Links for Keyword: Movement Disorders

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By Lisa Sanders, M.D On Thursday we challenged Well readers to solve the difficult case of twin sisters who, in the prime of youth, developed a weakness that forced them to use their arms to rise from a chair. Nearly 300 of you wrote in with thoughts on this difficult case. Many of you recognized that this was likely to be a genetic disorder, though I greatly admired the “House”-ian thinking that led to a host of possible reasons why two sisters, living in different states, might develop the same symptoms independent of their shared DNA. It took this patient, Katie Buryk, four years to get her answer, which was: Late onset Tay-Sachs disease Although several of you made this difficult diagnosis, the first to do so was George Bonadurer, a second year medical student at Mayo Medical School in Rochester, Minn. He says he recently read about this disease in a book of unusual cases that had come to the Mayo clinic for help. This is actually Mr. Bonadurer’s second win of this contest. Strong work! Tay-Sachs disease was first identified by two physicians, independently, in the 1880s. Dr. Warren Tay was an ophthalmologist in London. Dr. Bernard Sachs was a neurologist in New York City. Each described a disease in infants that caused profound weakness, blindness and, usually by age 4, death. Careful consideration of cases over the following decades showed that the disease was inherited and often seen in children of Ashkenazi descent. Studying the patterns of inheritance, it became clear that both parents had to have the abnormal gene and that each of their children would have a one in four chance of being born with the disease. The terrible manifestations of the disease derive from an inherited inability to make an essential protein in the brain. This protein acts to break down discarded components of the cells. Without this protein, these discarded cell parts accumulate, interrupting normal nerve and brain cell functioning. This mechanism and the missing protein was identified in 1969, allowing for the development of a test for carriers. Since the development of this test, the incidence of Tay-Sachs in the United States has dropped by 90 percent. © 2015 The New York Times Company

Related chapters from BP7e: 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 13: Memory, Learning, and Development
Link ID: 20902 - Posted: 05.09.2015

By Emily Dwass In the frightening world of brain tumors, “benign” is a good word to hear. But even a nonmalignant tumor can be dangerous — especially if, as in my case, it goes undetected, becoming a stealth invader. “Anecdotally, we often hear about women who were originally misdiagnosed — sometimes for years,” said Tom Halkin, a spokesman for the patient advocacy nonprofit National Brain Tumor Society. When I developed tingling in my limbs 12 years ago, two Los Angeles neurologists diagnosed Guillain-Barré syndrome, a disorder in which the immune system attacks the nervous system. The symptoms of numbness and weakness ebbed and flowed for three years. Then one day, I couldn’t slide my right foot into a flip-flop. This got me a ride in a magnetic resonance imaging machine, which revealed a brain mass the size of a tennis ball. It was a benign meningioma, a tumor that grows in the membranes surrounding the brain and spinal cord. After the diagnosis, I consulted with Los Angeles surgeons. “We’re going to cut your head open like a pumpkin,” one told me. I chose someone else, who had a stellar reputation, who was compassionate, and who did not compare my skull to a squash. “You’re cured,” he said as I awoke in the operating room. Recovery took about six weeks and went smoothly, except for my right foot, which remains partly numb. I relearned to walk and to drive with my left foot, using adaptive equipment. Had my tumor been diagnosed earlier, I might have avoided a large craniotomy and permanent foot issues. “It’s critical to find these tumors when they are small, when radiosurgery is an option, rather than when they are very big or produce a lot of symptoms, at which point it’s not optimal to treat them without doing open surgery,” said Dr. Susan Pannullo, the director of neuro-oncology and neurosurgical radiosurgery at NewYork-Presbyterian Hospital and Weill Cornell Medical College. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20854 - Posted: 04.28.2015

By Maggie Fox and Jane Derenowski A new strain of the polio-like EV-D68 may be causing the rare and mystifying cases of muscle weakness that's affected more than 100 kids across the United States, researchers reported Monday. They say they've found the strongest evidence yet that the virus caused the polio-like syndrome, but they also say it appears to be rare and might have to do with the genetic makeup of the patients. No other germ appears to be responsible, the team reports in the journal Lancet Infectious Diseases. But because most kids were tested many days after they first got sick, it may be impossible to ever know for sure. The body will have cleared the virus itself by then, said Dr. Charles Chiu of the University of California San Francisco, who helped conduct the study. "This is a virus that causes the common cold," Chiu told NBC News. "Parents don't bring their kids in until they are really sick. By that time, typically, the viral levels may be very, very low or undetectable." "Every single virus that we found in the children corresponded to new strain of the virus, called B-1." Enterovirus D68 (EV-D68) is one of about 100 different enteroviruses that infect people. They include polio but also a range of viruses that cause cold-like symptoms. Polio's the only one that is vaccinated against; before widespread vaccination it crippled 35,000 people a year in the United States.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20739 - Posted: 03.31.2015

By Sandra G. Boodman Catherine Cutter’s voice was her livelihood. A professor of food science at Penn State University, the microbiologist routinely lectured to large classes about food safety in the meat and poultry industries. But in 2008, after Cutter’s strong alto voice deteriorated into a raspy whisper, she feared her academic career might be over.How could she teach if her students could barely hear her? The classroom wasn’t the only area of Cutter’s life affected by her voicelessness. The mother of two teenagers, Cutter, now 52, recalls that she “couldn’t yell — or even talk” to her kids and would have to knock on a wall or countertop to get their attention. Social situations became increasingly difficult as well, and going to a restaurant was a chore. Using the drive-through at her bank or dry cleaner was out of the question because she couldn’t be heard. “I just retreated,” said Cutter, who sought assistance from nearly two dozen specialists for her baffling condition. The remedies doctors prescribed — when they worked at all — resulted in improvement that was temporary at best. For two years Cutter searched in vain for help. It arrived in the form of a neurosurgeon she consulted for a second opinion about potentially risky surgery to correct a different condition. He suggested a disorder that had never been mentioned, a diagnosis that proved to be correct — and correctable. Until then, “everyone had been looking in the wrong place,” Cutter said.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20605 - Posted: 02.24.2015

By Nick Lavars Keeping ourselves upright is something most of us shouldn't need to think a whole lot about, given we've been doing it almost our entire lives. But when it comes to dealing with more precarious terrain, like walking on ice or some sort of tight rope, you might think some pretty significant concentration is required. But researchers have found that even in our moments of great instability, our subconsciousness is largely responsible for keeping us from landing on our backsides. This is due to what scientists are describing as a mini-brain, a newly mapped bunch of neurons in the spinal cord which processes sensory information and could lead to new treatment for ailing motor skills and balance. "How the brain creates a sensory percept and turns it into an action is one of the central questions in neuroscience," says Martin Goulding, senior author of the research paper and professor at the Salk Institute. "Our work is offering a really robust view of neural pathways and processes that underlie the control of movement and how the body senses its environment. We’re at the beginning of a real sea change in the field, which is tremendously exciting.” The work of Goulding and his team focuses on how the body processes light touch, in particular the sensors in our feet that detect changes in the surface underfoot and trigger a reaction from the body. "Our study opens what was essentially a black box, as up until now we didn’t know how these signals are encoded or processed in the spinal cord," says Goulding. "Moreover, it was unclear how this touch information was merged with other sensory information to control movement and posture."

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 20561 - Posted: 02.07.2015

by Bethany Brookshire The windup before the pitch. The take-away before the golf swing. When you learn to pitch a softball, swing a golf club or shoot a basketball, you learn that preparation is important. You also learn about follow-through — the upswing of the golf club or the bend in the elbow after a softball pitch. It’s the preparation and the execution that get the ball across the plate, so why should we care about follow-through? In theory, once the ball has left your hands or sailed away from your club or racket, there’s no movement you could make that could affect what happens next. So while some follow-through might be important to diffuse the energy you just put into your shot, it shouldn’t really matter whether you swing your golf club up in an arc, whip it off to the side or club your opponent over the head with it. But follow-through is in fact quite important, and not just as an extension of the movements that preceded it. Consistent follow-through actually helps performance, reports neuroscientist Ian Howard and colleagues at the University of Plymouth in England. The finding gives coaches some science to back up their training, and helps scientists understand how the brain accesses motor memories. Howard has always been interested in how the brain learns movement tasks. “The first study we did looked at the preparation movement — you move backwards and then you move forwards [as in a golf swing],” he says. His lab found that the preparation before a particular motion had a strong effect on how our brains learn and recall motor movements. © Society for Science & the Public 2000 - 2015.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20549 - Posted: 02.05.2015

Ewen Callaway Since August 2014, more than 100 children and young adults in the United States have developed a mysterious paralysis. Many of them had fevers before losing strength in one or more limbs, and the cases coincided with a wider epidemic of a little-known respiratory pathogen. That virus, enterovirus D68 (EV-D68), is the leading candidate for the cause of the paralysis, which few children have recovered from. Yet researchers have not definitively linked the two, or determined how the virus could cause the children’s symptoms. A study published on 28 January in The Lancet1 that describes a cluster of cases from Denver, Colorado, strengthens the link, but falls short of providing a 'smoking gun'. Here is what we know about the virus — and what scientists are trying to find out. It belongs to the enterovirus family, which includes poliovirus and the pathogens that cause common colds; it is most similar to the rhinoviruses that cause respiratory infections. Although EV-D68 was first isolated in the 1960s, it is relatively uncommon among enteroviruses circulating worldwide. However, since August 2014, the virus has been linked to more than 1,000 respiratory infections in the United States, some of them severe, and France has seen cases, too. John Watson, a medical epidemiologist at the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, says that last year, EV-D68 was the predominant type of enterovirus circulating in the country. “That’s a first,” he says. Genome sequencing2 of viruses recovered from respiratory cases in St Louis, Missouri, shows that the EV-D68 strain circulating in the United States is most closely related to viruses that caused a pneumonia-like illness in three children in Thailand in 20113. What is the evidence that links EV-D68 to the cases of paralysis? © 2015 Nature Publishing Group

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20533 - Posted: 01.29.2015

By Peter Holley "Lynchian," according to David Foster Wallace, "refers to a particular kind of irony where the very macabre and the very mundane combine in such a way as to reveal the former's perpetual containment within the latter." Perhaps no other word better describes the onetime fate of Martin Pistorius, a South African man who spent more than a decade trapped inside his own body involuntarily watching "Barney" reruns day after day. "I cannot even express to you how much I hated Barney," Martin told NPR during the first episode of a new program on human behavior, "Invisibilia." The rest of the world thought Pistorius was a vegetable, according to NPR. Doctors had told his family as much after he'd fallen into a mysterious coma as a healthy 12-year-old before emerging several years later completely paralyzed, unable to communicate with the outside world. The nightmarish condition, which can be caused by stroke or an overdose of medication, is known as "total locked-in syndrome," and it has no cure, according to the National Institute of Neurological Disorders and Stroke. In a first-person account for the Daily Mail, Pistorius described the period after he slipped into a coma: I was completely unresponsive. I was in a virtual coma but the doctors couldn’t diagnose what had caused it. When he finally did awaken in the early 1990s, around the age of 14 or 15, Pistorius emerged in a dreary fog as his mind gradually rebooted itself.

Related chapters from BP7e: 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 Consciousness
Link ID: 20484 - Posted: 01.14.2015

By CATHERINE SAINT LOUIS A nationwide outbreak of a respiratory virus last fall sent droves of children to emergency departments. The infections have now subsided, as researchers knew they would, but they have left behind a frightening mystery. Since August, 103 children in 34 states have had an unexplained, poliolike paralysis of an arm or leg. Each week, roughly three new cases of so-called acute flaccid myelitis are still reported to the Centers for Disease Control and Prevention. Is the virus, called enterovirus 68, really the culprit? Experts aren’t certain: Unexplained cases of paralysis in children happen every year, but they are usually scattered and unrelated. After unusual clusters of A.F.M. appeared this fall, enterovirus 68 became the leading suspect, and now teams of researchers are racing to figure out how it could have led to such damage. “It’s unsatisfying to have an illness and not know what caused it,” said Dr. Samuel Dominguez, an epidemiologist and an infectious disease specialist at Children’s Hospital Colorado, which has had the largest cluster of patients. For many families, the onset of persistent limb paralysis has been a bewildering experience. Roughly two thirds of the children with A.F.M. have reported some improvement, according to the C.D.C. About a third show none. Only one child has fully recovered. In August, Jack Wernick, a first grader in Kingsport, Tenn., developed a “crummy little cold,” said his father, Dan Wernick, who works for a paper company. It seemed ordinary, until Jack complained that his right arm was heavy, his face began drooping and pain started shooting down his right leg. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20477 - Posted: 01.13.2015

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

Related chapters from BP7e: 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 13: Memory, Learning, and Development
Link ID: 20259 - Posted: 10.29.2014

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.

Related chapters from BP7e: 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 13: Memory, Learning, and Development
Link ID: 20190 - Posted: 10.11.2014

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.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20175 - Posted: 10.08.2014

By CATHERINE SAINT LOUIS Driven by a handful of reports of poliolike symptoms in children, federal health officials have asked the nation’s physicians to report cases of children with limb weakness or paralysis along with specific spinal-cord abnormalities on a magnetic resonance imaging test. As a respiratory illness known as enterovirus 68 is sickening thousands of children from coast to coast, officials are trying to figure out if the weakness could be linked to the virus. The emergence of several cases of limb weakness among children in Colorado put doctors on alert in recent months. The Centers for Disease Control and Prevention issued an advisory on Friday, and this week, other cases of unexplained muscle weakness or paralysis came to light in Michigan, Missouri and Massachusetts. The C.D.C. is investigating the cases of 10 children hospitalized at Children’s Hospital Colorado with unexplained arm or leg weakness since Aug. 9. Some of the children, who range in age from 1 to 18, also developed symptoms like facial drooping, double vision, or difficulty swallowing or talking. Four of them tested positive for enterovirus 68, also known as enterovirus D68, which has recently caused severe respiratory illness in children in 41 states and the District of Columbia. One tested positive for rhinovirus, which can cause the common cold. Two tested negative. Two patients’ specimens are still being processed; another was never tested. It is unclear whether the muscle weakness is connected to the viral outbreak. “It’s one possibility we are looking at, but certainly not the only possibility,” said Mark Pallansch, director of the C.D.C.’s division of viral diseases. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20150 - Posted: 10.02.2014

By Jocelyn Kaiser A virus that shuttles a therapeutic gene into cells has strengthened the muscles, improved the motor skills, and lengthened the lifespan of mice afflicted with two neuromuscular diseases. The approach could one day help people with a range of similar disorders, from muscular dystrophy to amyotrophic lateral sclerosis, or ALS. Many of these diseases involve defective neuromuscular junctions—the interface between neurons and muscle cells where brain signals tell muscles to contract. In one such disease, a form of familial limb-girdle myasthenia, people carry two defective copies of the gene called DOK7, which codes for a protein that’s needed to form such junctions. Their hip and shoulder muscles atrophy over many years, and some eventually have trouble breathing or end up in a wheelchair. Mice similarly missing a properly working Dok7 gene are severely underweight and die within a few weeks. In the new study, researchers led by molecular biologist Yuji Yamanashi of the University of Tokyo first injected young mice engineered to have defective Dok7 with a harmless virus carrying a good copy of the Dok7 gene, which is expressed only in muscle. Within about 7 weeks, the rodents recovered. Their muscle cells cranked out the DOK7 protein, and under a microscope their muscles had larger neuromuscular junctions than those of untreated mice with defective Dok7. What’s more, the mice grew to a healthy body weight and had essentially normal scores on tests of motor skills and muscle strength. © 2014 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 20096 - Posted: 09.19.2014

Ian Sample, science editor Scientists have prevented muscle wastage in mice with a form of muscular dystrophy by editing the faulty gene that causes the disease. The radical procedure could not be performed in humans, but researchers believe the work raises hopes for future gene-editing therapies to stop the disease from progressing in people. Duchenne muscular dystrophy is caused by mutations in a gene on the X chromosome and affects around one in 3,500 boys. Because girls have two X chromosomes they tend not to be affected, but can be carriers of the disease. The pivotal gene is used to make a protein called dystrophin which is crucial for muscle fibre strength. Without the protein, muscles in the body, including the heart and skeletal muscles, weaken and waste away. Most patients die by the age of 25 from breathing or heart problems. Researchers in the US used a powerful new gene-editing procedure called CRISPR to correct mutations in the dystrophin gene in mice that were destined to develop the disease. They extracted mouse embryos from their mothers and injected them with the CRISPR biological machinery, which found and corrected the faulty gene. After the injections, the mouse embryos were reimplanted in females and carried to term. Tests on the mice found that the therapy helped to restore levels of dystrophin, and that their skeletal muscle performed normally, even when only 17% of their cells contained corrected genes. The procedure could not be done in humans, but the proof-of-principle experiment demonstrates that correcting only a small proportion of cells could lead to a dramatic improvement for patients. © 2014 Guardian News and Media Limited

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 19966 - Posted: 08.16.2014

Dr. Mark Saleh Bell's palsy is a neurological condition frequently seen in emergency rooms and medical offices. Symptoms consist of weakness involving all muscles on one side of the face. About 40,000 cases occur annually in the United States. Men and women are equally affected, and though it can occur at any age, people in their 40s are especially vulnerable. The facial weakness that occurs in Bell's palsy prevents the eye of the affected side from blinking properly and causes the mouth to droop. Because the eyelid doesn't close sufficiently, the eye can dry and become irritated. Bell's palsy symptoms progress fairly rapidly, with weakness usually occurring within three days. If the progression of weakness is more gradual and extends beyond a week, Bell's palsy may not be the problem, and other potential causes should be investigated. Those with certain medical conditions, such as diabetes or pregnancy, are at greater risk of developing Bell's palsy, and those who have had one episode have an 8 percent chance of recurrence. Bell's palsy is thought to occur when the seventh cranial (facial) nerve becomes inflamed. The nerve controls the muscles involved in facial expression and is responsible for other functions, including taste perception, eye tearing and salivation. The cause of the inflammation is unknown, although the herpes simplex virus and autoimmune inflammation are possible causes. © 2014 Hearst Communications, Inc.

Related chapters from BP7e: 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: 19637 - Posted: 05.20.2014

by Clare Wilson A genetic tweak can make light work of some nervous disorders. Using flashes of light to stimulate modified neurons can restore movement to paralysed muscles. A study demonstrating this, carried out in mice, lays the path for using such "optogenetic" approaches to treat nerve disorders ranging from spinal cord injury to epilepsy and motor neuron disease. Optogenetics has been hailed as one of the most significant recent developments in neuroscience. It involves genetically modifying neurons so they produce a light-sensitive protein, which makes them "fire", sending an electrical signal, when exposed to light. So far optogenetics has mainly been used to explore how the brain works, but some groups are exploring using it as therapy. One stumbling block has been fears about irreversibly genetically manipulating the brain. In the latest study, a team led by Linda Greensmith of University College London altered mouse stem cells in the lab before transplanting them into nerves in the leg – this means they would be easier to remove if something went wrong. "It's a very exciting approach that has a lot of potential," says Ziv Williams of Harvard Medical School in Boston. Greensmith's team inserted an algal gene that codes for a light-responsive protein into mouse embryonic stem cells. They then added signalling molecules to make the stem cells develop into motor neurons, the cells that carry signals to and from the spinal cord to the rest of the body. They implanted these into the sciatic nerve – which runs from the spinal cord to the lower limbs – of mice whose original nerves had been cut. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 19450 - Posted: 04.05.2014

Walking backward may seem a simple task, but researchers don’t know how the mind controls this behavior. A study published online today in Science provides the first glimpse of the brain circuit responsible—at least in fruit flies. Geneticists created 3500 strains of the insects, each with a temperature-controlled switch that turned random networks of neurons on when the flies entered an incubator. One mutant batch of fruit flies started strolling in reverse when exposed to warmth (video, right panel), which the team dubbed “moonwalkers,” in honor of Michael Jackson’s famous dance. Two neurons were responsible for the behavior. One lived in the brain and extended its connections to the end of the ventral nerve cord—the fly’s version of a spine, which runs along its belly. The other neuron had the opposite orientation—it started at the bottom of the nerve cord and sent its messaging cables—or axons—into the brain. The neuron in the brain acted like a reverse gear in a car; when turned on, it triggered reverse walking. The researchers say this neuron is possibly a command center that responds to environmental cues, such as, “Hey! I see a wall in front of me.” The second neuron functioned as the brakes for forward motion, but it couldn’t compel the fly to moonwalk. It may serve as a fail-safe that reflexively prevents moving ahead, such as when the fly accidentally steps onto a very cold floor. Using the two neurons as a starting point, the team will trace their links to sensory neurons for touch, sight, and smell, which feed into and control the moonwalking network. No word yet on the neurons responsible for the Macarena. © 2014 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 19445 - Posted: 04.05.2014

For years, some biomedical researchers have worried that a push for more bench-to-bedside studies has meant less support for basic research. Now, the chief of one of the National Institutes of Health’s (NIH’s) largest institutes has added her voice—and hard data—to the discussion. Story Landis describes what she calls a “sharp decrease” in basic research at her institute, a trend she finds worrisome. In a blog post last week, Landis, director of the $1.6 billion National Institute of Neurological Disorders and Stroke (NINDS), says her staff started out asking why, in the mid-2000s, NINDS funding declined for R01s, the investigator-initiated grants that are the mainstay of most labs. After examining the aims and abstracts of grants funded between 1997 and 2012, her staff found that the portion of NINDS competing grant funding that went to basic research has declined (from 87% to 71%) while applied research rose (from 13% to 29%). To dig deeper, the staffers divided the grants into four categories—basic/basic; basic/disease-focused; applied/translational; and applied/clinical. Here, the decline in basic/basic research was “striking”: It fell from 52% to 27% of new and competing grants, while basic/disease-focused has been rising (see graph). The same trend emerged when the analysts looked only at investigator-initiated grants, which are proposals based on a researcher’s own ideas, not a solicitation by NINDS for proposals in a specific area. The shift could reflect changes in science and “a natural progression of the field,” Landis writes. Or it could mean researchers “falsely believe” that NINDS is not interested in basic studies and they have a better shot at being funded if they propose disease-focused or applied studies. The tight NIH budget and new programs focused on translational research could be fostering this belief, she writes. When her staff compared applications submitted in 2008 and 2011, they found support for a shift to disease-focused proposals: There was a “striking” 21% decrease in the amount of funding requested for basic studies, even though those grants had a better chance of being funded. © 2014 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 1: An Introduction to Brain and Behavior
Link ID: 19440 - Posted: 04.02.2014

By James Gallagher Health and science reporter, BBC News US doctors are warning of an emerging polio-like disease in California where up to 20 people have been infected. A meeting of the American Academy of Neurology heard that some patients had developed paralysis in all four limbs, which had not improved with treatment. The US is polio-free, but related viruses can also attack the nervous system leading to paralysis. Doctors say they do not expect an epidemic of the polio-like virus and that the infection remains rare. Polio is a dangerous and feared childhood infection. The virus rapidly invades the nervous system and causes paralysis in one in 200 cases. It can be fatal if it stops the lungs from working. There have been 20 suspected cases of the new infection, mostly in children, in the past 18 months, A detailed analysis of five cases showed enterovirus-68 - which is related to poliovirus - could be to blame. In those cases all the children had been vaccinated against polio. Symptoms have ranged from restricted movement in one limb to severe weakness in both legs and arms. Dr Emanuelle Waubant, a neurologist at the University of California, San Francisco, told the BBC: "There has been no obvious increase in the pace of new cases so we don't think we're about to experience an epidemic, that's the good news. BBC © 2014

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 19283 - Posted: 02.24.2014