By BENEDICT CAREY BEDFORD, Mass. — In a small room banked by refrigerators of preserved brains, a pathologist held a specimen up to the light in frank admiration. Then it was time to cut — once in half and then a thick slice from the back, the tissue dense and gray-pink, teeming with folds and swirls. It was the brain of a professional running back. “There,” said Dr. Ann McKee, the chief of neuropathology at the V.A. Boston Healthcare System and a professor of neurology and pathology at Boston University’s medical school, pointing to a key area that had an abnormal separation. “That’s one thing we look for right away.” Over the past several years, Dr. McKee’s lab, housed in a pair of two-story brick buildings in suburban Boston, has repeatedly made headlines by revealing that deceased athletes, including at least 90 former N.F.L. players, were found to have had a degenerative brain disease called chronic traumatic encephalopathy, or C.T.E., that is believed to cause debilitating memory and mood problems. This month, after years of denying or playing down a connection, a top N.F.L. official acknowledged at a hearing in Washington that playing football and having C.T.E. were “certainly” linked. His statement effectively ended a very public dispute over whether head blows sustained while playing football are associated with the disorder. But it will not resolve a quieter debate among scientists about how much risk each football player has of developing it, or answer questions about why some players seem far more vulnerable to it than others. Some researchers worry that the rising drumbeat of C.T.E. diagnoses is far outpacing scientific progress in pinpointing the symptoms, risks and prevalence of the disease. The American Academy of Clinical Neuropsychology, an organization of brain injury specialists, is preparing a public statement to point out that much of the science of C.T.E. is still unsettled and to contend that the evidence to date should not be interpreted to mean that parents must keep their children off sports teams, officials of the group say. © 2016 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 22040 - Posted: 03.28.2016

By ALAN SCHWARZ, WALT BOGDANICH and JACQUELINE WILLIAMS With several of its marquee players retiring early after a cascade of frightening concussions, the league formed a committee in 1994 that would ultimately issue a succession of research papers playing down the danger of head injuries. Amid criticism of the committee’s work, physicians brought in later to continue the research said the papers had relied on faulty analysis. Now, an investigation by The New York Times has found that the N.F.L.’s concussion research was far more flawed than previously known. For the last 13 years, the N.F.L. has stood by the research, which, the papers stated, was based on a full accounting of all concussions diagnosed by team physicians from 1996 through 2001. But confidential data obtained by The Times shows that more than 100 diagnosed concussions were omitted from the studies — including some severe injuries to stars like quarterbacks Steve Young and Troy Aikman. The committee then calculated the rates of concussions using the incomplete data, making them appear less frequent than they actually were. After The Times asked the league about the missing diagnosed cases — more than 10 percent of the total — officials acknowledged that “the clubs were not required to submit their data and not every club did.” That should have been made clearer, the league said in a statement, adding that the missing cases were not part of an attempt “to alter or suppress the rate of concussions.” One member of the concussion committee, Dr. Joseph Waeckerle, said he was unaware of the omissions. But he added: “If somebody made a human error or somebody assumed the data was absolutely correct and didn’t question it, well, we screwed up. If we found it wasn’t accurate and still used it, that’s not a screw-up; that’s a lie.” These discoveries raise new questions about the validity of the committee’s findings, published in 13 peer-reviewed articles and held up by the league as scientific evidence that brain injuries did not cause long-term harm to its players. It is also unclear why the omissions went unchallenged by league officials, by the epidemiologist whose job it was to ensure accurate data collection and by the editor of the medical journal that published the studies. © 2016 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 22035 - Posted: 03.26.2016

By Jordana Cepelewicz Last week a senior National Football League official acknowledged for the first time the link between head injuries in professional football and a degenerative brain disease called chronic traumatic encephalopathy. The admission—which has been compared with Big Tobacco’s 1997 disclosure that smoking causes cancer—comes at a time when the dangers of less severe traumatic brain injuries (TBIs), including concussions, have also been making headlines. Scientists do not yet understand the biological mechanisms underlying the detrimental effects of TBI—and as a result, effective treatments remain elusive. In fact, how to deal with even a mild concussion is the subject of debate: Some doctors prescribe rest for several weeks whereas others claim this may have negative consequences and urge patients to stay active. Now it turns out that the type of rest patients get may be key. In a study on rats published this week in The Journal of Neuroscience a team of researchers at University Hospital Zurich (UHZ) found that enhancing the slow-wave cycle of sleep after a traumatic head injury preserves brain function and minimizes damage to axons, the long projections from neurons that send signals to other cells in the brain. Previous research has shown that TBIs cause axonal damage as well as the buildup of neurotoxic molecular waste products that result from injury. In the new study the researchers examined two different methods of inducing a slow-wave sleep state—the deepest sleep stage characterized by low-frequency, high-amplitude waves. During this stage, the brain clears out protein buildup, leading the researchers to question whether it could help treat rats that had suffered a brain injury. © 2016 Scientific American

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 10: Biological Rhythms and Sleep
Link ID: 22023 - Posted: 03.24.2016

By KEN BELSON and ALAN SCHWARZ Perhaps no one will remember the setting, a hearing room for the House Energy and Commerce Committee, or the person who asked the question, a member of the House of Representatives from Illinois. But seven words spoken in the Rayburn House Office Building in Washington on Monday could profoundly affect the country’s most popular sport. After years of the N.F.L.‘s disputing evidence that connected football to chronic traumatic encephalopathy, the degenerative brain disease found in nearly 100 former players, a top official for the league for the first time acknowledged the link. To many, it was an echo of big tobacco’s confession in 1997 that smoking causes cancer and heart disease. Representative Jan Schakowsky, Democrat of Illinois, asked during a round-table discussion about concussions whether “there is a link between football and degenerative brain disorders like C.T.E.” Jeff Miller, the N.F.L.’s senior vice president for health and safety policy, said, “The answer to that is certainly, yes.” His response signaled a stunning about-face for the league, which has been accused by former players and independent experts of hiding the dangers of head injuries for decades. His reply came moments after a leading C.T.E. researcher — Dr. Ann McKee — had presented her findings, showing that dozens of former players who had died were afflicted with the disease. “The comments made by Jeff Miller yesterday accurately reflect the view of the N.F.L.,” Brian McCarthy, a league spokesman, said Tuesday, confirming that Mr. Miller had not misspoken. © 2016 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21997 - Posted: 03.16.2016

A senior British doctor, who has been an expert defence witness for parents accused of killing their children, has been found guilty of multiple charges that include giving misleading evidence in court. The Medical Practitioners Tribunal Service said that Waney Squier, a consultant pathologist at John Radcliffe Hospital in Oxford, UK, had failed to work within the limits of her competence, failed to be objective and unbiased, and failed to heed the views of other experts. In many of the cases investigated, her actions were deliberately misleading and irresponsible. The MPTS had considered Squier’s work as an expert witness in six child abuse cases and one appeal in which parents faced charges of non-accidental head injury, formerly known as shaken-baby syndrome. Squier is prominent among several researchers worldwide who have challenged a long-standing belief that a trio of symptoms of head injury provide unequivocal evidence of abusive behaviour. Squier has argued in the scientific literature and in court that the symptoms in question – haemorrhages on the surface of the brain, haemorrhages in the retinas, and a swollen brain – can have innocent causes, such as choking or other difficulties in breathing. These symptoms, they say, can also arise from the birthing process itself. Michele Codd, chair of the tribunal, gave examples of where the panel felt Squier’s court evidence had strayed outside her field of expertise. These included offering opinions on biomechanics in relation to injuries from falling, pathology of the eyes, and paediatric medicine. © Copyright Reed Business Information Ltd.

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 4: Development of the Brain
Link ID: 21982 - Posted: 03.14.2016

By Bob Roehr Retired American soccer star Brandi Chastain recently agreed to donate her brain to concussion research after her death. Females are often an unseen part of the concussion story even though they suffer more concussions than males, have more severe symptoms and are slower to recover. Just why is not completely clear, but the deficit in knowledge is slowly beginning to change thanks to women’s advocates behind Pink Concussions. The group gathered last weekend at Georgetown University to review the science behind concussions, and also to develop recommendations on gender-specific prevention protocols and clinical practices on how best to treat females with concussions. In comparable sports “female rates of concussions are much higher than those of their male counterparts,” says Zachary Kerr, director of the National Collegiate Athletic Association (NCAA) Injury Surveillance Program. Over a five-year period the rates per 1000 athlete-exposures were 6.3 in females versus 3.4 in males in soccer, 6.0 in females versus 3.9 in males in basketball and 3.3 in females versus 0.9 in males in baseball and softball. Only in swimming and diving did male rates (0.3) exceed those of females (0.5). Headache, dizziness and difficulty concentrating were roughly similar among both sexes, Kerr says. But among injured high school athletes, “larger portions of females are reporting sensitivity to light, sensitivity to noise, nausea and drowsiness,” he says. They were also slower to return to normal activity. The difference between the incidence and severity of concussions between the sexes does not start at birth, because infants and young children of both sexes have similar rates and symptoms with concussions. Puberty, however, which marks a significant developmental fork in the road for males and females, also marks a divergence for concussions. © 2016 Scientific American

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 8: Hormones and Sex
Link ID: 21973 - Posted: 03.10.2016

By Jordana Cepelewicz As the Panthers and Broncos faced off in the third quarter of last night’s Super Bowl, wide receiver Philly Brown suffered a possible concussion—and to the disappointment of Panthers fans, he never returned to the game. But for good reason: concussions are now known to be much more serious injuries than once thought. And the danger may not be limited to the immediate repercussions. Researchers have already linked more severe traumatic brain injury to later suicide—particularly in military veterans and professional athletes—and have more recently explored the connection between concussion and depression. Now, new research published in the Canadian Medical Association Journal shows that even mild concussions sustained in ordinary community settings might be more detrimental than anyone anticipated; the long-term risk of suicide increases threefold in adults if they have experienced even one concussion. That risk increases by a third if the concussion is sustained on a weekend instead of a weekday—suggesting recreational concussions are riskier long-term than those sustained on the job. “The typical patient I see is a middle-aged adult, not an elite athlete,” says Donald Redelmeier, a senior scientist at the University of Toronto and one of the study’s lead authors. “And the usual circumstances for acquiring a concussion are not while playing football; it is when driving in traffic and getting into a crash, when missing a step and falling down a staircase, when getting overly ambitious about home repairs—the everyday activities of life.” Redelmeier and his team wanted to examine the risks of the concussions acquired under those circumstances. © 2016 Scientific American

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21875 - Posted: 02.09.2016

Laura Sanders The brain can bounce back after a single head hit, but multiple hits in quick succession don’t give the brain time to recover, a new study suggests. Although the finding comes from mice, it may help scientists better understand the damage caused by repetitive impacts such as those sustained in football, soccer and other contact sports. The results, published in the March issue of the American Journal of Pathology, hint that a single, mild head hit isn’t necessarily cause for alarm. “There are things to be afraid of after a concussion,” says study coauthor Mark Burns of Georgetown University Medical Center in Washington, D.C. “But not every concussion is going to cause long-term damage.” Burns and his colleagues subjected some mice to a single, mild head hit. The relatively weak hit consistently slowed anesthetized mice’s return to consciousness, but didn’t cause major trauma. The impact was designed to mimic a mild traumatic brain injury, or concussion, in a person. Tests a day after the impact showed that about 13 percent of dendritic spines, docking sites that help connect brain cells, had vanished in a particular part of the brain. Three days after the injury, these missing connections reappeared, even surpassing the original number of connections. This fluctuating number of dendritic spines may actually help the brain recover, Burns says. “The cells weren’t dying,” he says. “They were responding to the injury.” © Society for Science & the Public 2000 - 2016.

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21867 - Posted: 02.06.2016

By JOHN BRANCH Shortly before he died in July, the former N.F.L. quarterback Ken Stabler was rushed away by doctors, desperate to save him, in a Mississippi hospital. His longtime partner followed the scrum to the elevator, holding his hand. She told him that she loved him. Stabler said that he loved her, too. “I turned my head to wipe the tears away,” his partner, Kim Bush, said recently. “And when I looked back, he looked me dead in the eye and said, ‘I’m tired.’ ” They were the last words anyone in Stabler’s family heard him speak. “I knew that was it,” Bush said. “I knew that he had gone the distance. Because Kenny Stabler was never tired.” The day after Stabler died on July 8, a victim of colon cancer at 69, his brain was removed during an autopsy and ferried to scientists in Massachusetts. It weighed 1,318 grams, or just under three pounds. Over several months, it was dissected for clues, as Stabler had wished, to help those left behind understand why his mind seemed to slip so precipitously in his final years. On the neuropathologist’s scale of 1 to 4, Stabler had high Stage 3 chronic traumatic encephalopathy, or C.T.E., the degenerative brain disease believed to be caused by repeated blows to the head, according to researchers at Boston University. The relationship between blows to the head and brain degeneration is still poorly understood, and some experts caution that other factors, like unrelated mood problems or dementia, might contribute to symptoms experienced by those later found to have had C.T.E. Stabler, well known by his nickname, the Snake (“He’d run 200 yards to score from 20 yards out,” Stabler’s junior high school coach told Sports Illustrated in 1977), is one of the highest-profile football players to have had C.T.E. The list, now well over 100 names long, includes at least seven members of the Pro Football Hall of Fame, including Junior Seau, Mike Webster and Frank Gifford. © 2016 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21861 - Posted: 02.04.2016

AUDIE CORNISH, HOST: It's unusual for an NFL player - a current player - to criticize the league, especially its handling of controversial issues like concussions or domestic violence, but author Johnny Anonymous has done just that. He's an offensive lineman who's written a book under that pseudonym. It's called "NFL Confidential." In it, he details his 2014 season, including training camp and his big break after a starting player gets injured. He's worried about being fired, so we've masked his voice. First, Johnny Anonymous says getting hurt is always on the mind of the player. ANONYMOUS: It's absolutely constant. The NFL's the only league, the only job you'll find in the world where we have a 100 percent injury rate. CORNISH: So walk us through the questions that come to mind for a player when they first hear that, you know, sickening sound and they're lying there on the field. What are you thinking? ANONYMOUS: For some guys, it's fear, which is why you'll see them kicking and screaming and crying, and some guys it's shock. I know for most of us - and probably all of us - the first thing you think is, I'm done; that's it. You think the injury's going to take the game away from you. CORNISH: So in a way, you know, this is how it happens, right, this discussion of, like, why do people take all the painkillers, you know, like, why do people defy doctors? ANONYMOUS: You have to. It's the only way you make it through. I can tell you right now, honestly, that if I am playing a game, I cannot complete that game without painkillers. I will not be an effective player. © 2016 npr

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21766 - Posted: 01.09.2016

By Josh Izaac Helmets can reduce the risk of traumatic brain injury by almost 20%. But what if we take so many risks when wearing them that we lose the protective edge they provide? This could be the case, according to a study published this week. Researchers observed 80 cyclists under the guise of an “eye-tracking experiment,” pretending to track their eye-motion via a head-mounted camera as the participants inflated a virtual balloon. For some of the participants, the “eye-tracking devices” were mounted on helmets, while others just wore baseball caps, as can be seen in the picture of the equipment above. The further they inflated the balloon without it popping, the higher their reward and their risk-taking score. Participants wearing helmets inflated their balloons on average 30% more than those who wore caps, the team reports in Psychological Science. The finding could affect how we approach safety design and training, the authors say, as increased risk-taking behavior when using safety equipment might counteract the perceived benefit of the equipment. But what causes this effect in the first place? The underlying mechanism might be related to the concept of “social priming,” where people’s actions towards others are altered subconsciously due to exposure to particular words, cues, objects, or symbols. Importantly, this is the first time social priming has been shown to change people’s behaviour even when they are not interacting with others, providing potential new insights into human behavior. So, next time you’re out riding with a helmet, think twice before attempting that wheelie. © 2016 American Association for the Advancement of Science

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21765 - Posted: 01.09.2016

A 25-year-old former college football player showed signs of a type of brain degeneration from repeated trauma, say researchers who described the autopsy-confirmed case. Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder associated with repetitive head impacts. Symptoms may include memory loss, impaired judgment, depression and progressive dementia. CTE can only be diagnosed after death by examining the brain. Monday's issue of JAMA Neurology includes a letter describing CTE in a 25-year-old man born with a heart valve disorder. He died of cardiac arrest secondary to a heart infection after playing football for 16 years and experiencing an estimated more than 10 concussions while playing. Dr. Ann McKee and Dr. Jesse Mez of Boston University School of Medicine ran neuropsychological tests on the man when he showed symptoms a year before his death, and then conducted an autopsy, reviewed his medical records and interviewed family members. "Focal lesions of CTE have been found in athletes as young as 17 years; however, widespread CTE pathology, as found in this case, is unusual in such a young football player," they wrote. To their knowledge, it's the first such case to include neuropsychological testing to document the type of cognitive issues with CTE. In this case, the athlete started playing football when he was six, including three years of college football as a defensive linebacker. His first concussion occurred at age eight. ©2015 CBC/Radio-Canada.

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21750 - Posted: 01.05.2016

By KEN BELSON When St. Louis Rams quarterback Case Keenum sustained a concussion in a game in Baltimore last month, commentators focused on how he wobbled as he got up and questioned why he was not taken out of the game. Few mentioned that he had slammed his head on the turf. In the rush to reduce head trauma in sports, doctors, researchers, leagues and equipment makers have looked at everything from improving helmets to teaching safer tackling techniques. But one little-explored cause of concussions is the field beneath the feet of the millions of athletes who play football, lacrosse, soccer and other sports. A new report compiled by the Concussion Legacy Foundation called attention to the link between head injuries and poorly maintained fields, especially the growing number of those made of synthetic turf. The foundation urged groundskeepers, athletic directors and sports associations to treat their fields as seriously as other protective sports equipment. “We have no national conversation on the technology underneath an athlete’s feet,” the authors wrote in their report, the Role of Synthetic Turf in Concussion. “Helmet technology is an area of great attention and investment, and surfaces deserve the same attention.” The report, which is based on more than a dozen academic studies, cites research that shows that 15.5 percent of concussions in high school sports occur when players hit their head on a playing surface. Another study found that 10 percent of concussions sustained by high school and college football players came after players hit their head on a field. In the N.F.L., about one in seven concussions occurs when a player’s head strikes a synthetic or grass field. © 2015 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21737 - Posted: 12.30.2015

By KEN BELSON Researchers at several universities and research institutes were awarded almost $16 million Tuesday to find a way to diagnose, while victims are alive, chronic traumatic encephalopathy, a degenerative brain disease linked to repeated head hits in contact sports. The National Institutes of Health and the National Institute of Neurological Disorders and Stroke issued the seven-year grant as part of a long-term study of brain disease in former N.F.L. and college football players, many of whom sustained multiple concussions on the field. Despite the implications that the research may have on football players and the N.F.L., no league money will be used to help pay for the grant. For years, researchers have been able to diagnose C.T.E. only by examining the brains of players who died and whose families agreed to donate the organ, a limitation that has slowed efforts to determine who is susceptible to having the disease. The new study, considered among the most ambitious in the field of sports-related brain injury, aims to develop ways to spot the disease in the living and figure out why certain players get it and others do not. A more comprehensive understanding of the disease, the researchers said, may lead to ways to prevent it. “There are so many critical unanswered questions about C.T.E.,” Dr. Robert Stern, the lead principal investigator and a professor at Boston University School of Medicine, said in a statement. “We are optimistic that this project will lead to many of these answers, by developing accurate methods of detecting and diagnosing C.T.E. during life, and by examining genetic and other risk factors for this disease.” © 2015 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21723 - Posted: 12.24.2015

Nicole Fisher , We know that the brain is neuroplastic — adapts to changes in behavior, environment, thinking and emotions — and may even rewire itself in certain ways. Life experience also teaches us that the tongue is a learning tool that shapes our brain. During early development, babies test everything by placing it in their mouths. As children age they stick out their tongues when concentrating on tasks such as drawing. Even as adults we let our tongue tell us about the world around us through eating, drinking and kissing. During basketball games, some players stick out their tongues while shooting. Now, knowing that there is such a rich nerve connection to the brain, scientists and doctors are turning to the tongue as a way to possibly stimulate the brain for neural retraining and rehabilitation after traumatic injuries or disease. The team at Helius Medical Technologies believe combining physical therapy with stimulation of the tongue may improve impairment of brain function and associated symptoms of injury. “We have already seen that stimulation of various nerves can improve symptoms of a range of neurological diseases. However, we believe the tongue is a much more elegant and direct pathway for stimulating brain structures and inducing neuroplasticity. We are focused on investigating the tongue as a gateway to the brain to hopefully ease the disease of brain injury,” said Dr. Jonathan Sackier, CMO at Helius. It has been argued by some that the era of small molecule is gone. Instead, recognition that the entire body is a closed electrical circuit, is leading to new therapeutic modalities that are known in certain circles as “electroceuticals.”

Related chapters from BN: Chapter 9: Hearing, Balance, Taste, and Smell; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 6: Hearing, Balance, Taste, and Smell; Chapter 15: Language and Lateralization
Link ID: 21595 - Posted: 11.03.2015

By Bob Grant Scientists delving into the neurological underpinnings of traumatic brain injuries (TBI) are finding that there may be crucial differences in the long-term effects of the events that depend not only on the insult, but also on the victim. “No two brain injuries are identical,” University of Pennsylvania neuroscientist Akiva Cohen said during a press conference held at the Society for Neuroscience (SfN) annual meeting in Chicago on Monday (October 19). “Brain injury, like many pathologies these days, constitutes a spectrum.” In addition to a severity spectrum that spans mild to severe, brain injuries may differ in terms of how male and female animals respond to them, according to Ramesh Raghupathi, a neurobiologist at Drexel University. Raghupathi and his colleagues have found that young male mice suffer more depressive behaviors than female mice at both four and eight weeks after mild TBI, and females display more headache-like symptoms after similar insults, which can include concussion. “All of these animals at these times after injury are cognitively normal,” Raghupathi told reporters. “And they do not have any movement problems.” Raghupathi and his colleagues also found molecular differences that may underlie the sex differences in TBI response that they observed. “In the male mice,” he said, “there is a dramatic difference in dopamine transmission” compared to the uninjured mice.” Researchers have previously linked impaired dopamine signaling to depression. Raghupathi’s team tested for the lingering effects of TBI in mice by subjecting the animals to certain swimming tests—which are accepted as proxies for depression—and by using a thin filament to touch the faces of the rodents and recording their sensitivity as a measure of headache-like behaviors.

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 8: Hormones and Sex
Link ID: 21558 - Posted: 10.24.2015

Neuroscientist Dr. Charles Tator has asked the family of former NHL enforcer Todd Ewen to donate Ewen's brain so he can study it. This week, Ewan's death was ruled a suicide and Tator wants to examine his brain to determine whether it has signs of degeneration. In particular, he's interested in what Ewen's brain may have in common with the other brains of athletes he's studying as part of the Canadian Sports Concussion Project. Brent Bambury speaks with Dr. Tator about how concussions can affect athletes and what big unanswered questions remain when it comes to the links between concussions, brain injury and self-harm. This conversation has been edited for clarity and length. Brent Bambury: You and your team already have examined the brains of eighteen former professional athletes. What do you hope to learn by looking at Todd Ewen's brain? Dr. Charles Tator: Well we want to know if he had C.T.E. In other words, was this the cause of his decline in terms of depression, for example. BB: What is C.T.E. ? CT: Well C.T.E. is chronic traumatic encephalopathy which is a specific type of brain degeneration that occurs after repetitive trauma like multiple concussions. BB: Is that something that you can only determine by examining the brain from a cadaver? CT: Unfortunately, even though we are getting clues about it from other tests like M.R.I., at this point in 2015, you have to do an autopsy to be sure that it's C.T.E. So with the Todd Ewen donation, if we're fortunate enough to have that opportunity to examine his brain, we would want to see if there were any manifestations of these previous concussions that he had in his career. ©2015 CBC/Radio-Canada

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21450 - Posted: 09.28.2015

By CLYDE HABERMAN Perhaps no crime staggers the mind, or turns the stomach, more than the murder of a baby, and so it is not a surprise when law enforcement comes down hard on the presumed killers. Often enough, these are men and women accused of having succumbed to sudden rage or simmering frustration and literally shaken the life out of a helpless infant who would not stop crying or would not fall asleep. Shaken baby syndrome has been a recognized diagnosis for several decades, though many medical professionals now prefer the term abusive head trauma. It is defined by a constellation of symptoms known as the triad: brain swelling, bleeding on the surface of the brain and bleeding behind the eyes. For years, those three symptoms by themselves were uniformly accepted as evidence that a crime had been committed, even in the absence of bruises, broken bones or other signs of abuse. While many doctors, maybe most, still swear by the diagnosis, a growing number have lost faith. Not that they doubt that some babies have been abused. But these skeptics assert that factors other than shaking, and having nothing to do with criminal behavior, may sometimes explain the triad. Has the syndrome been diagnosed too liberally? Are some innocent parents and other caretakers being wrongly sent to prison? Those questions, at the complex intersection of medicine and the law, can stir strong emotions among doctors, parents and prosecutors. They shape this first installment in a new series of Retro Report, video documentaries that explore major news stories of the past and their enduring consequences. The video’s starting point is a Massachusetts criminal case that introduced the concept of shaken baby syndrome to many Americans: the 1997 murder trial of Louise Woodward, an 18-year-old British au pair accused of having shaken an 8-month-old boy, Matthew Eappen, so aggressively that he died. Matthew also had injuries that may have predated Ms. Woodward’s joining the Eappen family in Newton, outside Boston. The focus, however, was on the triad of symptoms. To prosecution witnesses, they proved that the baby had been shaken violently, his head hitting some hard surface. © 2015 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 4: Development of the Brain
Link ID: 21405 - Posted: 09.14.2015

Every brain cell has a nucleus, or a central command station. Scientists have shown that the passage of molecules through the nucleus of a star-shaped brain cell, called an astrocyte, may play a critical role in health and disease. The study, published in the journal Nature Neuroscience, was partially funded by the National Institutes of Health (NIH). “Unexpectedly we may have discovered a hidden pathway to understanding how astrocytes respond to injury and control brain processes. The pathway may be common to many brain diseases and we’re just starting to follow it,” said Katerina Akassoglou, Ph.D., a senior investigator at the Gladstone Institute for Neurological Disease, a professor of neurology at the University of California, San Francisco, and a senior author of the study. Some neurological disorders are associated with higher than normal brain levels of the growth factor TGF-beta, including Alzheimer's disease and brain injury. Previous studies found that after brain injury, astrocytes produce greater amounts of p75 neurotrophin receptor (p75NTR), a protein that helps cells detect growth factors. The cells also react to TGF-beta by changing their shapes and secreting proteins that alter neuronal activity. Dr. Akassoglou’s lab showed that eliminating the p75NTR gene prevented hydrocephalus in mice genetically engineered to have astrocytes that produce higher levels of TGF-beta. Hydrocephalus is a disorder that fills the brain with excess cerebral spinal fluid. Eliminating the p75NTR gene also prevented astrocytes in the brains of the mice from forming scars after injuries and restored gamma oscillations, which are patterns of neuronal activity associated with learning and memory.

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 4: Development of the Brain
Link ID: 21307 - Posted: 08.18.2015

Rachel Martin The National Football League held its annual hall of fame induction ceremony Saturday night, in Canton, Ohio. Eight players were given football's highest honor, including a posthumous induction for Junior Seau, the former linebacker for the San Diego Chargers who killed himself in 2012. After his death, Seau's brain showed signs of chronic damage — the same kind of damage that has been found in dozens of other former NFL players. Scientific studies have shown that the kind of repeated hits NFL players take is linked to chronic traumatic encephalopathy, or CTE, a degenerative brain disease. CTE is associated with memory loss, impulse control problems, depression and eventually dementia. Some players are rethinking their careers — like up-and-coming linebacker Chris Borland, who quit after his first season with the 49ers a few months ago — for fear of head injuries. Parents are weighing the risks as well. So when someone like Chicago Bears coach Mike Ditka talks, they listen. When host Bryant Gumbel asked Ditka on HBO's Real Sports earlier this year whether, if he had an 8-year-old now, he would want him to play football. "No," he answered. "That's sad. I wouldn't, and my whole life was football. I think the risk is worse than the reward." Tregg Duerson's father, Dave Duerson, a defensive back who played most of his pro football career with the Chicago Bears, killed himself in 2011 in his Miami home. Duerson was part of the legendary '85 team that won the Superbowl, and five years later helped the New York Giants win their own championship. © 2015 NPR

Related chapters from BN: Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 15: Language and Lateralization
Link ID: 21281 - Posted: 08.10.2015