to learn to approach and touch the board and to understand the meaning of the symbols. All 23 horses learned the entire task within 14 days. They were then tested in various weather conditions to see whether they could use the board to tell their trainers about their blanket preferences. The scientists report online in Applied Animal Behaviour Science that the horses did not touch the symbols randomly, but made their choices based on the weather. If it was wet, cold, and windy, they touched the "blanket on" icon; horses that were already wearing a blanket nosed the “no change” image. But when the weather was sunny, the animals touched the "blanket off" symbol; those that weren’t blanketed pressed the “no change” icon. The study’s strong results show that the horses understood the consequences of their choices, say the scientists, who hope that other researchers will use their method to ask horses more questions. © 2016 American Association for the Advancement of Science.
By Rajeev Raizada These brain maps show how accurately it was possible to predict neural activation patterns for new, previously unseen sentences, in different regions of the brain. The brighter the area, the higher the accuracy. The most accurate area, which can be seen as the bright yellow strip, is a region in the left side of the brain known as the Superior Temporal Sulcus. This region achieved statistically significant sentence predictions in 11 out of the 14 people whose brains were scanned. Although that was the most accurate region, several other regions, broadly distributed across the brain, also produced significantly accurate sentence predictions Credit: University of Rochester graphic / Andrew Anderson and Xixi Wang. Used with permission Words, like people, can achieve a lot more when they work together than when they stand on their own. Words working together make sentences, and sentences can express meanings that are unboundedly rich. How the human brain represents the meanings of sentences has been an unsolved problem in neuroscience, but my colleagues and I recently published work in the journal Cerebral Cortex that casts some light on the question. Here, my aim is to give a bigger-picture overview of what that work was about, and what it told us that we did not know before. To measure people's brain activation, we used fMRI (functional Magnetic Resonance Imaging). When fMRI studies were first carried out, in the early 1990s, they mostly just asked which parts of the brain "light up,” i.e. which brain areas are active when people perform a given task. © 2016 Scientific American
By Meredith Wadman Last year, in a move to counter charges that it has neglected the health and safety of its players, the National Football League (NFL) tapped Elizabeth “Betsy” Nabel as its first chief health and medical adviser, a paid position to which she told The Boston Globe she devotes about 1 day a month, plus some nights and weekends. (She and NFL have not disclosed her salary.) And last week, Nabel answered Science’s questions on the heels of NFL’s 14 September announcement that it will devote $40 million in new funding to medical research, primarily neuroscience relevant to repetitive head injuries—with grant applications judged by an NFL-convened panel of scientists, rather than by National Institutes of Health (NIH) study sections. Nabel is well known to many medical scientists as the cardiologist who directed the National Heart, Lung, and Blood Institute at NIH, then left that job in 2009 to become president of a prestigious Harvard University–affiliated teaching hospital: Brigham and Women’s Hospital in Boston. Nabel’s new role with NFL came under media scrutiny in May, when a report by Democrats on the House of Representatives Energy and Commerce Committee found that NFL inappropriately tried to influence the way its “unrestricted” donation to NIH was spent. It revealed, for example, that last year Nabel contacted NIH’s neurology institute director Walter Koroshetz to question the objectivity of an NIH study section and of a principal investigator whose team the peer reviewers had just awarded a $16 million grant. Robert Stern and his group at Boston University, with others, were proposing to image the brains and chart the symptoms of scores of college and professional football players across time. NFL suggested that the scientists, who have led in establishing the link between repetitive head injury and the neurodegenerative brain disease chronic traumatic encephalopathy (CTE), were not objective; Nabel described them in one email as “a more marginal group” whose influence it would be well to “dilute.” The scientists were to have been paid from $30 million that NFL donated to NIH in 2012. After the league objected to its $16 million going to fund the Boston University–led team—it did offer to fund $2 million of the amount—NIH’s neurology institute ended up wholly funding the 7-year grant with its own money. © 2016 American Association for the Advancement of Scienc
Keyword: Brain Injury/Concussion
Link ID: 22669 - Posted: 09.20.2016
By Christof Koch Flies, birds, mice, dogs, monkeys and people all need to sleep. That is, they show daily periods of relative immobility and lack of response to external stimuli, such as light, sound or touch. This reduced sensitivity to external events distinguishes sleep from quiet resting, whereas the capacity to awaken from slumber distinguishes sleep from coma. Why sleep should be such a prominent feature of daily life across the animal kingdom, despite the fact that it leaves the sleeper unable to confront potential threats, remains mysterious. Still, much progress in characterizing the physiology and capabilities of the sleeping brain has occurred over the past century, driven by the ability to record electrical activity of the brain (via electroencephalography, or EEG, on the surface of the skull), of the eyes (via electrooculography, or EOG), and of facial or other muscles (via electromyography, or EMG). For scientists, it is this triad of simultaneous measurements that operationally defines the state of sleep, leading to both surprising and counterintuitive insights. Even without these tools, there are some basic things we do know about sleep. It is essential for our brain to function properly. Most of us have pulled all-nighters or have wanted to sleep but could not, unable to switch off our mind. The next day we are irritable, have trouble keeping our eyes open, and are terrible at tasks that demand sustained attention. Indeed, sleep deprivation causes many traffic accidents—the reason countries have laws that mandate a minimum rest period and maximum working hours for truck drivers. © 2016 Scientific American,
By JAMES GORMAN Who’s a good dog? Well, that depends on whom you’re asking, of course. But new research suggests that the next time you look at your pup, whether Maltese or mastiff, you might want to choose your words carefully. “Both what we say and how we say it matters to dogs,” said Attila Andics, a research fellow at Eotvos Lorand University in Budapest. Dr. Andics, who studies language and behavior in dogs and humans, along with Adam Miklosi and several other colleagues, reported in a paper to be published in this week’s issue of the journal Science that different parts of dogs’ brains respond to the meaning of a word, and to how the word is said, much as human brains do. Photo A dog waiting for its brain activity to be measured in a magnetic resonance imaging machine for research reported in the journal Science. Credit Enik Kubinyi As with people’s brains, parts of dogs’ left hemisphere react to meaning and parts of the right hemisphere to intonation — the emotional content of a sound. And, perhaps most interesting to dog owners, only a word of praise said in a positive tone really made the reward system of a dog’s brain light up. The experiment itself was something of an achievement. Dr. Andics and his colleagues trained dogs to enter a magnetic resonance imaging machine and lie in a harness while the machine recorded their brain activity. A trainer spoke words in Hungarian — common words of praise used by dog owners like “good boy,” “super” and “well done.” The trainer also tried neutral words like “however” and “nevertheless.” Both the praise words and neutral words were offered in positive and neutral tones. The positive words spoken in a positive tone prompted strong activity in the brain’s reward centers. All the other conditions resulted in significantly less action, and all at the same level. © 2016 The New York Times Company
By RACHEL RABKIN PEACHMAN New research shows that athletes who leave the game immediately after a concussion recover twice as fast as athletes who keep playing. Credit Fabrizio Costantini for The New York Times High school athletes who kept playing in the minutes after a concussion took nearly twice as long to recover as those who left the game immediately after the head trauma, a new study shows. The finding, published in the journal Pediatrics, is believed to be the first to focus on one of the most difficult social challenges of treating concussions: a pervasive sports culture that encourages young athletes to keep playing through pain. Medical guidelines call for benching the athlete immediately after the head injury to prevent long-term complications and the potentially devastating consequences of a second hit. “Kids are often reluctant to acknowledge a concussion,” said Dawon Dicks, a youth football coach with CoachUp in Andover, Mass. “The kid may want a scholarship and want to go to college, or it could be that ‘Dad or Coach wants me to play.’ That’s when they’re going to start to be a little dishonest in what they’re truly feeling.” The latest study tracked the neurological symptoms of 69 athletes who visited the University of Pittsburgh Medical Center Sports Medicine Concussion Program after suffering head trauma during a contact sport. The athletes, who ranged from 12 to 19 years old, came from football, soccer, ice hockey, volleyball, field hockey, basketball, wrestling and rugby. The sample included 35 athletes who were removed from games right after getting a concussion and compared their symptoms and recovery to 34 athletes who kept playing in the game or match after taking a hit. The study found that players who stayed in the game after head trauma took an average of 44 days to recover. By comparison, athletes who left a game immediately after signs of concussion took only an average of 22 days to recover. © 2016 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 22614 - Posted: 08.30.2016
Nicola Davis Children who suffer a traumatic brain injury, including mild concussion from a blow to the head, are less likely to do well at school and are at increased risk of early death, researchers have revealed. As adults they are also more likely to receive a disability pension, have failed to gain secondary school qualifications and nearly twice as likely to have been hospitalised for psychiatric reasons. The team analysed data from more than a million people born between 1973 and 1985, finding that around 9% had been diagnosed with at least one traumatic brain injury before the age of 25. More than 75% of these were mild injuries. The researchers compared the outcomes for these individuals with those of others who had not experienced a head injury, as well as carrying out a second comparison, where possible, with siblings who had not been injured. Once factors such as age and sex were taken into account, the team found that those diagnosed with a traumatic brain injury have an increased risk of experiencing a number of health and social problems. Those who had suffered a traumatic brain injury were 76% more likely to receive a disability pension, 58% more likely to have failed to gain secondary school qualifications and nearly twice as likely to have been hospitalised for psychiatric reasons, compared to those who had sustained no injury. When the researchers looked at patients who had siblings that had not sustained a traumatic brain injury, they found similar - although smaller - effects, suggesting that genetics could also play a role. © 2016 Guardian News and Media Limited
Scientists and clinicians have long dreamed of helping the injured brain repair itself by creating new neurons, and an innovative NIH-funded study published today in Nature Medicine may bring this goal much closer to reality. A team of researchers has developed a therapeutic technique that dramatically increases the production of nerve cells in mice with stroke-induced brain damage. The therapy relies on the combination of two methods that show promise as treatments for stroke-induced neurological injury. The first consists of surgically grafting human neural stem cells into the damaged area, where they mature into neurons and other brain cells. The second involves administering a compound called 3K3A-APC, which the scientists have shown helps neural stem cells grown in a petri dish develop into neurons. However, it was unclear what effect the molecule, derived from a human protein called activated protein-C (APC), would have in live animals. A month after their strokes, mice that had received both the stem cells and 3K3A-APC performed significantly better on tests of motor and sensory functions compared to mice that received neither or only one of the treatments. In addition, many more of the stem cells survived and matured into neurons in the mice given 3K3A-APC. “This USC-led animal study could pave the way for a potential breakthrough in how we treat people who have experienced a stroke,” added Jim Koenig, Ph.D., a program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which funded the research. “If the therapy works in humans, it could markedly accelerate the recovery of these patients.”
By Daniel Barron After prepping for the day’s cases, “Mike Brennan,” a 63-year-old cardiology technician, sat down for his morning coffee and paper. On the front page, he discovered something troubling: he could no longer read. No matter how long he stared at a word, its meaning was lost on him. With a history of smoking and hypertension, he worried that he might have had a stroke. So, leaving his coffee, he walked himself down the hall to the emergency department, where neurologists performed a battery of tests to tease out what had happened. Mike still recognized individual letters and, with great difficulty, could sound out small words. But even some simple vocabulary presented problems, for example, he read “desk” as “dish” or “flame” as “thame.” Function words such as prepositions and pronouns gave him particular trouble. Mike couldn’t read, but there was nothing wrong with his eyes. Words heard were no problem. He could recognize colors, faces, and objects. He could speak, move, think and even write normally. Mike had “pure alexia,” meaning he could not read but showed no other impairments. An M.R.I. scan of Mike’s brain revealed a pea-sized stroke in his left inferior occipitotemporal cortex, a region on the brain’s surface just behind the left ear. © 2016 Scientific American
Link ID: 22586 - Posted: 08.23.2016
By Roni Caryn Rabin Dementia is a general term for a set of symptoms that includes severe memory loss, a significant decline in reasoning and severely impaired communication skills; it most commonly strikes elderly people and used to be referred to as “senility.” Alzheimer’s disease is a specific illness that is the most common cause of dementia. Though many diseases can cause dementia, Alzheimer’s accounts for 60 percent to 80 percent of dementia cases, “which is why you’ll often hear the terms used interchangeably,” said Heather Snyder, the senior director of medical and scientific operations for the Alzheimer’s Association. She said the question comes up frequently because patients may receive an initial diagnosis of dementia followed by an evaluation that yields the more specific diagnosis of Alzheimer’s disease, and they may be confused. The second most common form of dementia is vascular dementia, which is caused by a stroke or poor blood flow to the brain. Other diseases that can lead to dementia include Huntington’s disease, Parkinson’s disease and Creutzfeldt-Jakob disease. Some patients may have more than one form of dementia. Dementia is caused by damage to brain cells. In the case of Alzheimer’s disease, that damage is characterized by telltale protein fragments or plaques that accumulate in the space between nerve cells and twisted tangles of another protein that build up inside cells. In Alzheimer’s disease, dementia gets progressively worse to the point where patients cannot carry out daily activities and cannot speak, respond to their environment, swallow or walk. Although some treatments may temporarily ease symptoms, the downward progression of disease continues and it is not curable. © 2016 The New York Times Company
Link ID: 22559 - Posted: 08.16.2016
By NICHOLAS ST. FLEUR Orangutan hear, orangutan do. Researchers at the Indianapolis Zoo observed an orangutan mimic the pitch and tone of human sounds, for the first time. The finding, which was published Wednesday, provides insight into the evolutionary origin of human speech, the team said. “It really redefines for us what we know about the capabilities of orangutans,” said Rob Shumaker, director of the zoo and an author on the paper. “What we have to consider now is the possibility that the origins of spoken language are not exclusively human, and that they may have come from great apes.” Rocky, an 11-year-old orangutan at the zoo, has a special ability. He can make sounds using his vocal folds, or voice box, that resemble the vowel “A,” and sound like “Ah.” The noises, or “wookies” as the researchers called them, are variations of the same vocalization. Sometimes the great ape would say high-pitched “wookies” and sometimes he would say his “Ahs” in a lower pitch. The researchers note that the sounds are specific to Rocky and ones that he used everyday. No other orangutan, captive or wild, made these noises. Rocky, who had never lived in the rain forest, apparently learned the skill during his time as an entertainment orangutan before coming to the zoo. He was at one point the most seen orangutan in movies and commercials, according to the zoo. The researchers said that Rocky’s grunts show that great apes have the capacity to learn to control their muscles to deliberately alter their sounds in a “conversational” manner. The findings, which were published in the journal Scientific Reports, challenge the notion that orangutans — an endangered species that shares about 97 percent of it DNA with humans — make noises simply in response to something, sort of like how you might scream when you place your hand on a hot stove. © 2016 The New York Times Company
Laura Sanders Under duress, nerve cells get a little help from their friends. Brain cells called astrocytes send their own energy-producing mitochondria to struggling nerve cells. Those gifts may help the neurons rebound after injuries such as strokes, scientists propose in the July 28 Nature. It was known that astrocytes — star-shaped glial cells that, among other jobs, support neurons — take in and dispose of neurons’ discarded mitochondria. Now it turns out that mitochondria can move the other way, too. This astrocyte-to-neuron transfer is surprising, says neuroscientist Jarek Aronowski of the University of Texas Health Science Center at Houston. “Bottom line: It’s sort of shocking.” Study coauthor Eng Lo of Massachusetts General Hospital and Harvard Medical School cautions that the work is at a very early stage. But he hopes that a deeper understanding of this process might ultimately point out new ways to protect the brain from damage. Mitochondria produce the energy that powers cells in the body. Scientists have spotted the organelles moving into damaged cells in other parts of the body, including the lungs, heart and liver. The new study turns up signs of this mitochondrial generosity in the brain. Astrocytes produce mitochondria and shunt them out into the soup that surrounds cells, Lo and colleagues found. The researchers then put neurons into this mitochondria-rich broth. When starved of glucose and oxygen — a situation that approximates a stroke — the neurons took in the astrocyte-made organelles. |© Society for Science & the Public 2000 - 2016
By Emily Underwood If your car’s battery dies, you might call on roadside assistance—or a benevolent bystander—for a jump. When damaged neurons lose their “batteries,” energy-generating mitochondria, they call on a different class of brain cells, astrocytes, for a boost, a new study suggests. These cells respond by donating extra mitochondria to the floundering neurons. The finding, still preliminary, might lead to novel ways to help people recover from stroke or other brain injuries, scientists say. “This is a very interesting and important study because it describes a new mechanism whereby astrocytes may protect neurons,” says Reuven Stein, a neurobiologist at The Rabin Institute of Neurobiology in Tel Aviv, Israel, who was not involved in the study. To keep up with the energy-intensive work of transmitting information throughout the brain, neurons need a lot of mitochondria, the power plants that produce the molecular fuel—ATP—that keeps cells alive and working. Mitochondria must be replaced often in neurons, in a process of self-replication called fission—the organelles were originally microbes captured inside a cell as part of a symbiosis. But if mitochondria are damaged or if they can’t keep up with a cell’s needs, energy supplies can run out, killing the cell. In 2014, researchers published the first evidence that cells can transfer mitochondria in the brain—but it seemed more a matter of throwing out the trash. When neurons expel damaged mitochondria, astrocytes swallow them and break them down. Eng Lo and Kazuhide Hayakawa, both neuroscientsists at Massachusetts General Hospital in Charlestown, wondered whether the transfer could go the other way as well—perhaps astrocytes donated working mitochondria to neurons in distress. Research by other groups supported that idea: A 2012 study, for example, found that stem cells from bone marrow can donate mitochondria to lung cells after severe injury. © 2016 American Association for the Advancement of Science
An orangutan copying sounds made by researchers offers new clues to how human speech evolved, scientists say. Rocky mimicked more than 500 vowel-like noises, suggesting an ability to control his voice and make new sounds. It had been thought these great apes were unable to do this and, since human speech is a learned behaviour, it could not have originated from them. Study lead Dr Adriano Lameira said this "notion" could now be thrown "into the trash can". Dr Lameira, who conducted the research at Amsterdam University prior to joining Durham University, said Rocky's responses had been "extremely accurate". The team wanted to make sure the ape produced a new call, rather than adapting a "normal orangutan call with a personal twist" or matching sounds randomly or by coincidence, he said. The new evidence sets the "start line for scientific inquiry at a higher level", he said. "Ultimately, we should be now in a better position to think of how the different pieces of the puzzle of speech evolution fit together." The calls Rocky made were different from those collected in a large database of recordings, showing he was able to learn and produce new sounds rather than just match those already in his "vocabulary". In a previous study Dr Lameira found a female orangutan at Cologne Zoo in Germany was able to make sounds with a similar pace and rhythm to human speech. Researchers were "astounded" by Tilda's vocal skills but could not prove they had been learned, he said. However, the fact that "other orangutans seem to be exhibiting equivalent vocal skills shows that Rocky is not a bizarre or abnormal individual", Dr Lameira said. © 2016 BBC.
By Tim Page When I returned to California, I brought my diaries into the back yard every afternoon and read them through sequentially, with the hope of learning more about the years before my brain injury. I remembered much of what I’d done professionally, and whatever additional information I needed could usually be found on my constantly vandalized Wikipedia page. Here was the story of an awkward, imperious child prodigy who made his own films and became famous much too early; a music explainer who won a Pulitzer Prize; a driven and obsessive loner whose fascinations led to collaborations with Glenn Gould, Philip Glass and Thomas Pynchon. In 2000, at age 45, I was diagnosed with Asperger’s syndrome. In retrospect, the only surprise is that it took so long. But the diaries offered a more intimate view. Reading them was slow going, and I felt as though my nose was pressed up against the windowpane of my own life. The shaggy-dog accretion of material — phone numbers, long-ago concert dates, coded references to secret loves — all seemed to belong to somebody else. My last clear memory was of a muggy, quiet Sunday morning in July, three months earlier, as I waited for a train in New London, Conn. It was 11:13 a.m., and the train was due to arrive two minutes later. I was contented, proud of my punctuality and expecting an easy ride to New York in the designated “quiet car,” with just enough time to finish whatever book I was carrying. There would be dinner in Midtown with a magical friend, followed by overnight family visits in Baltimore and Washington, and then a flight back to Los Angeles and the University of Southern California, at which point a sabbatical semester would be at an end.
By Ann Grisold, Oscar, 6, sits at the family dinner table and endures the loneliest hour of his day. The room bustles with activity: Oscar’s sister passes plates and doles out broccoli florets. His father and uncle exchange playful banter. Oscar’s mother emerges from the kitchen carrying a platter of carved meat; a cousin pulls up an empty chair. “Chi fan le!” shouts Oscar’s older sister, in Mandarin Chinese. Time for dinner! “Hao,” her grandfather responds from the other room. Okay. Family members tell stories and rehash the day, all in animated Chinese. But when they turn to Oscar, who has autism, they speak in English. “Eat rice,” Oscar’s father says. “Sit nice.” Except there is no rice on the table. In Chinese, ‘eat rice’ can refer to any meal, but its meaning is lost in translation. Pediatricians, educators and speech therapists have long advised multilingual families to speak one language — the predominant one where they live — to children with autism or other developmental delays. The reasoning is simple: These children often struggle to learn language, so they’re better off focusing on a single one. However, there are no data to support this notion. In fact, a handful of studies show that children with autism can learn two languages as well as they learn one, and might even thrive in multilingual environments. Lost in translation: It’s not just children with autism who miss out when parents speak only English at home — their families, too, may experience frustrating miscommunications. Important instructions, offhand remarks and words of affection are often lost in translation when families swap their heritage language for English, says Betty Yu, associate professor of special education and communicative disorders at San Francisco State University. © 2016 Scientific American,
By Sara Chodosh There has long been debate about a link between serious blows to the head and the development of neurodegenerative diseases later in life. Research has made cases for and against a relationship between traumatic brain injuries and neurological ailments such as Alzheimer’s, Parkinson’s and general dementia. Now the question is drawing ever more scrutiny as the alarming extent of these injuries becomes better known—and new research is finally casting some light on this murky and often quietly terrifying topic. A large-scale analysis of three separate studies published this week in JAMA Neurology found no association between unconsciousness-causing traumatic brain injuries (TBI) and Alzheimer’s disease or general dementia—but it did find a strong association between TBI and Parkinson’s disease. “I can’t decide if the positive or negative findings are more surprising,” says one of the study’s investigators, physician and Alzheimer’s researcher Paul Crane at the University of Washington. The positive association his team found between Parkinson’s and TBI was not entirely novel, but Crane says the magnitude of the link was unexpected. The researchers found the risk of Parkinson’s rose threefold for people whose head injuries had caused them to go unconscious for more than an hour. The more contentious finding is the lack of an association between TBI and Alzheimer’s. Prior research has been divided on whether there is a link, but many of the previous studies have been smaller in scale and conducted less-comprehensive analyses. “Although early studies suggested a clear link between TBI and an increased risk for Alzheimer’s disease, this has not been replicated,” explains Frances Corrigan at the University of Adelaide, who studies how TBI influences neurodegeneration. © 2016 Scientific American,