Chapter 5. The Sensorimotor System
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|By Sandra Upson Jan Scheuermann is not your average experimental subject. Diagnosed with spinocerebellar degeneration, she is only able to move her head and neck. The paralysis, which began creeping over her muscles in 1996, has been devastating in many ways. Yet two years ago she seized an opportunity to turn her personal liability into an extraordinary asset for neuroscience. In 2012 Scheuermann elected to undergo brain surgery to implant two arrays of electrodes on her motor cortex, a band of tissue on the surface of the brain. She did so as a volunteer in a multi-year study at the University of Pittsburgh to develop a better brain-computer interface. When she visits the lab, researchers hook up her brain to a robotic arm and hand, which she practices moving using her thoughts alone. The goal is to eventually allow other paralyzed individuals to regain function by wiring up their brains directly to a computer or prosthetic limb. The electrodes in her head record the firing patterns of about 150 of her neurons. Specific patterns of neuronal activity encode her desire to perform different movements, such as swinging the arm to the left or clasping the fingers around a cup. Two thick cables relay the data from her neurons to a computer, where software can identify Scheuermann’s intentions. The computer can then issue appropriate commands to move the robotic limb. On a typical workday, Jan Scheuermann arrives at the university around 9:15 am. Using her chin, she maneuvers her electric wheelchair into a research lab headed by neuroscientist Andrew Schwartz and settles in for a day of work. Scientific American Mind spoke to Scheuermann to learn more about her experience as a self-proclaimed “guinea pig extraordinaire.” © 2014 Scientific American,
Link ID: 20276 - Posted: 11.04.2014
Colin Barras It's the sweetest relief… until it's not. Scratching an itch only gives temporary respite before making it worse – we now know why. Millions of people experience chronic itching at some point, as a result of conditions ranging from eczema to kidney failure to cancer. The condition can have a serious impact on quality of life. On the face of it, the body appears to have a coping mechanism: scratching an itch until it hurts can bring instant relief. But when the pain wears off the itch is often more unbearable than before – which means we scratch even harder, sometimes to the point of causing painful skin damage. "People keep scratching even though they might end up bleeding," says Zhou-Feng Chen at the Washington University School of Medicine in St Louis, Missouri, who has now worked out why this happens. His team's work in mice suggests it comes down to an unfortunate bit of neural crosstalk. We know that the neurotransmitter serotonin helps control pain, and that pain – from the heavy scratching – helps soothe an itch, so Chen's team set out to explore whether serotonin is also involved in the itching process. They began by genetically engineering mice to produce no serotonin. Normally, mice injected with a chemical that irritates their skin will scratch up a storm, but the engineered mice seemed to have almost no urge to scratch. Genetically normal mice given a treatment to prevent serotonin leaving the brain also avoided scratching after being injected with the chemical, indicating that the urge to scratch begins when serotonin from the brain reaches the irritated spot. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 20270 - Posted: 11.03.2014
BY Laura Sanders The first time Nathan Whitmore zapped his brain, he had a college friend standing by, ready to pull the cord in case he had a seizure. That didn’t happen. Instead, Whitmore started experimenting with the surges of electricity, and he liked the effects. Since that first cautious attempt, he’s become a frequent user of, and advocate for, homemade brain stimulators. Depending on where he puts the electrodes, Whitmore says, he has expanded his memory, improved his math skills and solved previously intractable problems. The 22-year-old, a researcher in a National Institute on Aging neuroscience lab in Baltimore, writes computer programs in his spare time. When he attaches an electrode to a spot on his forehead, his brain goes into a “flow state,” he says, where tricky coding solutions appear effortlessly. “It’s like the computer is programming itself.” Whitmore no longer asks a friend to keep him company while he plugs in, but he is far from alone. The movement to use electricity to change the brain, while still relatively fringe, appears to be growing, as evidenced by a steady increase in active participants in an online brain-hacking message board that Whitmore moderates. This do-it-yourself community, some of whom make their own devices, includes people who want to get better test scores or crush the competition in video games as well as people struggling with depression and chronic pain, Whitmore says. As reckless as it sounds to juice a brain at home with a 9-volt battery and 40 dollars’ worth of spare parts, this technology’s buzz is based on legit science. Small laboratory studies suggest that carefully controlled brain stimulation can boost a person’s memory and math abilities, hone attention and fast-track learning. The U. S. military is interested and is funding studies to test brain stimulation as a way to boost soldiers’ alertness and vigilance. The technique may even be a viable treatment for pernicious mental disorders such as major depression, according to other laboratory-based studies. © Society for Science & the Public 2000 - 2014.
By Rachel Feltman Sometimes the process of scientific discovery can be a real headache. In a recent Danish study, scientists were thrilled to give painful migraines to 86 percent of their study subjects. Migraines are a particularly painful mystery for researchers to solve: More than 10 percent of people worldwide are affected by these intense headaches, but no one has been able to pinpoint a specific cause. What makes these headaches, which can cause incapacitating pain and nausea, different from all other headaches? That's why scientists had to make their patients suffer -- researchers keep trying to trigger migraines using different mechanisms. The more successful they are, the more likely it is that the mechanism being tested is actually a common cause of migraines. And once we know what the common causes are, we can try to develop better treatments that target them. In this case the 86 percent "success" rate, which the researchers say is much higher than results with other triggers, was owed to increases of a naturally occurring substance called cyclic AMP, or cAMP. Our bodies use cAMP to dilate blood vessels, so an increase of it can increase the flow of blood. To see if cAMP might cause migraines, the researchers dosed their subjects with cilostazol, a drug that increases cAMP concentrations in the body.
Keyword: Pain & Touch
Link ID: 20264 - Posted: 11.01.2014
By CATHERINE SAINT LOUIS More than 50 children in 23 states have had mysterious episodes of paralysis to their arms or legs, according to data gathered by the Centers for Disease Control and Prevention. The cause is not known, although some doctors suspect the cases may be linked to infection with enterovirus 68, a respiratory virus that has sickened thousands of children in recent months. Concerned by a cluster of cases in Colorado, the C.D.C. last month asked doctors and state health officials nationwide to begin compiling detailed reports about cases of unusual limb weakness in children. Experts convened by the agency plan next week to release interim guidelines on managing the condition. That so many children have had full or partial paralysis in a short period is unusual, but officials said that the cases seemed to be extremely rare. “At the moment, it looks like whatever the chances are of getting this syndrome are less than one in a million,” said Mark A. Pallansch, the director of the division of viral diseases at the C.D.C. Some of the affected children have lost the use of a leg or an arm, and are having physical therapy to keep their muscles conditioned. Others have sustained more extensive damage and require help breathing. Marie, who asked to be identified by her middle name to protect her family’s privacy, said her 4-year-old son used to climb jungle gyms. But in late September, after the whole family had been sick with a respiratory illness, he started having trouble climbing onto the couch. He walked into Boston Children’s Hospital the day he was admitted. But soon his neck grew so weak, it “flopped completely back like he was a newborn,” Marie said. Typically, the time from when weakness begins until it reaches its worst is one to three days. But for her son, eight mornings in a row, he awoke with a "brand new deficit" until he had some degree of weakness in each limb and had trouble breathing. He was eventually transferred to a Spaulding rehabilitation center, where he is now. © 2014 The New York Times Company
by Bethany Brookshire In many scientific fields, the study of the body is the study of boys. In neuroscience, for example, studies in male rats, mice, monkeys and other mammals outnumber studies in females 5.5 to 1. When scientists are hunting for clues, treatments or cures for a human population that is around 50 percent female, this boys-only club may miss important questions about how the other half lives. So in an effort to reduce this sex bias in biomedical studies, National Institutes of Health director Francis Collins and Office of Research on Women’s Health director Janine Clayton announced in May a new policy that will roll out practices promoting sex parity in research, beginning with a requirement that scientists state whether males, females or both were used in experiments, and moving on to mandate that both males and females are included in all future funded research. The end goal will be to make sure that NIH-funded scientists “balance male and female cells and animals in preclinical studies in all future [grant] applications” to the NIH. In 1993, the NIH Revitalization Act mandated the inclusion of women and minorities in clinical trials. This latest move extends that inclusion to cells and animals in preclinical research. Because NIH funds the work of morethan 300,000 researchers in the United States and other countries, many of whom work on preclinical and basic biomedical science, the new policy has broad implications for the biomedical research community. And while some scientists are pleased with the effort, others are worried that the mandate is ill-conceived and underfunded. In the end, whether it succeeds or fails comes down to interpretation and future implementation. © Society for Science & the Public 2000 - 2014
By BENEDICT CAREY A Polish man who was paralyzed from the chest down after a knife attack several years ago is now able to get around using a walker and has recovered some sensation in his legs after receiving a novel nerve-regeneration treatment, according to a new report that has generated both hope and controversy. The case, first reported widely by the BBC and other British news outlets, has stirred as much excitement on the Internet as it has extreme caution among many experts. “It is premature at best, and at worst inappropriate, to draw any conclusions from a single patient,” said Dr. Mark H. Tuszynski, director of the translational neuroscience unit at the medical school of the University of California, San Diego. That patient — identified as Darek Fidyka, 40 — is the first to recover feeling and mobility after getting the novel therapy, which involves injections of cultured cells at the site of the injury and tissue grafts, the report said. The techniques have shown some promise in animal studies. But the medical team, led by Polish and English doctors, also emphasized that the results would “have to be confirmed in a larger group of patients sustaining similar types of spinal injury” before the treatment could be considered truly effective. The case report was published in the journal Cell Transplantation. The history of spinal injury treatment is studded with false hope and miracle recoveries that could never be replicated, experts said. In previous studies, scientists experimented with some of the same methods used on Mr. Fidyka, with disappointing results. © 2014 The New York Times Company
By Fergus Walsh Medical correspondent A paralysed man has been able to walk again after a pioneering therapy that involved transplanting cells from his nasal cavity into his spinal cord. Darek Fidyka, who was paralysed from the chest down in a knife attack in 2010, can now walk using a frame. The treatment, a world first, was carried out by surgeons in Poland in collaboration with scientists in London. Prof Wagih El Masri Consultant spinal injuries surgeon Details of the research are published in the journal Cell Transplantation. BBC One's Panorama programme had unique access to the project and spent a year charting the patient's rehabilitation. Darek Fidyka, 40, from Poland, was paralysed after being stabbed repeatedly in the back in the 2010 attack. He said walking again - with the support of a frame - was "an incredible feeling", adding: "When you can't feel almost half your body, you are helpless, but when it starts coming back it's like you were born again." He said what had been achieved was "more impressive than man walking on the moon". UK research team leader Prof Geoff Raisman: Paralysis treatment "has vast potential" The treatment used olfactory ensheathing cells (OECs) - specialist cells that form part of the sense of smell. OECs act as pathway cells that enable nerve fibres in the olfactory system to be continually renewed. In the first of two operations, surgeons removed one of the patient's olfactory bulbs and grew the cells in culture. Two weeks later they transplanted the OECs into the spinal cord, which had been cut through in the knife attack apart from a thin strip of scar tissue on the right. They had just a drop of material to work with - about 500,000 cells. About 100 micro-injections of OECs were made above and below the injury. BBC © 2014
BY Tina Hesman Saey SAN DIEGO — A Golden retriever that inherited a genetic defect that causes muscular dystrophy doesn’t have the disease, giving scientists clues to new therapies for treating muscle-wasting diseases. The dog, Ringo, was bred to have a mutation that causes Duchenne muscular dystrophy in both animals and people. His weak littermates that inherited the same mutation could barely suckle at birth. But Ringo was healthy, with muscles that function normally. One of Ringo’s sons also has the mutation but doesn’t have the disease, said geneticist Natassia Vieira of Boston Children’s Hospital and Harvard University October 19 at the annual meeting of the American Society of Human Genetics. The dogs without the disease had a second genetic variant that caused their muscles to make more of a protein called Jagged 1, Vieira and her colleagues discovered. That protein allows muscles to repair themselves. Making more of Jagged 1 appears to compensate for the wasting effect of the muscular dystrophy mutation, although the researchers don’t yet know the exact mechanism. The finding suggests that researchers may one day be able to devise treatments for people with muscular dystrophies by boosting production of Jagged 1 or other muscle repair proteins. N. M. Vieira. The muscular dystrophies: Revealing the genetic and phenotypic variability. American Society of Human Genetics Annual Meeting, San Diego, October 19, 2014. © Society for Science & the Public 2000 - 2014
by Flora Graham This glowing blue web of neurons is usually what researchers examine when searching for a cure for Parkinson's. But a new study, part-funded by Parkinson's UK, hones in on the tiny yellow dots. These are the connections between brain cells known as synapses, has discovered a killer that targets these links, potentially paving the way for new treatments. Soledad Galli at University College London and her colleagues have found that the death of synapses in mice may be due to malfunctioning proteins called Wnt proteins. "If we confirm that Wnt is involved in the early stages of Parkinson's, this throws up exciting possibilities, not just for new treatment targets, but also for new ways to identify people with Parkinson's early on in their condition," says Galli. Most patients currently depend on the drug levodopa, which is over 50 years old and can have severe side-effects, in addition to becoming less effective over time. Moreover, it only masks the symptoms: there is no cure for Parkinson's and no way to stop its progression. Journal reference: Nature Communications, DOI: 10.1038/ncomms5992 © Copyright Reed Business Information Ltd
|By Amy Yee Pouring a bucket of ice water over one’s head may seem like a distant summer memory. But although the “ice bucket challenge” craze has died down, public awareness of amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrig’s disease, has never been stronger. The viral video campaign raised $115 million from more than 3 million donors for the ALS Association. In one month, from July 29 to August 29, donors raised $100.9 million, compared with $2.8 million during the same period the previous year. In early October, the ALS Association began spending that money. It approved $21.7 million of funding for six programs and initiatives by groups that include the academic-industry partnership ALS Accelerated Therapeutics, the New York Genome Center, three California labs that form the Neuro Collaborative, and Project MinE, which will map the genomes of 15,000 people with ALS (about 10 percent of ALS patients have a family member with the disease). The grants focus on developing gene therapies for common ALS genes and exploring approaches to counter two major contributors to the disease, the inflammation of nervous tissue and misfolded proteins in brain cells that control movement. These efforts may not only someday lead to new treatments, but may also point to the cause of ALS. At the level of basic research, scientists do not have a dominant theory from which to work, notes Tom Jessell, a neuroscientist and co-director of Columbia University’s new Zuckerman Mind Brain Behavior Institute. Jessell is also the chair of the research advisory board of Project ALS, a nonprofit that identifies and funds ALS research. © 2014 Scientific American
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20213 - Posted: 10.18.2014
By Carl T. Hall Even Clayton Kershaw, the Los Angeles Dodgers’ pitching ace, makes mistakes now and then. And although very few of his mistakes seemed to do Giants hitters much good this season, a team of San Francisco scientists found a way to take full advantage. A new study by UCSF researchers revealed a tendency of the brain’s motion-control system to run off track in a predictable way when we try to perform the same practiced movement over and over. The scientists found the phenomenon first in macaque monkeys, then documented exactly the same thing in Kershaw’s game video. Although he struggled in a playoff appearance last week, the left-hander’s pitching performance during the regular season was among the best on record. It included a minuscule 1.77 earned run average, a nearly flawless no-hitter in June, 239 strikeouts and only 31 walks. He led the major leagues with 10.85 strikeouts per nine innings pitched. In what turned out to be an early warm-up to the playoffs, UCSF scientists Kris Chaisanguanthum, Helen Shen and Philip Sabes delved into the motor-control system of the primate brain. Their study, published in the Journal of Neuroscience, could help design better prosthetic limbs — or make robots that move less like robots and more like Kershaw. Unlike most machines, our brains seem to never stop trying to adapt to new information, making subtle adjustments each time we repeat a particular movement no matter how practiced. This trial-by-trial form of learning has obvious advantages in a fast-changing world, but also seems prone to drift away from spot-on accuracy as those small adjustments go too far.
Keyword: Learning & Memory
Link ID: 20193 - Posted: 10.11.2014
by Andy Coghlan Ten years after the death of everyone's favourite Superman, Christopher Reeve, his son Matthew Reeve is pushing ahead with a spine-tingling clinical trial You're planning a large study of a paralysis treatment that has already helped four young men. What will it entail? This study will include 36 people with spinal cord injuries who will be treated with epidural stimulation – a technique in which a device is used to apply electrical current to the spinal cord. If we see the same results as we did in the first four, this therapy could have a profound impact on thousands of people living with paralysis. It has the potential to become as commonplace as the pacemaker is for cardiac patients. How well has the treatment worked for the four men who have already received it? Prior to epidural stimulation, they had all suffered chronic injuries caused by completely severed spinal cords. All four have seen dramatic improvements, including the ability to voluntarily move their toes, feet, ankles and legs, and even stand at times, when the device is on. One unexpected bonus has been the return of autonomic function, such as bladder and bowel control and sexual function. From a quality-of-life point of view, this is the biggest improvement. Also unexpectedly, these autonomic functions continue in all four men even when the device is switched off, although they still need it to stand, move their legs and do exercises. © Copyright Reed Business Information Ltd.
Posted by Rachel Dolhun, MD, The ability to quit smoking, especially “cold turkey” or on the first attempt, has been heralded as a marker of strong willpower and determination. But could the ease with which one eschews cigarettes also serve as an early sign of Parkinson’s disease (PD)? This is the conclusion drawn by Beate Ritz, MD, PhD, and colleagues from the University of California, Los Angeles in a recent study published in Neurology. Researchers compared lifelong tobacco use, use of nicotine substitutes, and individual’s rating of their difficulty in trying to quit tobacco among 1,808 Danish people with PD and 1,876 control volunteers. They found that those with PD were less inclined to ever pick up the smoking habit, but, even if they did, they were less likely to need nicotine replacement therapies and able to more effortlessly stop smoking cigarettes. Therefore, ease of quitting smoking may be a sign of early PD. This joins a short list of other symptoms — smell loss, constipation and REM sleep behavior disorder — that usually predate diagnosis and are strongly associated with PD. Physicians rely heavily on such information to help confirm the diagnosis of Parkinson’s, given that biomarkers, objective measurements of disease, are currently lacking. Research led by The Michael J. Fox Foundation is ongoing to identify biological markers of PD, which could help diagnose and treat people earlier. In the meantime, doctors must look for symptoms and behaviors to help identify Parkinson’s. Researchers have long known that tobacco use was linked to a lower risk of PD. An ongoing Foundation-funded study is investigating whether nicotine might guard against or slow the progression of PD.
By Elizabeth Pennisi Four years ago, Igor Spetic lost his right arm in an industrial accident. Doctors outfitted him with a prosthetic arm that restored some function, but they couldn't restore his sense of touch. Without it, simple tasks like picking up a glass or shaking hands became hit-or-miss propositions. The lack of touch also robs Spetic of basic pleasures. “I would love to feel my wife’s hand,” he says. In time, he may regain that pleasure: Two independent research teams have now equipped artificial hands with sensors that send signals to the wearer’s nerves to recreate this missing sense. The sensing technologies work only in the lab, but they have proved durable, and amputees who have tried them, including Spetic, say that they are effective. One technology advances the range of touch sensations available, while the other promises to enable touch through a better way to attach the prosthesis. “All of these results are very positive,” says Mandayam Srinivasan, a neuroengineer at the Massachusetts Institute of Technology in Cambridge, who was not involved in either project. “Each of them fills a piece of the puzzle in terms of [prosthesis] development.” Almost 40 years ago, researchers tried to provide sensory feedback by adding pressure sensors to prostheses that relayed the sensation through electrodes attached to nerves. But for the most part, they just made it seem like the hand was tingling. And durability has been an issue in such efforts, too. In February, Silvestro Micera, a neuroengineer at the Sant'Anna School of Advanced Studies in Pisa, Italy, and the Swiss Federal Institute of Technology in Lausanne and his team showed that it was possible for sensor-equipped prosthetic arms to gently or powerfully grab objects and even to distinguish a round from a square object. But the study lasted just 4 weeks, in part because of the delicate interface with the body. © 2014 American Association for the Advancement of Science.
by Colin Barras LOCKED in but not shut out: for the first time people who have lost the ability to move or talk because of a stroke may be able to communicate with their loved ones using a brain-computer interface. Brain injuries can leave people aware but almost completely paralysed, a condition called locked-in syndrome. Brain-computer interfaces (BCIs) can help some people communicate by passing signals from electrodes attuned to their brain activity as they watch a screen displaying letters. Subtle changes in neural activity let researchers know when a person wishes to select a particular on-screen item, allowing them to spell out messages by thought alone. Until now, BCIs have only been tested on healthy volunteers and people with amyotrophic lateral sclerosis, a neurodegenerative disease that leads to muscle wasting. But no one had tested whether the technology could help people locked in after a brain stem stroke. Now Eric Sellers and his colleagues at East Tennessee State University in Johnson City have tested the technique on a 68-year-old man. After more than a year of training he learned to communicate reliably via the BCI. He took the opportunity to thank his wife for her hard work, and to give his thoughts on gift purchases for his children (Science Translational Medicine, DOI: 10.1126/scitranslmed.3007801). © Copyright Reed Business Information Ltd.
|By Tara Haelle The first step to treating or preventing a disease is often finding out what drives it. In the case of neurodegenerative disorders, the discovery two decades ago of what drives them changed the field: all of them—including Alzheimer's, Parkinson's, Huntington's and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease)—involve the accumulation of misfolded proteins in brain cells. Typically when a protein misfolds, the cell destroys it, but as a person ages, this quality-control mechanism starts to fail and the rogue proteins build up. In Huntington's, for example, huntingtin protein—used for many cell functions—misfolds and accumulates. Symptoms such as muscular difficulties, irritability, declining memory, poor impulse control and cognitive deterioration accompany the buildup. Mounting evidence suggests that not only does the accumulation of misfolded proteins mark neurodegenerative disease but that the spread of the proteins from one cell to another causes the disease to progress. Researchers have seen misfolded proteins travel between cells in Alzheimer's and Parkinson's. A series of experiments reported in Nature Neuroscience in August suggests the same is true in Huntington's. In their tests, researchers in Switzerland showed that mutated huntingtin protein in diseased brain tissue could invade healthy brain tissue when the two were placed together. And when the team injected the mutated protein into a live mouse's brain, it spread through the neurons within a month—similar to the way prions spread, says Francesco Paolo Di Giorgio of the Novartis Institutes for BioMedical Research in Basel, who led the research. Prions are misfolded proteins that travel through the body and confer their disease-causing characteristics onto other proteins, as seen in mad cow disease. But it is not known if misfolded proteins involved in Huntington's convert other proteins as true prions do, according to Di Giorgio. © 2014 Scientific American
Link ID: 20181 - Posted: 10.08.2014
|By Tori Rodriguez Imagining your tennis serve or mentally running through an upcoming speech might help you perform better, studies have shown, but the reasons why have been unclear. A common theory is that mental imagery activates some of the same neural pathways involved in the actual experience, and a recent study in Psychological Science lends support to that idea. Scientists at the University of Oslo conducted five experiments investigating whether eye pupils adjust to imagined light as they do to real light, in an attempt to see whether mental imagery can trigger automatic neural processes such as pupil dilation. Using infrared eye-tracking technology, they measured the diameter of participants' pupils as they viewed shapes of varying brightness and as they imagined the shapes they viewed or visualized a sunny sky or a dark room. In response to imagined light, pupils constricted 87 percent as much as they did during actual viewing, on average; in response to imagined darkness, pupils dilated to 56 percent of their size during real perception. Two other experiments ruled out the possibility that participants were able to adjust their pupil size at will or that pupils were changing in response to mental effort, which can cause dilation. The finding helps to explain why imagined rehearsals can improve your game. The mental picture activates and strengthens the very neural circuits—even subconscious ones that control automated processes like pupil dilation—that you will need to recruit when it is time to perform. © 2014 Scientific American
Keyword: Learning & Memory
Link ID: 20176 - Posted: 10.08.2014
By Julie Rehmeyer Eight years ago, collapsed on a neurologist’s examining table, I asked a naive question that turned out to be at the center of a long-running controversy: “So what is chronic fatigue syndrome?” I had just been diagnosed with the illness, which for six years had been gradually overtaking me. A week earlier, I had woken up barely able to walk. Fatigue hardly described what I felt. Paralysis was more like it. My legs seemed to have been amputated and replaced with tubes of liquid concrete, and just shifting them on the table made me grunt like an Olympic weightlifter. My bones hurt; my brain felt like a swollen mass. Speaking required tracking down and spearing each word individually as it scampered away from me. I felt as capable of writing an article about science — my job — as of killing a rhino with my teeth. “We don’t understand it very well,” my neurologist said, his face blank. He could recommend no tests, no treatments, no other doctors. I came to understand that, for him, the term chronic fatigue syndrome meant “I can’t help you.” My neurologist’s understanding of the illness mirrored that of many doctors, who believe two things about CFS: that it’s probably psychosomatic and that there’s nothing doctors can do for it. One survey found that nearly half of doctors thought that CFS was or might be psychosomatic, and 58 percent said there wasn’t enough information available to help them diagnose it. An examination of medical textbooks found that CFS was underrepresented, even compared with less-prevalent illnesses.
By Gretchen Reynolds Encourage young boys and girls to run, jump, squeal, hop and chase after each other or after erratically kicked balls, and you substantially improve their ability to think, according to the most ambitious study ever conducted of physical activity and cognitive performance in children. The results underscore, yet again, the importance of physical activity for children’s brain health and development, especially in terms of the particular thinking skills that most affect academic performance. The news that children think better if they move is hardly new. Recent studies have shown that children’s scores on math and reading tests rise if they go for a walk beforehand, even if the children are overweight and unfit. Other studies have found correlations between children’s aerobic fitness and their brain structure, with areas of the brain devoted to thinking and learning being generally larger among youngsters who are more fit. But these studies were short-term or associational, meaning that they could not tease out whether fitness had actually changed the children’s’ brains or if children with well-developed brains just liked exercise. So for the new study, which was published in September in Pediatrics, researchers at the University of Illinois at Urbana-Champaign approached school administrators at public elementary schools in the surrounding communities and asked if they could recruit the school’s 8- and 9-year-old students for an after-school exercise program. This group was of particular interest to the researchers because previous studies had determined that at that age, children typically experience a leap in their brain’s so-called executive functioning, which is the ability to impose order on your thinking. Executive functions help to control mental multitasking, maintain concentration, and inhibit inappropriate responses to mental stimuli. © 2014 The New York Times Company