Links for Keyword: Movement Disorders

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By Alison F. Takemura Bodies like to keep their pH close to 7.4, whether that means hyperventilating to make the blood alkaline, or burning energy, shifting to anaerobic metabolism, and producing lactate to make the blood acidic. The lungs and kidneys can regulate pH changes systemically, but they may not act quickly on a local scale. Because even small pH changes can dramatically affect the nervous system, a study led by Sten Grillner of Karolinska Institute in Sweden looked for a mechanism for pH homeostasis in the spinal cord. Using the lamprey as a model system, the researchers observed that a type of spinal canal neuron, called CSF-c, fired more rapidly when they bathed it with high pH (7.7) or low pH (7.1) media. They could suspend the elevated activity by blocking two ion channels: PKD2L1 channels, which stimulate neurons in alkaline conditions, or ASIC3 channels, which, the team showed previously, do the same in acidic states. As the neurons fired, they released the hormone somatostatin, which inhibited the lamprey’s locomotor network. These results suggest that, whichever direction pH deviates, “the response of the system is just to reduce activity as much as possible,” Grillner says. The pH-regulating role of CSF-c neurons is likely conserved among animals, the authors suspect, given the presence of these neurons across vertebrate taxa. © 1986-2016 The Scientist

Related chapters from BP7e: 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: 22688 - Posted: 09.24.2016

By Michael Price A soft brush that feels like prickly thorns. A vibrating tuning fork that produces no vibration. Not being able to tell which direction body joints are moving without looking at them. Those are some of the bizarre sensations reported by a 9-year-old girl and 19-year-old woman in a new study. The duo, researchers say, shares an extremely rare genetic mutation that may shed light on a so-called “sixth sense” in humans: proprioception, or the body’s awareness of where it is in space. The new work may even explain why some of us are klutzier than others. The patients’ affliction doesn’t have a name. It was discovered by one of the study’s lead authors, pediatric neurologist Carsten Bönnemann at the National Institutes of Health (NIH) in Bethesda, Maryland, who specializes in diagnosing unknown genetic illnesses in young people. He noticed that the girl and the woman shared a suite of physical symptoms, including hips, fingers, and feet that bent at unusual angles. They also had scoliosis, an unusual curvature of the spine. And, significantly, they had difficulty walking, showed an extreme lack of coordination, and couldn’t physically feel objects against their skin. Bönnemann screened their genomes and looked for mutations that they might have in common. One in particular stood out: a catastrophic mutation in PIEZO2, a gene that has been linked to the body’s sense of touch and its ability to perform coordinated movements. At about the same time, in a “very lucky accident,” Bönnemann attended a lecture by Alexander Chesler, a neurologist also at NIH, on PIEZO2. Bönnemann invited Chesler to help study his newly identified patients. © 2016 American Association for the Advancement of Science.

Related chapters from BP7e: 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: 22683 - Posted: 09.22.2016

By SABRINA TAVERNISE WASHINGTON — The Food and Drug Administration approved the first drug to treat patients with the most common childhood form of muscular dystrophy, a vivid example of the growing power that patients and their advocates wield over the federal government’s evaluation of drugs. The agency’s approval went against the recommendation of its experts. The main clinical trial of the drug was small, involving only 12 boys with the disease known as Duchenne muscular dystrophy, and did not have an adequate control group of boys who had the disease but did not take the drug. A group of independent experts convened by the agency this spring said there was not enough evidence that it was effective. But the vote was close. Large and impassioned groups of patients, including boys in wheelchairs, and their advocates, weighed in. The muscular dystrophy community is well organized and has lobbied for years to win approval for the drug, getting members of Congress to write letters to the agency. A decision on the drug had been delayed for months. The approval was so controversial that F.D.A. employees fought over it, a dispute that was taken to the agency’s commissioner, Dr. Robert M. Califf, who ultimately decided that it would stand. The approval delighted the drug’s advocates and sent the share price of the drug’s maker, Sarepta Therapeutics, soaring. But it was taken as a deeply troubling sign among drug policy experts who believe the F.D.A. has been far too influenced by patient advocates and drug companies, and has allowed the delicate balance in drug approvals to tilt toward speedy decisions based on preliminary data and away from more conclusive evidence of effectiveness and safety. © 2016 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: 22671 - Posted: 09.20.2016

By CATHERINE SAINT LOUIS In seven countries that recently experienced Zika outbreaks, there were also sharp increases in the numbers of people suffering from a form of temporary paralysis, researchers reported Wednesday. The analysis, published online in The New England Journal of Medicine, adds to substantial evidence that Zika infections — even asymptomatic ones — may bring on a paralysis called Guillain-Barré syndrome. The syndrome can be caused by a number of other factors, including infection with other viruses. Researchers studying the Zika epidemic in French Polynesia had estimated that roughly 1 in 4,000 people infected with the virus could develop the syndrome. The Centers for Disease Control and Prevention has said that the Zika virus is “strongly associated” with Guillain-Barré, but has stopped short of declaring it a cause of the condition. The new data suggest a telling pattern: Each country in the study saw unusual increases in Guillain-Barré that coincided with peaks in Zika infections, the researchers concluded. “It’s pretty obvious that in all seven sites there is a clear relationship,” said Dr. Marcos A. Espinal, the study’s lead author and the director of communicable diseases at the Pan American Health Organization, which collected data on confirmed and suspected cases of Zika infection and on the incidence of Guillain-Barré. “Something is going on.” In Venezuela, officials expected roughly 70 cases of Guillain-Barré from December 2015 to the end of March 2016, as mosquitoes were spreading the virus. Instead, there were 684 cases. Similarly, during five months in which the Zika virus was circulating in Colombia, officials recorded 320 cases of Guillain-Barré when there should have been about 100. From September 2015 to March 2016, while Zika infections peaked in El Salvador, cases of Guillain-Barré doubled to 184 from 92. © 2016 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: 22618 - Posted: 09.01.2016

By Kas Roussy, In a room at Sunnybrook Health Sciences Centre in Toronto, Brian Smith gives one last hug to his wife, Noreen. "You're doing really well, sweetheart," he says to her. Doctors have finished prepping the 76-year-old patient. She's clad in a blue hospital gown, her head has been shaved and metallic headgear is attached to her skull. Google's latest a spoon that steadies tremors New technology could help seniors stay independent longer She's ready to be wheeled into an MRI room, where she'll undergo a procedure that her doctors believe will revolutionize the way brain diseases are treated. Before that happens, Noreen leans into her husband for a kiss. "Best buddy," she whispers. Noreen Smith is among the three per cent of the Canadian population who suffer from a nervous system disorder called essential tremor. It causes uncontrollable shaking, most often in a person's hands. Smith noticed the first signs when she was 33. "It started developing in my dominant hand, which is my right hand," she said the day before her medical procedure from her home in Bobcaygeon, Ont. She went to a specialist who delivered the diagnosis: essential tremor. Media placeholder Smith ‘really, really excited’ about treatment’s potential0:48 Just as shocking was what he said next, alluding to a high-profile actor who had the condition. "This particular person wasn't terribly helpful because he said: 'Do you happen to know Katharine Hepburn? I'm going to give you some medication, and you can go home and get used to the idea that eventually you're going to end up looking like Katharine Hepburn.' I was devastated," says Smith. Medication helped for the first few years. But Smith's tremor was still severe and like others who suffer from this disorder, the shaking worsened with simple movements or everyday tasks like applying makeup or pouring a glass of water. ©2016 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 22603 - Posted: 08.25.2016

In a global study of myasthenia gravis, an autoimmune disease that causes muscle weakness and fatigue, researchers found that surgical removal of an organ called the thymus reduced patients’ weakness, and their need for immunosuppressive drugs. The study, published in the New England Journal of Medicine, was partially funded by the National Institutes of Health. “Our results support the idea that thymectomy is a valid treatment option for a major form of myasthenia gravis,” said Gil Wolfe, M.D., Professor and Irvin and Rosemary Smith Chair of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, New York, and a leader of the study. The Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone (MGTX) was a randomized, controlled study conducted on 126 patients aged 18-65 between 2006 and 2012. The researchers compared the combination of surgery and immunosuppression with the drug prednisone with prednisone treatment alone. They performed extended transternal thymectomies on 57 patients. This major surgical procedure aims to remove most of the thymus, which requires opening of a patient’s chest. On average the researchers found that the combination of surgery and prednisone treatment reduced overall muscle weakness more than prednisone treatment alone. After 36 months of prednisone treatment, both groups of patients had better QMG scores, a measure of muscle strength. Scores for the patients who had thymectomies and prednisone were 2.84 points better than patients who were on prednisone alone.

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: 22547 - Posted: 08.12.2016

Rae Ellen Bichell For Tim Goliver and Luther Glenn, the worst illness of their lives started in the same way — probably after having a stomach bug. Tim was 21 and a college student at the University of Michigan. He was majoring in English and biology and active in the Lutheran church. "I was a literature geek," says Tim. "I was really looking forward to my senior year and wherever life would take me." Luther was in his 50s. He'd spent most of his career as a U.S. military policeman and was working in security in Washington, D.C. He'd recently separated from his wife and had just moved into a new house with his two daughters, who were in their 20s. Both men recovered from their stomach bugs, but a few days later they started to feel sluggish. "Here we are trying to unpack, prepare ourselves for new life together and I'm flat out, dead tired," says Luther. He fell asleep in the car one morning and never made it out of the garage. Then he fell in the bathroom. For Tim, it started to feel like running a marathon just to lift a spoonful of soup. One morning, he tried to comb his hair and realized he couldn't lift his arm above his shoulder. "At that moment I started to freak out," he says. Both men got so weak that their families had to wheel them into the emergency room in wheelchairs. They got the same diagnosis: Guillain-Barre syndrome, a neurological disorder which can leave people paralyzed for weeks. © 2016 npr

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: 22217 - Posted: 05.16.2016

Sara Reardon Elite ski jumpers rely on extreme balance and power to descend the steep slopes that allow them to reach up to 100 kilometres per hour. But the US Ski and Snowboard Association (USSA) is seeking to give its elite athletes an edge by training a different muscle: the mind. Working with Halo Neuroscience in San Francisco, California, the sports group is testing whether stimulating the brain with electricity can improve the performance of ski jumpers by making it easier for them to hone their skills. Other research suggests that targeted brain stimulation can reduce an athlete’s ability to perceive fatigue1. Such technologies could aid recovery from injury or let athletes try 'brain doping' to gain a competitive advantage. Yet many scientists question whether brain stimulation is as effective as its proponents claim, pointing out that studies have looked at only small groups of people. “They’re cool findings, but who knows what they mean,” says cognitive psychologist Jared Horvath at the University of Melbourne in Australia. The USSA is working with Halo to judge the efficacy of a device that delivers electricity to the motor cortex, an area of the brain that controls physical skills. The company claims that the stimulation helps the brain build new connections as it learns a skill. It tested its device in an unpublished study of seven elite Nordic ski jumpers, including Olympic athletes. © 2016 Nature Publishing Group,

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21979 - Posted: 03.12.2016

Laura Sanders For some adults, Zika virus is a rashy, flulike nuisance. But in a handful of people, the virus may trigger a severe neurological disease. About one in 4,000 people infected by Zika in French Polynesia in 2013 and 2014 got a rare autoimmune disease called Guillain-Barré syndrome, researchers estimate in a study published online February 29 in the Lancet. Of 42 people diagnosed with Guillain-Barré in that outbreak, all had antibodies that signaled a Zika infection. Most also had recent symptoms of the infection. In a control group of hospital patients who did not have Guillain-Barré, researchers saw signs of Zika less frequently: Just 54 out of 98 patients tested showed signs of the virus. The message from this earlier Zika outbreak is that countries in the throes of Zika today “need to be prepared to have adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome,” writes study coauthor Arnaud Fontanet of the Pasteur Institute in Paris and colleagues, some of whom are from French Polynesia. The study, says public health researcher Ernesto Marques of the University of Pittsburgh, “tells us what I think a lot of people already thought: that Zika can cause Guillain-Barré syndrome.” As with Zika and the birth defect microcephaly (SN: 2/20/16, p. 16), though, more work needs to be done to definitively prove the link. Several countries currently hard-hit by Zika have reported upticks in Guillain-Barré syndrome. Colombia, for instance, usually sees about 220 cases of the syndrome a year. But in just five weeks between mid-December 2015 to late January 2016, doctors diagnosed 86 cases, the World Health Organization reports. Other Zika-affected countries, including Brazil, El Salvador and Venezuela, have also reported unusually high numbers of cases. © Society for Science & the Public 2000 - 2016. All rights reserved.

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: 21939 - Posted: 03.01.2016

Colombia says three people have died after contracting the Zika virus and developing a rare nerve disorder. Health Minister Alejandro Gaviria said there was a "causal connection" between Zika, the Guillain-Barre disorder and the three deaths. Earlier, Brazilian scientists said they had detected for the first time active samples of Zika in urine and saliva. However, it is not clear whether the virus can be transmitted through bodily fluids. Zika, a mosquito-borne disease, has been linked to cases of babies born in Brazil with microcephaly - underdeveloped brains. "We have confirmed and attributed three deaths to Zika," said the head of Colombia's National Health Institute, Martha Lucia Ospina. "In this case, the three deaths were preceded by Guillain-Barre syndrome." Guillain-Barre is a rare disorder in which the body's immune system attacks part of the nervous system. It isn't normally fatal. Ms Ospina said another six deaths were being investigated for possible links to Zika. "Other cases (of deaths linked to Zika) are going to emerge," she said. "The world is realising that Zika can be deadly. The mortality rate is not very high, but it can be deadly." Mr Gaviria said one of the fatalities took place in San Andres and the other two in Turbo, in Antioquia department. UK virologist Prof Jonathan Ball, of the University of Nottingham, told the BBC: "We have been saying Zika has been associated with Guillain-Barre. One of the complications of that could be respiratory failure. But it is still probably a very rare event." Although Zika usually causes mild, flu-like symptoms, it has been linked to thousands of suspected birth defects. However, it has not yet been proved that Zika causes either microcephaly or Guillain-Barre. © 2016 BBC

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: 21865 - Posted: 02.06.2016

By Ralph G. Neas In mid-February of 1979, I started experiencing tingling sensations in my feet and fingers. I told myself I was only feeling some residual effects from a bout with the flu several weeks before, and I caught the afternoon plane to Minneapolis to join my new boss, U.S. Sen. David Durenberger (R-Minn.), for several days of political meetings. That was on Sunday. On Tuesday, midway through a presentation, I began slurring my words and I found it hard to swallow. A local doctor, on hearing I’d had the flu, told me to go to my hotel room, take a couple of aspirin and call him in the morning. I spent the night moving from the bed to the couch to the chair to the floor, seeking relief from pain that was affecting more and more of my body. Just before dawn, I noticed that the right side of my face was paralyzed. On my way to the ER, the left side became paralyzed. I wasn’t having a recurrence of the flu. A spinal tap confirmed doctors’ suspicions that I’d come down with Guillain-Barré syndrome, or GBS, a rare neurological disorder that can cause total paralysis. Within 10 days I was so weakened by the spreading paralysis in my legs and arms that I could not get out of my bed at St. Mary’s, the Minneapolis hospital where I was being treated. Within three weeks, doctors performed a tracheostomy — connecting a mechanical respirator to my windpipe — because my ability to breathe was getting so poor.

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: 21777 - Posted: 01.12.2016

By NICHOLAS WADE After decades of disappointingly slow progress, researchers have taken a substantial step toward a possible treatment for Duchenne muscular dystrophy with the help of a powerful new gene-editing technique. Duchenne muscular dystrophy is a progressive muscle-wasting disease that affects boys, putting them in wheelchairs by age 10, followed by an early death from heart failure or breathing difficulties. The disease is caused by defects in a gene that encodes a protein called dystrophin, which is essential for proper muscle function. Because the disease is devastating and incurable, and common for a hereditary illness, it has long been a target for gene therapy, though without success. An alternative treatment, drugs based on chemicals known as antisense oligonucleotides, is in clinical trials. But gene therapy — the idea of curing a genetic disease by inserting the correct gene into damaged cells — is making a comeback. A new technique, known as Crispr-Cas9, lets researchers cut the DNA of chromosomes at selected sites to remove or insert segments. Three research groups, working independently of one another, reported in the journal Science on Thursday that they had used the Crispr-Cas9 technique to treat mice with a defective dystrophin gene. Each group loaded the DNA-cutting system onto a virus that infected the mice’s muscle cells, and excised from the gene a defective stretch of DNA known as an exon. Without the defective exon, the muscle cells made a shortened dystrophin protein that was nonetheless functional, giving all of the mice more strength. The teams were led by Charles A. Gersbach of Duke University, Eric N. Olson of the University of Texas Southwestern Medical Center and Amy J. Wagers of Harvard University. © 2016 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: 21745 - Posted: 01.02.2016

The clock is ticking for Ronald Cohn. He wants to use CRISPR gene editing to correct the genes of his friend’s 13-year-old son. The boy, Gavriel, has Duchenne muscular dystrophy, a genetic disease in which muscles degenerate. Breathing and heart problems often start by the time people with the condition are in their early twenties. Life expectancy is about 25 years. By the standards of science, the field of CRISPR gene editing is moving at a lightning fast pace. Although the technique was only invented a few years ago, it is already being used for research by thousands of labs worldwide to make extremely precise changes to DNA. A handful of people have already been treated using therapies enabled by the technology, and last week an international summit effectively endorsed the idea of gene editing embryos. It is too soon to try the technique out, but the summit concluded that basic research on embryos should be permitted, alongside a debate on how we should use the technology. But for people like Cohn, progress can’t come fast enough. Gavriel was diagnosed at age 4. He has already lost the use of his legs but still has some movement in his upper body, and uses a manual wheelchair. Cohn, a clinician at the Hospital for Sick Children in Toronto, estimates that he has three years to develop and test a CRISPR-based treatment if he is to help Gavriel. Muscular dystrophy is caused by a faulty gene for the protein dystrophin, which holds our muscles together. Gavriel has a duplicated version of the gene. This week, Cohn’s team published a paper describing how they grew Gavriel’s cells in a dish and used CRISPR gene-editing techniques to snip out the duplication. With the duplication removed, his cells produced normal dystrophin protein. © 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: 21698 - Posted: 12.14.2015

By Karen Weintraub Essential tremor is involuntary shaking – usually of the hands, but sometimes also of the neck, jaw, voice or legs. “Any fine tasks with the hands can be very difficult when the tremor is pronounced,” said Dr. Albert Hung, center director of the Massachusetts General Hospital National Parkinson Foundation Center of Excellence. Essential tremor can affect balance, walking, hearing and cognition, and can get worse over time, said Dr. Elan Louis, chief of the division of movement disorders at Yale School of Medicine. People with essential tremor run almost twice the risk of developing Alzheimer’s as the general population. Essential tremor appears with movement; if people let their hands sit still, they don’t tremble. That is the big difference between an essential tremor and the tremor of Parkinson’s disease, which can occur while at rest, Dr. Louis said. Essential tremor also tends to strike both hands while Parkinson’s is more one-sided at first, said Dr. Hung. The cause of essential tremor remains a mystery, though it seems to run in families. People of any age or sex can have the condition, though it is more common as people grow older. Roughly 4 percent of 40-year-olds have essential tremor, compared with about 20 percent of 90-year-olds, Dr. Louis said. Available treatments “aren’t great,” Dr. Louis said. Two medications – the beta blocker propranolol and the epilepsy drug primidone, sold under the brand name Mysoline – can reduce tremors by 10 to 30 percent, he said, but they work only in about half of patients. Deep brain stimulation – implanting electrodes into the brain to override faulty electrical signals – has been shown to markedly reduce hand tremor severity, he said. But the treatment can worsen cognitive and balance problems and “doesn’t cure the underlying disease. It merely and temporarily lessons a single symptom, which is the tremor.” © 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: 21653 - Posted: 11.24.2015

Ewen Callaway Ringo, a golden retriever born in 2003 in a Brazilian kennel, was never expected to live long. Researchers bred him and his littermates to inherit a gene mutation that causes severe muscular dystrophy. They hoped that the puppies would provide insight into Duchenne muscular dystrophy (DMD), an untreatable and ultimately fatal human disease caused by inactivation of the same gene. But Ringo’s muscles didn't waste away like his littermates', and researchers have now determined why: he was born with another mutation that seems to have protected him from the disease, according to a paper published in Cell1. Scientists hope that by studying Ringo’s mutation — which has never before been linked to muscular dystrophy — they can find new treatments for the disease. As many as 1 in 3,500 boys inherit mutations that produce a broken version of a protein called dystrophin, causing DMD. (The disease appears in boys because the dystrophin gene sits on the X chromosome, so girls must inherit two copies of the mutated gene to develop DMD.) The protein helps to hold muscle fibres together, and its absence disrupts the regenerative cycle that rebuilds muscle tissue. Eventually, fat and connective tissue replace muscle, and people with DMD often become reliant on a wheelchair before their teens. Few survive past their thirties. Some golden retriever females carry dystrophin mutations that cause a similar disease when passed onto male puppies. Dog breeders can prevent this through genetic screening. But Mayana Zatz, a geneticist at the University of São Paulo in Brazil, and her colleagues set out to breed puppies with the mutation to model the human disease. © 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: 21632 - Posted: 11.14.2015

Laura Sanders Scribes usually have pretty good handwriting. That’s not the case for one prolific 13th century writer known to scholars only as the Tremulous Hand of Worcester. Now scientists suggest the writer suffered from a neurological condition called essential tremor. Neurologist Jane Alty and historical handwriting researcher Deborah Thorpe, both of the University of York in England, made the retrospective diagnosis August 31 in Brain after studying the spidery wiggles that pervade the scribe’s writing. Essential tremor can cause shaking of the hands, head and voice and is distinct from other tremor-causing conditions such as Parkinson’s disease. Here, the anonymous writer’s peculiar script is evident (lighter portion of text) in an early Middle English version of the Nicene Creed, a summary of the Christian faith. Buried in the manuscript are clues that helped the researchers conclude that essential tremor plagued the Tremulous Hand. The Tremulous Hand of Worcester’s writing appeared in more than 20 books, including the Nicene Creed, a summary of the Christian faith. The writer’s distinctive script is the lighter portion of the text, about a third of the way down the page. Several clues led researchers to diagnose the scribe with essential tremor (see following images). © 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: 21482 - Posted: 10.07.2015

Ever waited for a bus rather than take the short walk to work? Headed for the escalator instead of the stairs? Humans clearly harbour a deep love of lethargy – and now we know how far people will go to expend less energy. We will change our walking style on the fly when our normal gait becomes even a little more difficult. The finding could have implications for the rehabilitation offered to people with spinal injuries. Jessica Selinger and her colleagues at Simon Fraser University in Burnaby, British Columbia, Canada, strapped volunteers into a lightweight robotic exoskeleton and put them on a treadmill. Initially, the team let the volunteers find their preferred walking rhythm – which turned out to be 1.8 steps per second, on average. Then the researchers switched on the exoskeleton, programming it to make it more difficult for the volunteers to walk at their preferred pace by preventing the knee from bending – and leg swinging – as freely. The exoskeleton didn’t interfere with the human guinea pigs’ ability to walk faster or slower than they preferred. Within minutes the volunteers had found a walking style that the exoskeleton would allow without offering resistance. Remarkably, though, they did so despite the fact that the exoskeleton only ever offered minimal resistance. By using breathing masks to analyse the volunteers’ metabolic activity, Selinger’s team found that subjects would shift to an awkward new gait even if the energy saving was only 5 per cent. “People are able to adapt and fine-tune in order to move in the most energetically optimal way,” says Selinger. “People will change really fundamental characteristics of their gait.” © 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: 21398 - Posted: 09.11.2015

By Jennifer Couzin-Frankel Some rare diseases pull researchers in and don’t let them go, and the unusual bone condition called fibrodysplasia ossificans progressiva (FOP) has long had its hooks in Aris Economides. “The minute you experience it it’s impossible to step back and forget it,” says the functional geneticist who runs the skeletal disease program at Regeneron Pharmaceuticals in Tarrytown, New York. “It’s devastating in the most profound way.” The few thousand or so people with FOP worldwide live with grueling uncertainty: Some of their muscles or other soft tissues periodically, and abruptly, transform into new bone that permanently immobilizes parts of their bodies. Joints such as elbows or ankles may become frozen in place; jaw motion can be impeded and the rib cage fixed, making eating or even breathing difficult. Twenty years after he first stumbled on FOP, Economides and his colleagues report today that the gene mutation shared by 97% of people with the disease can trigger its symptoms in a manner different than had been assumed—through a single molecule not previously eyed as a suspect. And by sheer chance, Regeneron had a treatment for this particular target in its freezers. The company tested that potential therapy, a type of protein known as a monoclonal antibody, on mice with their own form of FOP and lo and behold, they stopped growing unwelcome new bone. © 2015 American Association for the Advancement of Science.

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: 21377 - Posted: 09.03.2015

Boer Deng Palaeontologist Stephen Gatesy wants to bring extinct creatures to life — virtually speaking. When he pores over the fossilized skeletons of dinosaurs and other long-dead beasts, he tries to imagine how they walked, ran or flew, and how those movements evolved into the gaits of their modern descendents. “I'm a very visual guy,” he says. But fossils are lifeless and static, and can only tell Gatesy so much. So instead, he relies on XROMM, a software package that he developed with his colleagues at Brown University in Providence, Rhode Island. XROMM (X-ray Reconstruction of Moving Morphology) borrows from the technology of motion capture, in which multiple cameras film a moving object from different angles, and markers on the object are rendered into 3D by a computer program. The difference is that XROMM uses not cameras, but X-ray machines that make videos of bones and joints moving inside live creatures such as pigs, ducks and fish. Understanding how the movements relate to the animals' bone structure can help palaeontologists to determine what movements would have been possible for fossilized creatures. “It's a completely different approach” to studying evolution, says Gatesy. XROMM, released to the public in 2008 as an open-source package, is one of a number of software tools that are expanding what researchers know about how animals and humans walk, crawl and, in some cases, fly (see ‘Movement from inside and out’). That has given the centuries-old science of animal motion relevance to a wide range of fields, from studying biodiversity to designing leg braces, prostheses and other assistive medical devices.“We're in an intense period of using camera-based and computer-based approaches to expand the questions we can ask about motion,” says Michael Dickinson, a neuroscientist at the California Institute of Technology in Pasadena. © 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: 21370 - Posted: 09.01.2015

By David Noonan Leaping through the air with ease and spinning in place like tops, ballet dancers are visions of the human body in action at its most spectacular and controlled. Their brains, too, appear to be special, able to evade the dizziness that normally would result from rapid pirouettes. When compared with ordinary people's brains, researchers found in a study published early this year, parts of dancers' brains involved in the perception of spinning seem less sensitive, which may help them resist vertigo. For millions of other people, it is their whole world, not themselves, that suddenly starts to whirl. Even the simplest task, like walking across the room, may become impossible when vertigo strikes, and the condition can last for months or years. Thirty-five percent of adults older than 39 in the U.S.—69 million people—experience vertigo at one time or another, often because of damage to parts of the inner ear that sense the body's position or to the nerve that transmits that information to the brain. Whereas drugs and physical therapy can help many, tens of thousands of people do not benefit from existing treatments. “Our patients with severe loss of balance have been told over and over again that there's nothing we can do for you,” says Charles Della Santina, an otolaryngologist who studies inner ear disorders and directs the Johns Hopkins Vestibular NeuroEngineering Laboratory. Steve Bach's nightmare started in November 2013. The construction manager was at home in Parsippany, N.J. “All of a sudden the room was whipping around like a 78 record,” says Bach, now age 57. He was curled up on the living room floor in a fetal position when his daughter found him and called 911. He spent the next five days in the hospital. © 2015 Scientific American

Related chapters from BP7e: Chapter 9: Hearing, Vestibular Perception, Taste, and Smell; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 6: Hearing, Balance, Taste, and Smell; Chapter 5: The Sensorimotor System
Link ID: 21248 - Posted: 08.01.2015