Chapter 11. Motor Control and Plasticity
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
|William Mullen, Tribune reporter Researchers at Northwestern University say they have discovered a common cause behind the mysterious and deadly affliction of amyotrophic lateral sclerosis, or Lou Gehrig's disease, that could open the door to an effective treatment. Dr. Teepu Siddique, a neuroscientist with Northwestern's Feinberg School of Medicine whose pioneering work on ALS over more than a quarter-century fueled the research team's work, said the key to the breakthrough is the discovery of an underlying disease process for all types of ALS. The discovery provides an opening to finding treatments for ALS and could also pay dividends by showing the way to treatments for other, more common neurodegenerative diseases such as Alzheimer's, dementia and Parkinson's, Siddique said. The Northwestern team identified the breakdown of cellular recycling systems in the neurons of the spinal cord and brain of ALS patients that results in the nervous system slowly losing its ability to carry brain signals to the body's muscular system. Without those signals, patients gradually are deprived of the ability to move, talk, swallow and breathe. "This is the first time we could connect (ALS) to a clear-cut biomedical mechanism," Siddique said. "It has really made the direction we have to take very clear and sharp. We can now test for drugs that would regulate this protein pathway or optimize it, so it functions as it should in a normal state."
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20459 - Posted: 01.08.2015
|By Lindsey Konkel For 28 years, Bill Gilmore lived in a New Hampshire beach town, where he surfed and kayaked. “I’ve been in water my whole life,” he said. “Before the ocean, it was lakes. I’ve been a water rat since I was four.” Now Gilmore can no longer swim, fish or surf, let alone button a shirt or lift a fork to his mouth. Earlier this year, he was diagnosed with amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters. About five years ago, doctors at a New Hampshire hospital noticed a pattern in their ALS patients—many of them, like Gilmore, lived near water. Since then, researchers at Dartmouth-Hitchcock Medical Center have identified several ALS hot spots in lake and coastal communities in New England, and they suspect that toxic blooms of blue-green algae—which are becoming more common worldwide—may play a role. Now scientists are investigating whether breathing a neurotoxin produced by the algae may raise the risk of the disease. They have a long way to go, however: While the toxin does seem to kill nerve cells, no research, even in animals, has confirmed the link to ALS. As with all ALS patients, no one knows what caused Bill Gilmore’s disease. He was a big, strong guy—a carpenter by profession. One morning in 2011, his arms felt weak. “I couldn’t pick up my tools. I thought I had injured myself,” said Gilmore, 59, who lived half his life in Hampton and now lives in Rochester, N.H. © 2014 Scientific American
by Andy Coghlan To catch agile prey on the wing, dragonflies rely on the same predictive powers we use to catch a ball: that is, anticipating by sight where the ball will go and readying body and hand to snatch it from mid-air. Until now, dragonflies were thought to catch their prey without this predictive skill, instead blindly copying every steering movement made by their prey, which can include flies and bees. Now, sophisticated laboratory experiments have tracked the independent body and eye movements of dragonflies as they pursue prey, showing for the first time that dragonflies second guess where their prey will fly to next and then steer their flight accordingly. Throughout the pursuit, they lock on to their target visually while they orient their bodies and flight path for ultimate interception, rather than copying each little deviation in their prey's flight path in the hope of ultimately catching up with it. "The dragonfly lines up its body axis in the flight direction of the prey, but keeps the eyes in its head firmly fixed on the prey," says Anthony Leonardo of the Howard Hughes Medical Institute in Ashburn, Virginia. "It enables the dragonfly to catch the prey from beneath and behind, the prey's blind spot," he says. © Copyright Reed Business Information Ltd.
Link ID: 20412 - Posted: 12.13.2014
Injections of a new drug may partially relieve paralyzing spinal cord injuries, based on indications from a study in rats, which was partly funded by the National Institutes of Health. The results demonstrate how fundamental laboratory research may lead to new therapies. “We’re very excited at the possibility that millions of people could, one day, regain movements lost during spinal cord injuries,” said Jerry Silver, Ph.D., professor of neurosciences, Case Western Reserve University School of Medicine, Cleveland, and a senior investigator of the study published in Nature. Every year, tens of thousands of people are paralyzed by spinal cord injuries. The injuries crush and sever the long axons of spinal cord nerve cells, blocking communication between the brain and the body and resulting in paralysis below the injury. On a hunch, Bradley Lang, Ph.D., the lead author of the study and a graduate student in Dr. Silver’s lab, came up with the idea of designing a drug that would help axons regenerate without having to touch the healing spinal cord, as current treatments may require. “Originally this was just a side project we brainstormed in the lab,” said Dr. Lang. After spinal cord injury, axons try to cross the injury site and reconnect with other cells but are stymied by scarring that forms after the injury. Previous studies suggested their movements are blocked when the protein tyrosine phosphatase sigma (PTP sigma), an enzyme found in axons, interacts with chondroitin sulfate proteoglycans, a class of sugary proteins that fill the scars.
Link ID: 20394 - Posted: 12.04.2014
Stem cells can be used to heal the damage in the brain caused by Parkinson's disease, according to scientists in Sweden. They said their study on rats heralded a "huge breakthrough" towards developing effective treatments. There is no cure for the disease, but medication and brain stimulation can alleviate symptoms. Parkinson's UK said there were many questions still to be answered before human trials could proceed. The disease is caused by the loss of nerve cells in the brain that produce the chemical dopamine ,which helps to control mood and movement. To simulate Parkinson's, Lund University researchers killed dopamine-producing neurons on one side of the rats' brains. They then converted human embryonic stem cells into neurons that produced dopamine. Parkinson's Disease Parkinson's is one of the commonest neurodegenerative diseases These were injected into the rats' brains, and the researchers found evidence that the damage was reversed. There have been no human clinical trials of stem-cell-derived neurons, but the researchers said they could be ready for testing by 2017. Malin Parmar, associate professor of developmental and regenerative neurobiology, said: "It's a huge breakthrough in the field [and] a stepping stone towards clinical trials." A similar method has been tried in a limited number of patients. It involved taking brain tissue from multiple aborted foetuses to heal the brain. Clinical trials were abandoned after mixed results, but about a third of the patients had foetal brain cells that functioned for 25 years. BBC © 2014
Link ID: 20292 - Posted: 11.08.2014
By Kelly Servick Using data from old clinical trials, two groups of researchers have found a better way to predict how amyotrophic lateral sclerosis (ALS) progresses in different patients. The winning algorithms—designed by non-ALS experts—outperformed the judgments of a group of ALS clinicians given the same data. The advances could make it easier to test whether new drugs can slow the fatal neurodegenerative disease. The new work was inspired by the so-called ALS Prediction Prize, a joint effort by the ALS-focused nonprofit Prize4Life and Dialogue for Reverse Engineering Assessments and Methods, a computational biology project whose sponsors include IBM, Columbia University, and the New York Academy of Sciences. Announced in 2012, the $50,000 award was designed to bring in experts from outside the ALS field to tackle the notoriously unpredictable illness. Liuxia Wang, a data analyst at the marketing company Sentrana in Washington, D.C., was used to helping companies make business decisions based on big data sets, such as information about consumer choices, but says she “didn’t know too much about this life science thing” until she got an unusual query from a client. One of the senior managers she worked with revealed that her son had just been diagnosed with ALS and wondered if Sentrana’s analytics could apply to patient data, too. When Wang set out to investigate, she found the ALS Prediction Prize. The next step, she said, was to learn something about ALS. The disease destroys the neurons that control muscle movement, causing gradual paralysis and eventually killing about half of patients within 3 years of diagnosis. But the speed of its progression varies widely. About 10% of patients live a decade or more after being diagnosed. That makes it hard for doctors to answer patients’ questions about the future, and it’s a big problem for testing new ALS treatments. © 2014 American Association for the Advancement of Science.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20278 - Posted: 11.04.2014
|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
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 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 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.