Chapter 5. The Sensorimotor System
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by Jessica Hamzelou A single session of nerve stimulation has improved the movement of people with spinal cord injuries. Mimicking the passage of nerve signals by stimulating a muscle as well as the brain has boosted recovery and helped people to regain better control of their movements. Voluntary movement requires a signal from the brain, which is passed down the spinal cord and then to neurons in muscles. Damage to the spinal cord can interrupt this pathway, resulting in paralysis. To improve the control of movement in people with these injuries, Monica Perez and Karen Bunday at the University of Pittsburgh in Pennsylvania used electrical and magnetic stimulation to strengthen the connection between two nerves involved in voluntary movement of the index finger. The pair used transcranial magnetic stimulation (TMS), a non-invasive technique in which a magnetic field alters brain activity, to target the corticospinal tract. This bundle of nerves connects movement-associated parts of the brain with the spinal cord. "The corticospinal tract plays a major role in the recovery of motor function in spinal cord injury," says Perez. Just 1 to 2 milliseconds after stimulating the brain, they used an electrode to stimulate a nerve that innervates an index-finger muscle – mimicking normal brain-to-muscle nerve signalling. © Copyright Reed Business Information Ltd.
Link ID: 17554 - Posted: 12.01.2012
By JAMES GORMAN For the first time, researchers at the Massachusetts Institute of Technology report, brain imaging has been able to show in living patients the progressive damage Parkinson’s disease causes to two small structures deep in the brain. The new technique confirms some ideas about the overall progress of the disease in the brain. But the effects of Parkinson’s vary in patients, the researchers said, and in the future, the refinement in imaging may help doctors monitor how the disease is affecting different people and adjust treatment accordingly. The outward symptoms and progress of Parkinson’s disease — tremors, stiffness, weakness — have been well known since James Parkinson first described them in 1817. But its progress in the brain has been harder to document. Some of the structures affected by the disease have been buried too deep to see clearly even with advances in brain imaging. An important recent hypothesis about how the disease progresses was based on the examinations of brains of patients who had died. Now, a group of scientists at M.I.T. and Massachusetts General Hospital report that they have worked out a way to combine four different sorts of M.R.I. to get clear pictures of damage to two brain structures in people living with Parkinson’s. In doing so, they have added support to one part of the recent hypothesis, which is that the disease first strikes an area involved in movement and later progresses to a higher part of the brain more involved in memory and attention. Suzanne Corkin, a professor emerita of behavioral neuroscience at M.I.T. and the senior author on the paper published online Monday in The Archives of Neurology, said that this progression was part of the hypothesis put forward in 2003 by Heiko Braak, a German neuroscientist, based on autopsies. © 2012 The New York Times Company
Link ID: 17544 - Posted: 11.27.2012
By Maggie Fox, NBC News Seniors who fit in the most daily physical activity – from raking leaves to dancing – can have more gray matter in important brain regions, researchers reported on Monday. The scientists have images that show people who were the most active had 5 percent more gray matter than people who were the least active. Having more little gray brain cells translates into a lower risk of Alzheimer’s disease, other studies have shown. “People really want to know what they can do to reduce their risk of Alzheimer’s disease,” said Dr. Cyrus Raji of the University of California in Los Angeles, who presented his team’s findings to a meeting of the Radiological Society of North America. Raji’s team looked at the records of 876 adults, who were recruited into a larger study on heart health starting in 1989. They all got magnetic resonance imaging (MRI) brain scans in 1998 and 1999, when they were on average 78 years old, and filled out detailed questionnaires on exercise and other types of activity. Most of them were a little overweight – with a body mass index or BMI of 27. People with BMIs above 25 are considered overweight and at 30 they are considered clinically obese. The researchers found a huge difference in the amount of activity people reported. They were asked about everything from cycling to yard work, dancing and bicycle riding. © 2012 NBCNews.com
Link ID: 17543 - Posted: 11.27.2012
David Perlman With an ultimate goal to help paralyzed patients achieve a degree of independence, Stanford brain researchers report they have taken a promising step forward in efforts to link nerve centers in the human brain with computers controlled by only a person's thought. In their latest development, the Stanford scientists have successfully enabled a pair of rhesus monkeys to move a virtual cursor across a computer screen merely by thinking about their response to human commands. The monkeys' ability to manipulate a cursor without using a mouse is based on a powerful new algorithm, a mathematical computing program devised by Vikash Gilja, a Stanford electrical engineer and computer scientist. Four years ago, neurosurgeons at Brown University and Massachusetts General Hospital had demonstrated a simpler version of an algorithm that enabled completely paralyzed humans with implanted sensors in their brains to command a cursor to move erratically toward targets on a computer screen. But with Gilja's algorithm, called ReFit, the monkeys showed they could aim their virtual cursor, a moving dot of light, at another bright light on a computer screen, and hold it steadily there for 15 seconds - far more precisely than the humans four years ago. With the new algorithm, they were able to perform their thinking tasks faster and more accurately as they sat comfortably in a chair facing the computer. The development is "a big step toward clinically useful brain-machine technology that has faster, smoother, and more natural movements" than anything before it, said James Gnadt of the National Institute of Neurological Disorders and Stroke. © 2012 Hearst Communications Inc.
Link ID: 17537 - Posted: 11.26.2012
By David Pogue Okay, great: we can control Our phones with speech recognition and our television sets with gesture recognition. But those technologies don't work in all situations for all people. So I say, forget about those crude beginnings; what we really want is thought recognition. As I found out during research for a recent NOVA episode, it mostly appears that brain-computer interface (BCI) technology has not advanced very far just yet. For example, I tried to make a toy helicopter fly by thinking “up” as I wore a $300 commercial EEG headset. It barely worked. Such “mind-reading” caps are quick to put on and noninvasive. They listen, through your scalp, for the incredibly weak remnants of electrical signals from your brain activity. But they're lousy at figuring out where in your brain they originated. Furthermore, the headset software didn't even know that I was thinking “up.” I could just as easily have thought “goofy” or “shoelace” or “pickle”—whatever I had thought about during the 15-second training session. There are other noninvasive brain scanners—magnetoencephalography, positron-emission tomography and near-infrared spectroscopy, and so on—but each also has its trade-offs. Of course, you can implant sensors inside someone's skull for the best readings of all; immobilized patients have successfully manipulated computer cursors and robotic arms using this approach. Still, when it comes to controlling everyday electronics, brain surgery might be a tough sell. © 2012 Scientific American,
Link ID: 17518 - Posted: 11.21.2012
Scientists have reversed paralysis in dogs after injecting them with cells grown from the lining of their nose. The pets had all suffered spinal injuries which prevented them from using their back legs. The Cambridge University team is cautiously optimistic the technique could eventually have a role in the treatment of human patients. The study is the first to test the transplant in "real-life" injuries rather than laboratory animals. The only part of the body where nerve fibres continue to grow in adults is the olfactory system. Found in the at the back of the nasal cavity, olfactory ensheathing cells (OEC) surround the receptor neurons that both enable us to smell and convey these signals to the brain. The nerve cells need constant replacement which is promoted by the OECs. For decades scientists have thought OECs might be useful in spinal cord repair. Initial trials using OECs in humans have suggested the procedure is safe. In the study, funded by the Medical Research Council and published in the neurology journal Brain, the dogs had olfactory ensheathing cells from the lining of their nose removed. These were grown and expanded for several weeks in the laboratory. BBC © 2012
By JUSTIN HECKERT The girl who feels no pain was in the kitchen, stirring ramen noodles, when the spoon slipped from her hand and dropped into the pot of boiling water. It was a school night; the TV was on in the living room, and her mother was folding clothes on the couch. Without thinking, Ashlyn Blocker reached her right hand in to retrieve the spoon, then took her hand out of the water and stood looking at it under the oven light. She walked a few steps to the sink and ran cold water over all her faded white scars, then called to her mother, “I just put my fingers in!” Her mother, Tara Blocker, dropped the clothes and rushed to her daughter’s side. “Oh, my lord!” she said — after 13 years, that same old fear — and then she got some ice and gently pressed it against her daughter’s hand, relieved that the burn wasn’t worse. “I showed her how to get another utensil and fish the spoon out,” Tara said with a weary laugh when she recounted the story to me two months later. “Another thing,” she said, “she’s starting to use flat irons for her hair, and those things get superhot.” Tara was sitting on the couch in a T-shirt printed with the words “Camp Painless But Hopeful.” Ashlyn was curled on the living-room carpet crocheting a purse from one of the skeins of yarn she keeps piled in her room. Her 10-year-old sister, Tristen, was in the leather recliner, asleep on top of their father, John Blocker, who stretched out there after work and was slowly falling asleep, too. The house smelled of the homemade macaroni and cheese they were going to have for dinner. A South Georgia rainstorm drummed the gutters, and lightning illuminated the batting cage and the pool in the backyard. Without lifting her eyes from the crochet hooks in her hands, Ashlyn spoke up to add one detail to her mother’s story. “I was just thinking, What did I just do?” she said. © 2012 The New York Times Company
Keyword: Pain & Touch
Link ID: 17507 - Posted: 11.19.2012
By Laura Sanders The insidious spread of an abnormal protein may be behind Parkinson’s disease, a study in mice suggests. A harmful version of the protein crawls through the brains of healthy mice, killing brain cells and damaging the animals’ balance and coordination, researchers report in the Nov. 16 Science. If a similar process happens in humans, the results could eventually point to ways to stop Parkinson’s destruction in the brain. “I really think that this model will increase our ability to come up with Parkinson’s disease therapies,” says study coauthor Virginia Lee of the University of Pennsylvania Perelman School of Medicine in Philadelphia. The new study targets a hallmark of Parkinson’s disease — clumps of a protein called alpha-synuclein. The clumps, called Lewy bodies, pile up inside nerve cells in the brain and cause trouble, particularly in cells that make dopamine, a chemical messenger that helps control movement. Death of these dopamine-producing cells leads to the characteristic tremors and muscle rigidity seen in people with Parkinson’s. Lee and her team injected alpha-synuclein into the brains of healthy mice. After 30 days, the protein had spread to connected brain regions, suggesting that rouge alpha-synuclein moves from cell to cell, the scientists found. Months later, the spreading was even more extensive. © Society for Science & the Public 2000 - 2012
Link ID: 17499 - Posted: 11.17.2012
Women with migraines did not appear to experience a decline in cognitive ability over time compared to those who didn’t have them, according to a nine-year follow up study funded by the National Institutes of Health. The study also showed that women with migraine had a higher likelihood of having brain changes that appeared as bright spots on magnetic resonance imaging (MRI), a type of imaging commonly used to evaluate tissues of the body. "The fact that there is no evidence of cognitive loss among these women is good news," said Linda Porter, Ph.D., pain health science policy advisor in the Office of the Director at the National Institute of Neurological Disorders and Stroke (NINDS), which provided funding for the study. "We’ve known for a while that women with migraine tend to have these brain changes as seen on MRI. This nine-year study is the first of its kind to provide long-term follow-up looking for associated risk." "An important message from the study is that there seems no need for more aggressive treatment or prevention of attacks," said Mark C. Kruit, M.D., Ph.D., one of the principal investigators, and a neuroradiologist from Leiden University Medical Center, the Netherlands, which led the study. Dr. Kruit and associates evaluated MRIs for changes in the white matter, brainstem, and cerebellum that appeared on the scans as bright spots known as hyperintensities. Previous studies have shown an association between such hyperintensities and risk factors for atherosclerotic disease, increased risk of stroke and cognitive decline.
Keyword: Pain & Touch
Link ID: 17488 - Posted: 11.14.2012
by Greg Miller Seeing someone yawn or hearing someone laugh makes you likely to follow suit. The same goes for scratching an itch. Now, for the first time, researchers have investigated the neural basis of contagious itch, identifying several brain regions whose activity predicts how susceptible people are to feeling itchy when they see someone else scratch. Researchers in the United Kingdom showed volunteers video clips of people scratching an arm or a spot on their chest. Sure enough, subjects reported feeling more itchy, and most scratched themselves at least once during the experiment. When a subset of the volunteers watched the videos inside an functional magnetic resonance imaging scanner, the scans revealed activity in several of the same brain regions known to fire up in response to an itch-inducing histamine injection. Activity in three of these areas correlated with subjects' self-reported itchiness, the team reports online today in the Proceedings of the National Academy of Sciences. Personality tests suggest that the trait that best predicts susceptibility to contagious itch is neuroticism, not empathy, as some researchers have suggested. © 2010 American Association for the Advancement of Science
By Ben Thomas In the early 1990s, a team of neuroscientists at the University of Parma made a surprising discovery: Certain groups of neurons in the brains of macaque monkeys fired not only when a monkey performed an action – grabbing an apple out of a box, for instance – but also when the monkey watched someone else performing that action; and even when the monkey heard someone performing the action in another room. In short, even though these “mirror neurons” were part of the brain’s motor system, they seemed to be correlated not with specific movements, but with specific goals. Over the next few decades, this “action understanding” theory of mirror neurons blossomed into a wide range of promising speculations. Since most of us think of goals as more abstract than movements, mirror neurons confront us with the distinct possibility that those everyday categories may be missing crucial pieces of the puzzle – thus, some scientists propose that mirror neurons might be involved in feelings of empathy, while others think these cells may play central roles in human abilities like speech. Some doctors even say they’ve discovered new treatments for mental disorders by reexamining diseases through the mirror neuron lens. For instance, UCLA’s Marco Iacoboni and others have put forth what Iacoboni called the “broken mirror hypothesis” of autism – the idea that malfunctioning mirror neurons are likely responsible for the lack of empathy and theory of mind found in severely autistic people. © 2012 Scientific American,
Danish researchers Krogh and colleagues randomly 115 assigned depressed people to one of two exercise programs. One was a strenuous aerobic workout - cycling for 30 minutes, 3 times per week, for 3 months. The other was various stretching exercises. The idea was that stretching was a kind of placebo control group on the grounds that, while it is an intervention, it's not the kind of exercise that gets you fit. It doesn't burn many calories, it doesn't improve your cardiovascular system, etc. Aerobic exercise is the kind that's most commonly been proposed as having an antidepressant effect. So what happened? Not much. Both groups got less depressed but there was zero difference between the two conditions. The cyclists did get physically fitter than the stretchers, losing more weight and improving on other measures. But they didn't feel any better. If this is true, it might mean that the antidepressant effects of aerobic exercise are psychological rather than physical - it's about the idea of 'exercising', not the process of becoming fitter. While many trials have found modest beneficial effects of exercise vs a "control condition", the control condition was often just doing nothing much - such as being put on a waiting-list. So the placebo effect or the motivational benefits of 'doing something', rather than the effects of exercise per se, could be behind it. In the current study though the stretching avoided that problem.
Link ID: 17463 - Posted: 11.07.2012
By Meghan Rosen Michael McAlpine’s shiny circuit doesn’t look like something you would stick in your mouth. It’s dashed with gold, has a coiled antenna and is glued to a stiff rectangle. But the antenna flexes, and the rectangle is actually silk, its stiffness melting away under water. And if you paste the device on your tooth, it could keep you healthy. The electronic gizmo is designed to detect dangerous bacteria and send out warning signals, alerting its bearer to microbes slipping past the lips. Recently, McAlpine, of Princeton University, and his colleagues spotted a single E. coli bacterium skittering across the surface of the gadget’s sensor. The sensor also picked out ulcer-causing H. pylori amid the molecular medley of human saliva, the team reported earlier this year in Nature Communications. At about the size of a standard postage stamp, the dental device is still too big to fit comfortably in a human mouth. “We had to use a cow tooth,” McAlpine says, describing test experiments. But his team plans to shrink the gadget so it can nestle against human enamel. McAlpine is convinced that one day, perhaps five to 10 years from now, everyone will wear some sort of electronic device. “It’s not just teeth,” he says. “People are going to be bionic.” McAlpine belongs to a growing pack of tech-savvy scientists figuring out how to merge the rigid, brittle materials of conventional electronics with the soft, curving surfaces of human tissues. Their goal: To create products that have the high performance of silicon wafers — the crystalline material used in computer chips — while still moving with the body. © Society for Science & the Public 2000 - 2012
Link ID: 17455 - Posted: 11.05.2012
Kerry Grens Fewer than five percent of patients prescribed narcotics to treat chronic pain become addicted to the drugs, according to a new analysis of past research. The finding suggests that concerns about the risk of becoming addicted to prescription painkillers might be "overblown," said addiction specialist Dr. Michael Fleming at Northwestern University's Feinberg School of Medicine. "If you're a person that doesn't have a history of addiction and doesn't have any major psychiatric problems, narcotics are relatively safe as long as your doctor doesn't give you too much and uses the right medication," Fleming, who was not involved in the new study, told Reuters Health. Some recent research has concluded the same thing, but another expert remained skeptical about the new report because many of the studies it included were not considered the best quality research, and they varied widely in their results. Advertise | AdChoices "I think the jury's still out" on how worrisome prescription opioid addiction is, said Joseph Boscarino of the Geisinger Clinic in Danville, Pennsylvania, who studies pain and addiction. Opioid painkillers, which include oxycodone, fentanyl and morphine, have only recently become available for patients with chronic pain, said Boscarino, who was not part of the new study. © 2012 NBCNews.com
By Katherine Harmon With a juicy insect dinner perched on a leaf above the water, what is a hungry little archer fish down below to do? Knock it down with a super-powered, super-precise jet of water that packs six times the power the fish could generate with its own muscles, according to new findings published online October 24 in PLoS ONE. The stunning spitting power of the amazing archer fish (Toxotes jaculatrix) was first described in the 18th century. The creature lives in mostly in mangrove forests and estuaries where insects are prevalent—above water, that is. And these tasty treats are not easily knocked off of the plants that hang over the archer fish’s territory. The insects, such as grasshoppers, can hang on with a force some 10 times their own body weight. So the archer fish has developed an impressive strategy for fetching food that not many other fish can reach. Its water jet can target and dislodge a single insect so that it falls into the water for the fish to eat. Just how the fish manages to do this—and in less than a second—had remained a mystery. Many scientists figured that the source must be a special organ in the fish’s body. “The origin of the effectiveness of the jet squirted by the archer fish has been searched for inside of the fish for nearly 250 years,” Alberto Vailati, a physicist at the University of Milan and co-author of the new paper, said in a prepared statement. © 2012 Scientific American
By ANAHAD O'CONNOR Remaining physically active as you age, a new study shows, may help protect parts of your brain from shrinking, a process that has been linked to declines in thinking and memory skills. Physical exercise not only protected against such age-related brain changes, but also had more of an effect than mentally and socially stimulating activities. In the new report, published in the journal Neurology, a team at the University of Edinburgh followed more than 600 people, starting at age 70. The subjects provided details on their daily physical, mental and social activities. Three years later, using imaging scans, the scientists found that the subjects who engaged in the most physical exercise, including walking several times a week, had less shrinkage and damage in the brain’s white matter, which is considered the “wiring” of the brain’s communication system. The relationship remained even after the researchers controlled for things like age, health status, social class and I.Q. As far as mental exercise, “we can only say we found no benefit in our sample,” said Dr. Alan J. Gow, an author of the study and a senior research fellow at Edinburgh. He added: “There might be associations earlier in the life course. Such activities also have important associations with well-being and quality of life, so we would certainly agree it is important for older adults to continue to pursue them.” Copyright 2012 The New York Times Company
Link ID: 17427 - Posted: 10.27.2012
by Helen Thomson Paralysis may no longer mean life in a wheelchair. A man who is paralysed from the trunk down has recovered the ability to stand and move his legs unaided thanks to training with an electrical implant. Andrew Meas of Louisville, Kentucky, says it has changed his life (see "I suddenly noticed I can move my pinkie", below). The stimulus provided by the implant is thought to have either strengthened persistent "silent" connections across his damaged spinal cord or even created new ones, allowing him to move even when the implant is switched off. The results are potentially revolutionary, as they indicate that the spinal cord is able to recover its function years after becoming damaged. Previous studies in animals with lower limb paralysis have shown that continuous electrical stimulation of the spinal cord below the area of damage allows an animal to stand and perform locomotion-like movements. That's because the stimulation allows information about proprioception – the perception of body position and muscle effort – to be received from the lower limbs by the spinal cord. The spinal cord, in turn, allows lower limb muscles to react and support the body without any information being received from the brain (Journal of Neuroscience, doi.org/czq67d). Last year, Susan Harkema and Claudia Angeli at the Frazier Rehab Institute and University of Louisville in Kentucky and colleagues tested what had been learned on animals in a man who was paralysed after being hit by a car in 2006. He was diagnosed with a "motor complete" spinal lesion in his neck, which means that no motor activity can be recorded below the lesion. © Copyright Reed Business Information Ltd
Link ID: 17420 - Posted: 10.25.2012
Why some people respond to treatments that have no active ingredients in them may be down to their genes, a study in the journal PLoS ONE suggests. The so-called "placebo effect" was examined in 104 patients with irritable bowel syndrome (IBS) in the US. Those with a particular version of the COMT gene saw an improvement in their health after placebo acupuncture. The scientists warn that while they hope their findings will be seen in other conditions, more work is needed. Edzard Ernst, a professor of complementary medicine at the University of Exeter, said: "This is a fascinating but very preliminary result. "It could solve the age-old question of why some individuals respond to placebo, while others do not. "And if so, it could impact importantly on clinical practice. "But we should be cautious - the study was small, we need independent replications, and we need to know whether the phenomenon applies just to IBS or to all diseases." Gene variants The placebo effect is when a patient experiences an improvement in their condition while undergoing an inert treatment such as taking a sugar pill or, in this case, placebo acupuncture, where the patient believes they are receiving acupuncture but a sham device prevents the needles going into their body. BBC © 2012
By Michelle Roberts Health editor, BBC News online Exercising in your 70s may stop your brain from shrinking and showing the signs of ageing linked to dementia, say experts from Edinburgh University. Brain scans of 638 people past the age of retirement showed those who were most physically active had less brain shrinkage over a three-year period. Exercise did not have to be strenuous - going for a walk several times a week sufficed, the journal Neurology says. But giving the mind a workout by doing a tricky crossword had little impact. The study found no real brain-size benefit from mentally challenging activities, such as reading a book, or other pastimes such as socialising with friends and family. When the researchers examined the brain's white matter - the wiring that transmits messages round the brain - they found that the people over the age of 70 who were more physically active had fewer damaged areas than those who did little exercise. And they had more grey matter - the parts of the brain where the messages originate. Experts already know that our brains tend to shrink as we age and that this shrinkage is linked to poorer memory and thinking. BBC © 2012
Link ID: 17410 - Posted: 10.23.2012
By Dan Cossins There’s a new suspect in the search for the causes of Parkinson’s disease—deformities in the nuclear membrane of neural stem cells. Scientists observed the same defects, caused by a single gene mutation, in brain tissue samples from deceased Parkinson’s patients, suggesting that nuclear deterioration—and the mutation that drives it—could play a role in the pathology of the disease. The study, published today (October 17) in Nature, also shows that correcting the mutation reverses this phenotype, pointing to new ways to treat this cause of neurodegeneration. “I don’t recall anyone ever suggesting this as a major phenotype [for Parkinson’s], so that’s really quite a big new direction for the field,” said Mark Cookson, a neuroscientist at the National Institutes of Health in Bethesda, Maryland, who did not participate in the study. Parkinson’s disease has traditionally been attributed to a loss of dopamine-generating neurons, which leads to the degenerative muscle control that is characteristic of the disease. But Parkinson’s also causes many other sensory problems, which cannot be explained by a dopaminergic mechanism. Over the past 5 years, several groups have shown that disruption of the structure of the nuclear envelope—the lipid bilayer that separates nucleus from cytoplasm—is correlated with aging and certain age-related pathologies in the human brain, though the precise role of nuclear defects in the diseases remained unclear. Meanwhile, since 2004 scientists including Cookson have demonstrated that a mutation in the luceine-rich repeat kinase 2 (LRRK2) gene is correlated with Parkinson’s. However, the molecular and cellular mechanisms by which the LRRK2 mutation might drive disease progression remained a mystery. © 1986-2012 The Scientist
Link ID: 17392 - Posted: 10.20.2012