By JAMES GORMAN SEATTLE — To hear Michael Dickinson tell it, there is nothing in the world quite as wonderful as a fruit fly. And it’s not because the fly is one of the most important laboratory animals in the history of biology, often used as a simple model for human genetics or neuroscience. “I don’t think they’re a simple model of anything,” he says. “If flies are a great model, they’re a great model for flies. “These animals, you know, they’re not like us,” he says, warming to his subject. “We don’t fly. We don’t have a compound eye. I don’t think we process sensory information the same way. The muscles that they use are just incredibly much more sophisticated and interesting than the muscles we use. “They can taste with their wings,” he adds, as his enthusiasm builds. “No one knows any reason why they have taste cells on their wing. Their bodies are just covered with sensors. This is one of the most studied organisms in the history of science, and we’re still fundamentally ignorant about many features of its basic biology. It’s like having an alien in your lab. “And,” he says, pausing, seeming puzzled that the world has not joined him in open-mouthed wonder for his favorite creature, “they can fly!” If he had to define his specialty, Dr. Dickinson, 50, who counts a MacArthur “genius” award among his honors, would call himself a neuroethologist. As such, he studies the basis of behavior in the brain at the University of Washington, in Seattle. In practice he is a polymath of sorts who has targeted the fruit fly, Drosophila melanogaster, and its flying behavior for studies that involve physics, mathematics, neurobiology, computer vision, muscle physiology and other disciplines. © 2013 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 18762 - Posted: 10.08.2013

Lying in bed, unable to move a muscle, so-called locked-in patients have few ways to communicate with the outside world. But researchers have now found a way to use the widening and narrowing of the pupils to send a message, potentially helping these patients break the silence. Doctors use the constriction of pupils under bright light to test whether a patient’s brain stem is intact. But our pupils also show the opposite response—dilation—based on our thoughts and emotions, says Wolfgang Einhäuser, a neurophysicist at Philipps University of Marburg in Germany. Einhäuser had been struggling to interpret changes in pupil size during decision-making when he began to wonder about a different application. He contacted Steven Laureys, a member of the Coma Science Group at the University Hospital of Liège in Belgium, to explore how the pupil could be used to communicate a choice. Laureys works with locked-in patients, who have normal mental acuity but are paralyzed and unable to express thoughts to those around them. Many can control only the muscles that move their eyes; some, not even that. They can learn to communicate using EEG technology, in which electrodes on the scalp detect changes in brain activity. But applying the electrode cap is time-consuming, and the equipment is expensive, Einhäuser says. “If you imagine doing that every day, basically to communicate, that’s troublesome.” To find a different technique, Einhäuser, Laureys, and colleagues reached back in time. “The pieces have been there since the early ’60s,” Einhäuser says. A 1964 study showed that our pupils dilate when we perform mental arithmetic, like attempting to multiply 27 and 15 with no pencil and paper, and that harder tasks led to more dramatic dilation. The team set up a camera and a laptop to explore this automatic response. © 2012 American Association for the Advancement of Science.

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 14: Attention and Higher Cognition
Link ID: 18466 - Posted: 08.06.2013

Brendan Maher Hugh Rienhoff says that his nine-year-old daughter, Bea, is “a fire cracker”, “a tomboy” and “a very sassy, impudent girl”. But in a forthcoming research paper, he uses rather different terms, describing her hypertelorism (wide spacing between the eyes) and bifid uvula (a cleft in the tissue that hangs from the back of the palate). Both are probably features of a genetic syndrome that Rienhoff has obsessed over since soon after Bea’s birth in 2003. Unable to put on much muscle mass, Bea wears braces on her skinny legs to steady her on her curled feet. She is otherwise healthy, but Rienhoff has long worried that his daughter’s condition might come with serious heart problems. Rienhoff, a biotech entrepreneur in San Carlos, California, who had trained as a clinical geneticist in the 1980s, went from doctor to doctor looking for a diagnosis. He bought lab equipment so that he could study his daughter’s DNA himself — and in the process, he became a symbol for the do-it-yourself biology movement, and a trailblazer in using DNA technologies to diagnose a rare disease (see Nature 449, 773–776; 2007). “Talk about personal genomics,” says Gary Schroth, a research and development director at the genome-sequencing company Illumina in San Diego, California, who has helped Rienhoff in his search for clues. “It doesn’t get any more personal than trying to figure out what’s wrong with your own kid.” Now nearly a decade into his quest, Rienhoff has arrived at an answer. Through the partial-genome sequencing of his entire family, he and a group of collaborators have found a mutation in the gene that encodes transforming growth factor-β3 (TGF-β3). Genes in the TGF-β pathway control embryogenesis, cell differentiation and cell death, and mutations in several related genes have been associated with Marfan syndrome and Loeys–Dietz syndrome, both of which have symptomatic overlap with Bea’s condition. The mutation, which has not been connected to any disease before, seems to be responsible for Bea’s clinical features, according to a paper to be published in the American Journal of Medical Genetics. © 2013 Nature Publishing Group,

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 18329 - Posted: 07.01.2013

by Mara Hvistendahl and Martin Enserink A mysterious group of viruses known for their circular genome has been detected in patients with severe disease on two continents. In papers published independently this week, researchers report the discovery of agents called cycloviruses in Vietnam and in Malawi. The studies suggest that the viruses—one of which also widely circulates in animals in Vietnam—could be involved in brain inflammation and paraplegia, but further studies are needed to confirm a causative link. The discovery in Vietnam grew out of a frustrating lack of information about the causes of some central nervous system (CNS) infections such as encephalitis and meningitis, which can be fatal or leave lasting damage. "There are a lot of severe cases in the hospitals here, and very often we can't come to a diagnosis," says H. Rogier van Doorn, a clinical virologist with the Oxford University Clinical Research Unit in the Hospital for Tropical Diseases, Ho Chi Minh City. Extensive diagnostic tests turn up pathogens in only about half of patients with such infections, he says. Van Doorn and colleagues in Vietnam and at the University of Amsterdam's Academic Medical Center hoped that they might uncover new pathogens using a powerful new technique called next-generation sequencing. The group sequenced all the genetic material in cerebrospinal fluid (CSF) samples taken from more than 100 patients with undiagnosed CNS infections. One sample batch returned a promising lead: a viral sequence belonging to the Circoviridae family. © 2010 American Association for the Advancement of Science

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 18311 - Posted: 06.25.2013

The paralyzing syndrome Guillain-Barré syndrome isn't linked to receiving common vaccines, according to a U.S. study. Concerns about the association of Guillain-Barré syndrome with vaccines have "flourished" since there was a hint of an increased risk after the 1976 swine flu vaccine campaign. It hasn’t been clearly linked since then. The syndrome is an acute inflammatory disease that results in destruction of a nerve’s myelin sheath and some nerves, which in severe cases can progress to complete paralysis and even death. Researchers from the U.S. Centers for Disease Control and Prevention and Kaiser Permanente Vaccine Study Center in Oakland, Calif. looked back at cases of GBS over 13 years in the state that were confirmed by a neurologist who reviewed the medical records. In the 13-year study period 415 patients were confirmed with GBS only 25 had received a vaccine within six weeks before onset of the disease. "In summary, this study did not find any association between influenza vaccine or any other vaccine and development of GBS within six weeks following vaccination," Dr. Roger Baxter, co-director of the Kaiser Permanente Vaccine Study Center and his co-authors concluded in Monday's online issue of Clinical Infectious Diseases. © CBC 2013

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18306 - Posted: 06.25.2013

By ALLISON HERSH LONDON I’M in line at the supermarket holding three items close to my chest. But I might as well be juggling my Kleenex box, toothpaste tube and an orange. Because — as you’d surely notice if you were behind me in line — I‘m bent forward at a sharp angle, which makes holding things difficult. I know you don’t want to stare, but you do. Maybe you think you’re being considerate when you say, apropos of nothing, “You look like you’re in pain.” Well, thanks, I am — but I’ll resist replying the way I want (“You look like you’re having a bad hair day”). I’m sorry. I know you mean well. Anyway it’s my turn at the register which means I’m closer to being at home where I can lie down and wait for the spasms to subside. Besides, if I told you what my issue was, you would probably shrug and reply that you’d never heard of it. There aren’t any public service announcements about it or telethons. No Angelina Jolies to bravely inform the world. Just people like me, in supermarket checkout lines. And this, I realize, is at the core of a problem that extends beyond me and my condition and that affects the way all of us respond to illnesses, some of which are the subject of public attention — and resources — and some of which are not. I have dystonia, a neurological disorder. Some years ago, for reasons no one knows, the muscles in my back and neck began to spasm involuntarily; the spasms multiply quickly, fatigue the muscles and force the body into repetitive movements and awkward postures like mine. There is no cure, only treatment options like deep brain stimulation, which requires a surgery I underwent last year as a last resort. © 2013 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 5: The Sensorimotor System
Link ID: 18171 - Posted: 05.20.2013

Voluntary movements involve the coordinated activation of two brain pathways that connect parts of deep brain structures called the basal ganglia, according to a study in mice by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health. The findings, which challenge the classical view of basal ganglia function, were published online in Nature on Jan. 23. “By improving our understanding of how the basal ganglia control movements, these findings could aid in the development of treatments for disorders in which these circuits are disrupted, such as Parkinson’s disease, Huntington’s disease and addiction,” says NIAAA Acting Director Kenneth R. Warren, Ph.D. The predominant model of basal ganglia function proposes that direct and indirect pathways originating in a brain region called the striatum have opposing effects on movement. Activity of neurons in the direct pathway is thought to promote movement, while activity in the indirect pathway is thought to inhibit movement. Newer models, however, suggest that co-activation of these pathways is necessary to synchronize basal ganglia circuits during movement. “Testing these models has been difficult due to the lack of methods to measure specific neurons in the direct and indirect pathways in freely moving animals,” explains first author Guohong Cui, Ph.D., of the NIAAA Laboratory for Integrated Neuroscience (LIN). To overcome these difficulties, Dr. Cui and colleagues devised a new approach for measuring the activity of neurons deep within the brain during complex behaviors. Their technique uses fiber optic probes implanted in the mouse brain striatum to measure light emissions from neurons engineered to glow when activated.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 17729 - Posted: 01.29.2013

By Sandra G. Boodman, For the first decade of his life, every doctor who saw Jack DeWitt inevitably zeroed in on the harrowing circumstances of his premature birth. Delivered by emergency Caesarean section in December 1999, doctors universally ascribed his developmental problems to his being born six weeks early, said his mother, Ruth DeWitt. “It always came back to that.” When Jack’s walking became odd at age 5, doctors chalked it up to a mild form of cerebral palsy that can occur in children born too soon. “We were okay with it,” his mother said, because mild cerebral palsy would not “affect the length of his life or his enjoyment of it.” Jack’s parents were also reassured by his ability to catch up; with help, he mastered various skills: jumping, walking and writing in cursive. But by age 10, when his ability to walk badly deteriorated, a reevaluation by his doctors resulted in a very different diagnosis and prognosis. “We had all those years of feeling that he was a normal, healthy kid with some challenges,” his mother recalled. Discovering what was really wrong has been a heavy blow, magnified by Jack’s perceptive awareness of its implications. Ruth DeWitt, who lives with her family in Howell, Mich., outside Ann Arbor, was in the hospital undergoing a test for preeclampsia, or pregnancy-induced hypertension, when she began hemorrhaging, a sign of placental abruption. The life-threatening condition occurs when the placenta prematurely detaches from a woman’s uterus. Rushed into surgery, Jack was born weighing 3 pounds, 9 ounces, and was transferred to the neonatal intensive care unit at the University of Michigan Medical Center. Small but strong, he needed oxygen but no ventilator, and he came home 15 days later. © 1996-2012 The Washington Post

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 17615 - Posted: 12.18.2012

By ANDREW POLLACK An experimental drug preserved and even improved the walking ability of boys with Duchenne muscular dystrophy in a clinical trial, raising hopes that the first effective treatment for the disease may be on the horizon. Boys with the disease who received the highest dose of the drug had a slightly improved ability to walk after 48 weeks of treatment, the drug’s developer, Sarepta Therapeutics, announced Wednesday. By contrast, the boys who received a placebo suffered a sharp decline in how well they could walk. The drug, called eteplirsen, also appeared to restore levels of the crucial protein that muscular dystrophy patients lack to about half of normal levels, Sarepta said. “I think this changes the entire playing field for muscular dystrophy,” said Dr. Jerry R. Mendell, director of the gene therapy and muscular dystrophy programs at Nationwide Children’s Hospital in Columbus, Ohio, and the lead investigator in the trial. There are many caveats. The trial had only 12 patients, with only four receiving the high dose and four the placebo, and the data has not been reviewed by experts. It is also unclear how long the effects of the drug would last or if safety issues would arise with longer treatment. Also, eteplirsen would be appropriate for only about 13 percent to 15 percent of Duchenne patients, those with the particular genetic mutation the drug is meant to counteract. However, a similar approach might work for some other mutations. © 2012 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 17331 - Posted: 10.04.2012

by Jessica Hamzelou When something goes wrong in your brain, you'd think it would be a good idea to get rid of the problem. Turns out, sometimes it's best to keep hold of it. By preventing faulty proteins from being destroyed, researchers have delayed the symptoms of a degenerative brain disorder. SNAP25 is one of three proteins that together make up a complex called SNARE, which plays a vital role in allowing neurons to communicate with each other. In order to work properly, all the proteins must be folded in a specific way. CSP alpha is one of the key proteins that ensures SNAP25 is correctly folded. Cells have a backup system to deal with any misfolded proteins – they are destroyed by a bell-shaped enzyme called a proteasome, which pulls the proteins inside itself and breaks them down. People with a genetic mutation that affects the CSP alpha protein – and its ability to correctly fold SNAP25 – can develop a rare brain disorder called neuronal ceroid lipofuscinosis (NCL). The disorder causes significant damage to neurons – people affected gradually lose their cognitive abilities and struggle to move normally. To find out what role proteasomes might play in NCL, Manu Sharma and his colleagues at Stanford University in California blocked the enzyme in mice that were bred to lack CSP alpha. "We weren't sure what would happen," says Sharma. Either the misfolded SNAP25 would accumulate and harm the cells, or some of the misfolded proteins may work well enough to retain some of their function. © Copyright Reed Business Information Ltd.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 17173 - Posted: 08.16.2012

by Nicola Guttridge Whether a tree branch or a computer mouse is the target, reaching for objects is fundamental primate behaviour. Neurons in the brain prepare for such movements, and this neural activity can now be deciphered, allowing researchers to predict what movements will occur. This discovery could help us develop prosthetic limbs that can be controlled by thought alone. To find out what goes on in the brain when we reach for things, biomedical engineers Daniel Moran and Thomas Pearce at Washington University in St Louis, Missouri, trained two rhesus macaques to participate in a series of exercises. When the monkeys reached for items, electrodes measured the activity of neurons in their dorsal premotor cortex, a region of the brain that is involved in the perception of movement. The monkeys were trained to reach for a virtual object on a screen to receive a reward. In some tasks the monkeys had to reach directly for an object, in others they had to reach around an obstacle to get to the target. Impulsive grab Moran and Pearce managed to identify the neural activity corresponding with several aspects of the planned movement, such as angle of reach, hand position and the final target location. The findings could one day allow the design of prosthetic limbs that can be controlled with thought alone, which is "one of the reasons we did the study", says Moran. © Copyright Reed Business Information Ltd.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 17073 - Posted: 07.21.2012

By Scicurious Think about what happens when you walk. Really THINK about it. What does it take to walk? Well, your feet and legs have to move (far more complicated than they look), which means your muscles have to move, which means your nerves have to control your muscles, which means your brain has to send the signals in the first place. All of this is based on further information, knowing where you are in space and where you’re going, how fast you need to get there. And then there’s even more! How do you know where you are? How do you know how fast you’re going? How do you know which direction you’re headed? And behind all of this are thousands and millions of neurons firing, together and separately. And underlying THAT are thousands of biochemical processes which allow the neurons to fire… …now take that walking speed, and make it a run. The sheer number of neurobiological processes and number of things that need to happen to make you walk into your workplace every morning is the kind of thing that makes neuroscientists stop in their tracks with wonder. And today, we’re going to talk about a paper that may have worked out a tiny piece of how the brain might deal with things like increased speed. How does your brain keep up with your feet? By running a little faster. To understand how this works. We need to talk about two major things: place neurons, and oscillatory networks. © 2012 Scientific American

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 14: Attention and Higher Cognition
Link ID: 17059 - Posted: 07.18.2012

By Sandra G. Boodman, Liisa Ecola lay on the sofa in the living room of her Capitol Hill home counting the hours until she could see a specialist who, she fervently hoped, would tell her why she could no longer keep her eyes open. For several months, the 42-year-old transportation policy researcher for Rand had been squinting, even in the dark. Her puzzled optometrist had suggested she consult a neuro-ophthalmologist, a doctor who specializes in diseases of the eye originating in the central nervous system. Ecola had waited weeks to get an appointment, which was scheduled for Dec. 15, 2010. But the day before, Ecola recalled, “I opened my laptop and my eyes snapped shut.” To her horror, she discovered that her eyes would stay open only for a few minutes at a time. Panicked, she called the specialist to confirm the appointment, only to discover that she wouldn’t be seeing him at all. The office had no record of her. “I was really scared,” said Ecola, who called it the lowest moment in her quest for a diagnosis. “I was convinced I had a brain tumor.” Her problem turned out to be far less serious and far more easily treated. The following day she lucked into an appointment with another specialist, who explained the odd constellation of symptoms that had left her unable to leave her house. For several years, Ecola had suffered an unexplained, intermittent facial tic, in which she scrunched up her face as if she were tasting something awful. Because it seemed linked to stress, Ecola consulted a behavioral therapist in an effort to banish it through habit reversal training — using relaxation exercises and making a conscious effort to stop the tic. Until early 2010, the treatment usually worked, and Ecola seemed able to control it. © 1996-2012 The Washington Post

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 7: Vision: From Eye to Brain
Link ID: 16696 - Posted: 04.24.2012

By LISA SANDERS, M.D., Columnist On Thursday, we challenged Well readers to figure out the diagnosis for a 27-year-old woman with an odd walk and slowly progressive weakness of her hips and thighs. The correct diagnosis is… Adult-onset Tay-Sachs disease The first person to get it right was Jason Maley, a third-year medical student at Tulane University. His answer came in just after 1 a.m., an hour after the case was posted. He says that all the clues were there; he just had to put it all together. He’s planning to go into internal medicine. (I certainly hope that he will!) Tay-Sachs is an inherited disease in which the inability to get rid of discarded parts of the cell membrane causes the death of certain nerve cells. There are several forms of the disease. The most common affects infants. Babies born with this version of the disease usually die by age 4. Another form of the disease affects children who usually die before reaching adulthood. Late-onset Tay-Sachs, the form of the disease this patient has, doesn’t manifest itself until adolescence or young adulthood and causes a slow loss of strength and coordination. While the form seen in children was first described over a century ago, this version wasn’t recognized until the 1970s. Patients with this form of the disease can get rid of some but not all of the fatty components of the cell wall and so have a much slower rate of cell death and disability. The degree of disability varies widely in this group, and there are patients who have the disease but appear to be completely asymptomatic. For many with this disease, life expectancy is normal, but most eventually require a wheelchair. © 2012 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16621 - Posted: 04.07.2012

By ABIGAIL ZUGER, M.D. Just when it seems long past time for the age of memoir to be over — just when it seems impossible that any ailing person with literary inclinations could find anything new to say about illness, and the list of not-to-be-missed “patients are people too” books should be closed and locked — yet another book comes along. And despite all the above, no one with even a passing interest in the experience of illness should miss Robert C. Samuels’s “Blue Water, White Water,” a memoir drafted about 30 years ago and published without fanfare a few months ago; it stands head and shoulders above the crowd. The details are slightly obsolete, to be sure: Mr. Samuels endured his many months of dire illness tethered to a respirator back in the 1980s, the Stone Age of modern intensive-care treatment. Nonetheless, his story from the wrong end of the tubes is timeless; the technology may evolve briskly, but the experience changes glacially, if at all. A former beat reporter for The New York World-Telegram & Sun, Mr. Samuels covers his own story like a pro. He was healthy, 44, just returned from a trip around the world in December 1981, when he got out of bed one morning with a weak left leg. He wandered into the local emergency room half convinced he was imagining things. By the next day he was completely paralyzed with a respirator breathing for him: Guillain-Barré syndrome, an autoimmune disease, was rapidly and efficiently stripping his motor nerves of their myelin sheathing, short-circuiting them all. Only his eyes still moved a little, from left to right. Nothing was wrong with his brain. © 2012 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 16511 - Posted: 03.13.2012

Scottish research has shown it could be possible to reverse the muscle damage seen in children with a form of motor neurone disease. Spinal muscular atrophy (SMA) - 'floppy baby syndrome' - is the leading genetic cause of death in children. It affects one in 6,000 births, but 50% of those with the most severe form die before the age of two. The University of Edinburgh mouse study suggests a drug could boost levels of a protein and so reverse muscle damage. Children with SMA experience progressive muscle wastage, loss of mobility and motor function. Now 13, he was diagnosed at the age of three. "My wife first knew there was something wrong when he was two. He was just walking funnily. "But he wasn't diagnosed until the third time she took him to the doctors. "Initially there was a question as to whether it was SMA or muscular dystrophy. "We'd heard of muscular dystrophy - but not SMA. BBC © 2012

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 16437 - Posted: 02.27.2012

By Scicurious Humans walk well. More to the point, we walk EFFICIENTLY. As we evolved to walk upright, we also evolved to do so with great economy, expending fewer calories at an optimal walking pace, but then expending more calories when we either speed up or slow down. We also may be economically efficient runners as well as walkers, we’re average for mammals, but our long legs and ability for those legs to take repeated strain suggests we may be on the efficient end of primates (and we’re some of the BEST long distance runners on the planet, so we can preen a bit over that one). The jury is still out on running, but as far as walking goes we are the most efficient at a moderate speed (roughly 5 km/hr, or 3.1 miles/hour for men, a relatively brisk walk of 20 min a mile). So we’re good walkers, or at least economic ones. But the question is, what MAKES for this efficiency? How exactly are we burning fewer calories at a specific walking pace? Ideally, this means that our muscles, like our bodies overall, are at their most efficient at a moderate walking pace. The calories burned over time are the result of the total metabolic rate of all the muscles that produce locomotion. So since your metabolism is minimized at a moderate walking pace, creating the most efficiency, it would make theoretical sense that your individual MUSCLES are also minimizing their metabolism at that moderate walking pace, and the cumulative effect is one of energy efficiency. Theoretically, it makes sense. At a certain pace, you’re overall burning fewer calories and not working as hard, so your individual muscles must also not be working as hard. Right? Well…possibly wrong. © 2012 Scientific American,

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16204 - Posted: 01.03.2012

by Curtis Abraham, Uganda Large areas of northern Uganda are experiencing an outbreak of nodding syndrome, a mysterious disease that causes young children and adolescents to nod violently when they eat food. The disease, which may be an unusual form of epilepsy, could be linked to the parasitic worm responsible for river blindness, a condition that affects some 18 million people, most of them in Africa. The current outbreaks are concentrated in the districts of Kitgum, Pader and Gulu. In Pader alone, 66 children and teenagers have died. More than 1000 cases were diagnosed between August and mid-December. Onchocerca volvulus, a nematode worm that causes river blindness, is known to infest all three affected districts. Nearly all the children with nodding syndrome are thought to live near permanent rivers, another hint of a connection with river blindness. The link is not clear cut, though. "We know that [Onchocerca volvulus] is involved in some way, but it is a little puzzling because [the worm] is fairly common in areas that do not have nodding disease," says Scott Dowell, who researches paediatric infectious diseases and is lead investigator into nodding syndrome with the US Centers for Disease Control and Prevention. There is no known cure for nodding syndrome, so Uganda's Ministry of Health has begun using anticonvulsants such as sodium valproate to treat its signs and symptoms. Meanwhile the disease is continuing to spread, say Janet Oola, Pader's health officer, and Sam William Oyet, the district's medical entomology officer. © Copyright Reed Business Information Ltd.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 16177 - Posted: 12.23.2011

By Lonnae O’Neal Parker, That morning, I noticed first that I couldn’t spit. I was brushing my teeth, but I couldn’t close my lips around the toothbrush, and my mouth didn’t seem to work right. Weird, I thought, but I quickly put it out of my mind. I was on assignment for The Post and probably I was just tired from the overnight drive from Prince George’s County to Greensboro, N.C. Perhaps it was the two glasses of wine a couple of nights before. Maybe it was the flu. Whatever it was, I was sure I didn’t have time for it. I was traveling to Atlanta with two guys I was writing about, and as we grabbed breakfast before the second leg of our drive, my weird-face feeling intensified. Then my right eye began to ache, and a sudden fear iced my spine. I stepped outside the restaurant to stare at my reflection in the car window, and I couldn’t process what I was seeing. I couldn’t move the right side of my face, and my eye ached because I couldn’t close it. The parking lot started to swim, and I willed myself not to faint. “Something’s wrong with my face,” I told the guys haltingly. “I have to go to the emergency room when we get to Atlanta.” But they insisted on taking me immediately in Greensboro. I’m glad they did. “My face is paralyzed, and I can’t blink. I think I’m having a stroke,” I told the receptionist at the Moses Cone Urgent Care Center, though it all felt so surreal. I’m only 44, and I’m healthy! © 1996-2011 The Washington Post

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15859 - Posted: 10.01.2011

By JoNel Aleccia Health writer A cluster of cases of a rare illness that can lead to nerve damage and paralysis has been identified along a small stretch of the United States-Mexico border. An outbreak of food poisoning is the likely culprit, health officials in the two countries said. At least two dozen people in Yuma County, Ariz., and San Luis Rio Colorado, Sonora, Mexico, have been diagnosed with Guillain-Barré Syndrome in the past month, with some left drastically impaired by the illness that triggers the body's auto-immune reaction. “It’s really attacking the nerves,” said Shoana Anderson, office chief of infectious disease at the Arizona Department of Health Services. “All of the patients I’ve seen are not able to walk.” Most of the victims, including 17 from Mexico and seven from the U.S., are adults who range in age from 40 to 70, although younger people also have been affected, Anderson said. Some patients have muscle weakness in their upper bodies as well as in their legs, she added. It's not clear how quickly they may recover. Guillian-Barré Syndrome, or GBS, typically affects only about 1 in 100,000 people, according to government health statistics, so a cluster of 24 cases is cause for alarm, officials said. Although the condition often resolves on its own, recovery can be long and painful. And in rare cases, the illness can cause permanent disability and even death. © 2011 msnbc.com

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15599 - Posted: 07.26.2011