Links for Keyword: Movement Disorders

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 166

by Cleve R. Wootson Jr. Kailyn Griffin, 5, experienced temporary paralysis following a tick bite in Grenada, Miss., discovered on June 6. (WLBT) As soon as Kailyn Griffin's feet hit the floor Wednesday morning, she collapsed in a heap. The 5-year-old kept trying to stand but fell every time. She was also struggling to speak, said her mother, Jessica Griffin. Her daughter had been fine when the family went out to a T-ball game the night before, NBC-affiliate WLBT in Jackson, Miss., reported. Maybe Kailyn was having a hard time waking up Wednesday morning, or perhaps her legs were asleep. Then Griffin saw the tick. She had gathered Kailyn's hair to put it in a ponytail when she spotted the arachnid, embedded in the girl's scalp, swelled with the girl's blood. She pulled the tick out and placed it in a plastic bag, then rushed to the hospital with Kailyn, WTXL reported. Doctors told Griffin it was an uncommon condition called tick paralysis. “After tons of bloodwork and a CT of the head UMMC has ruled it as tick paralysis! PLEASE for the love of god check your kids for ticks! It’s more common in children than it is adults!” Griffin, of Grenada, Miss., wrote in a Facebook post Wednesday that seemed a mixture of worry and relief. “Scary is a UNDERSTATEMENT!” Griffin could not be immediately reached for comment. It was unclear where or when she thought her daughter had acquired the tick, or how long it had been on her body. Ticks are most active from April through September, The Washington Post has reported. Tick paralysis is caused by female ticks on the verge of laying eggs. After the tick eats a blood meal and is engorged, it secretes a neurotoxin into the host, according to the American Lyme disease Foundation. The symptoms can occur five to seven days after the tick starts feeding. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25081 - Posted: 06.12.2018

Researchers say they may have worked out why there is a natural loss of muscle in the legs as people age - and that it is due to a loss of nerves. In tests on 168 men, they found that nerves controlling the legs decreased by around 30% by the age of 75. This made muscles waste away, but in older fitter athletes there was a better chance of them being 'rescued' by nerves re-connecting. The scientists published their research in the Journal of Physiology. As people get older, their leg muscles become smaller and weaker, leading to problems with everyday movements such as walking up stairs or getting out of a chair. It is something that affects everyone eventually, but why it happens is not fully understood. Prof Jamie McPhee, from Manchester Metropolitan University, said young adults usually had 60-70,000 nerves controlling movement in the legs from the lumbar spine. But his research showed this changed significantly in old age. "There was a dramatic loss of nerves controlling the muscles - a 30-60% loss - which means they waste away," he said. "The muscles need to receive a proper signal from the nervous system to tell them to contract, so we can move around." The research team from Manchester Metropolitan University worked with researchers from the University of Waterloo, Ontario, and the University of Manchester. They looked at muscle tissue in detail using magnetic resonance imaging (MRI) and they recorded the electrical activity passing through the muscle to estimate the numbers and the size of surviving nerves. The good news is that healthy muscles have a form of protection: surviving nerves can send out new branches to rescue muscles and stop them wasting away. This is more likely to happen in fit people with large, healthy muscles, Prof McPhee said. © 2018 BBC.

Related chapters from BN8e: 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: 24737 - Posted: 03.12.2018

by Sandra G. Boodman “What are you doing ?” Laura Hsiung’s friends asked as she slowly loped across a Maryland handball court, her ankle off-kilter so that she was walking on the outside of her left foot. Hsiung recalls wondering the same thing. One minute she was walking normally, and then all of a sudden, she wasn’t. “I couldn’t figure it out,” Hsiung said. “I hadn’t rolled my ankle. But my left foot just would not function normally.” For the next two years, Hsiung consulted specialist after specialist — orthopedists, a podiatrist and a neurologist — each of whom was unable to explain what was causing her weird walk. She underwent surgery which didn’t help and felt increasingly desperate about the problem, which did not affect her right foot. “Doctors would literally say, ‘I don’t know what’s wrong with you,’ ” said Hsiung, who lives in Montgomery County. Nor, she said, did most of them seem interested in unearthing a probable cause. After nearly two years of frustration and anxiety, a consultation with a physical therapist ultimately led to a diagnosis, followed by treatment that has helped alleviate Hsiung’s unusual disorder. Although they met only twice, the impact of her encounters with that physical therapist had a galvanizing effect on another aspect of Hsiung’s life, pushing her to make a midlife career change she had been contemplating. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24677 - Posted: 02.19.2018

National Institutes of Health scientists developing a rapid, practical test for the early diagnosis of prion diseases have modified the assay to offer the possibility of improving early diagnosis of Parkinson’s disease and dementia with Lewy bodies. The group, led by NIH’s National Institute of Allergy and Infectious Diseases (NIAID), tested 60 cerebral spinal fluid samples, including 12 from people with Parkinson’s disease, 17 from people with dementia with Lewy bodies, and 31 controls, including 16 of whom had Alzheimer’s disease. The test correctly excluded all the 31 controls and diagnosed both Parkinson’s disease and dementia with Lewy bodies with 93 percent accuracy. Importantly, test results were available within two days, compared to related assays that require up to 13 days. The group conducted the tests using Real-Time Quaking-Induced Conversion (RT-QuIC), an assay developed and refined over the past decade at NIAID’s Rocky Mountain Laboratories. Scientists from the University of California San Diego, University of Verona in Italy, Indiana University School of Medicine, Indianapolis, and the Case Western Reserve University School of Medicine, Cleveland, collaborated on the project. The research findings were published in Acta Neuropathologica Communications. Multiple neurological disorders, including Parkinson’s disease and dementia with Lewy bodies, involve the abnormal clumping of a protein called alpha-synuclein into brain deposits called Lewy bodies. The pathological processes in these diseases resembles prion diseases in mammal brains. Like prion diseases, Parkinson’s disease and dementia with Lewy bodies result in progressive deterioration of brain functions and, ultimately, death. Parkinson’s disease is about 1,000 times more common than prion diseases, affecting up to 1 million people in the United States, with 60,000 new cases diagnosed each year. Lewy body dementia affects an estimated 1.4 million people in the United States, according to the Lewy Body Dementia Association.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24641 - Posted: 02.10.2018

By LISA SANDERS, M.D. “Something’s wrong,” the woman told the young doctor, her face lined with worry. “This is not my husband.” The 68-year-old man lay unmoving in the hospital bed, his eyes dull, his face expressionless. His wife stood by him, as she had for nearly four decades of marriage. You don’t know him, she said, but if you did, you’d know that something is not right. George Goshua, a doctor in his first year of residency, looked at the distressed woman and then back at the man in the bed. He had spent nearly an hour reviewing the man’s hospital chart before coming to see him, and he knew the patient had been dangerously ill in the intensive-care unit for the last week. It all began about two weeks before, the wife explained. They were preparing for their son’s wedding, and her husband, normally a workhorse, was not feeling well. He was a tough guy — he worked as an estimator for a local builder and constructed his own house pretty much single-handedly. But now he said he was exhausted. At one point, just two days before the wedding, he said, “I think I might die.” At the time, she was irritated, because she thought he was just trying to get out of the work. Now she knew otherwise. They made it through the wedding, but the next day he was a wreck. His neck was stiff, as if there were a crick on both sides. He went to the local urgent-care center. They thought it was probably just a sore muscle and gave him something for the pain. The day after that, he had a fever. And the following day he was so weak he couldn’t walk. When his wife realized he was too sick to see his own doctor, she called an ambulance. As she struggled to get him out of his pajamas and into his clothes, he slid off the couch onto the floor. He just lay there, unable to even sit up. She couldn’t lift him. When the E.M.T.s arrived, they loaded him into an ambulance, and she followed them to Yale New Haven Hospital, in New Haven, Conn. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24621 - Posted: 02.06.2018

By Keith Doucette, In what her mother calls a "Christmas miracle," a Nova Scotia woman who suffered a catastrophic brain injury in a 1996 car accident communicated one-on-one with her mother for the first time in 21 years. Louise Misner said her 37-year-old daughter Joellan Huntley used eye-motion cameras and software on an iPad to respond to a comment from Misner about her clothes. Huntley has been severely disabled since she was 15, unable to walk or talk and is fed through a tube. She has always responded to family members' presence by making sounds, but was unable to communicate any thoughts. The breakthrough occurred during a Christmas Day visit at the Kings Regional Rehabilitation Centre in Waterville, N.S. "I said, 'Joellan, I like your new Christmas outfit you got on,"' Misner said in a telephone interview on Friday. Misner said her daughter then used the technology to find an icon for a short-sleeved shirt. "And then she said no, and went to a long-sleeve shirt because she was trying to tell me what she had on." Misner said her reaction to the long-hoped-for communication was immediate. "Christmas miracle," she said. "It was God's way of telling me that she's finally achieved what she needed to since the accident." Settlement helped buy technology Huntley was thrown from a car that had swerved to avoid a dog running loose along a road in Centreville, N.S., on April 18, 1996. The accident claimed the life of her boyfriend and a young girl who was the sister of the driver. ©2017 CBC/Radio-Canada.

Related chapters from BN8e: 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: 24469 - Posted: 12.30.2017

By Helen Shen Brain-controlled prosthetic devices have the potential to dramatically improve the lives of people with limited mobility resulting from injury or disease. To drive such brain-computer interfaces, neuroscientists have developed a variety of algorithms to decode movement-related thoughts with increasing accuracy and precision. Now researchers are expanding their tool chest by borrowing from the world of cryptography to decode neural signals into movements. During World War II, codebreakers cracked the German Enigma cipher by exploiting known language patterns in the encrypted messages. These included the typical frequencies and distributions of certain letters and words. Knowing something about what they expected to read helped British computer scientist Alan Turing and his colleagues find the key to translate gibberish into plain language. Many human movements, such as walking or reaching, follow predictable patterns, too. Limb position, speed and several other movement features tend to play out in an orderly way. With this regularity in mind, Eva Dyer, a neuroscientist at the Georgia Institute of Technology, decided to try a cryptography-inspired strategy for neural decoding. She and her colleagues published their results in a recent study in Nature Biomedical Engineering. “I’ve heard of this approach before, but this is one of the first studies that’s come out and been published,” says Nicholas Hatsopoulos, a neuroscientist at the University of Chicago, who was not involved in the work. “It’s pretty novel.” © 2017 Scientific American,

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24462 - Posted: 12.28.2017

Michael May Carl Luepker suffers from a nerve disorder which causes involuntary muscle spasms. He lived with the symptoms for 30 years until he discovered he'd passed the genetic disorder on to his son. NOEL KING, HOST: Parents make all kinds of sacrifices for their children, but what do you do when you want to save your child from experiencing the same kind of suffering you have experienced? NPR's Michael May brings us the story of one father who's searching for a way to ease his son's discomfort that's caused by a shared genetic disorder. MICHAEL MAY, BYLINE: Carl Luepker suffers from dystonia, a disorder that causes involuntary muscle spasms. When I met him 30 years ago, Carl's spasms were in his right hand. Then they spread to the muscles of his face until they garbled his speech. Last December, Carl sat down in the office of his neurologist, Dr. Jerrold Vitek, to discuss a surgery called deep brain stimulation. CARL LUEPKER: My fears are - obviously, first is death. MAY: It's not an easy decision to let a doctor drill a hole in your skull and put electrodes deep in your brain. LUEPKER: Those are sort of my three biggest fears, are death, loss of cognition and any behavioral changes I might incur from the procedure. JERROLD VITEK: Well, Carl, what I would say is that the potential risk is about a 1 to 2 percent chance that there'd be a significant bleed. That's the greatest risk. The chance of benefit is marked. The vast majority of people will benefit. MAY: Deep brain stimulation has been called a pacemaker for the brain. It regulates the neurons that are misfiring. It's used for everything from Parkinson's disease to major depression. Scientists still don't understand exactly why DBS works. But for some patients, it dramatically reduces symptoms. At first, scientists literally destroyed the part of the brain that was malfunctioning. Vitek says there's a reason doctors would be willing to try something so brutal. VITEK: One word will answer that - desperation. © 2017 npr

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24456 - Posted: 12.26.2017

By RONI CARYN RABIN A. Bell’s palsy is a temporary partial facial paralysis that occurs when the nerve controlling the facial muscles is inflamed. But identifying the underlying cause of the inflammation “is a question for the ages,” said Dr. Joseph Safdieh, a neurologist at Weill Cornell Medicine and a fellow of the American Academy of Neurology. The current prevailing theory is that Bell’s palsy develops after a viral infection activates the immune system, Dr. Safdieh said, adding that “once the immune system is activated, it goes and attacks a nerve.” The condition usually affects only one side of the face, causing asymmetry or drooping on one side (the reason for that is not known either). Some experts believe Bell’s palsy is related to the herpes simplex or common cold sore virus. But several large randomized controlled trials that compared treatment with antiviral agents and prednisolone, an oral steroid that suppresses the immune system, found the steroid to be most effective. The results reinforce the idea that the condition is caused by an immune system reaction rather than the virus itself, Dr. Safdieh said. The condition has also been associated with recent vaccinations and upper respiratory infections, “but many people are vaccinated and have upper respiratory infections and don’t develop Bell’s palsy,” Dr. Safdieh said. “The ultimate answer is ‘we don’t know,’ but that many things that activate the immune system can trigger it.” One specific cause that should be ruled out is Lyme disease, especially if Bell’s palsy develops in the summer or early fall or in children, in whom it is less common, Dr. Safdieh said. Treatment will differ if the patient has Lyme disease. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24385 - Posted: 12.04.2017

By Jocelyn Kaiser CENTREVILLE, VIRGINIA—Nothing unusual jumps out upon meeting Evelyn, a bubbly almost-3-year-old with red curls—except that she should not be here, chatting with a visitor in her family’s living room, twirling in her tights to the Pharrell Williams song “Happy.” Evelyn’s older sister Josephine had spinal muscular atrophy type 1 (SMA1), a genetic disease that gradually paralyzes babies. She died at 15 months. Evelyn was an unexpected pregnancy, but her parents decided to have the baby despite one-in-four odds of a second tragedy. Soon after Evelyn was born in December 2014, they were devastated to learn from genetic testing that she, too, had SMA1. “We knew what we were dealing with: We’ll love her for as long as we can,” says her father, Milan Villarreal. But that same night, frantically searching the internet, they learned about a clinical trial in Ohio and sent an email. At 8 weeks old, Evelyn received a gene therapy treatment that gave her body a crucial missing protein. And now here she is, not so different from any healthy toddler. Although she has weak thighs and can’t run normally or jump, she can walk quickly, dance, trace letters, toss foam blocks, carry a small chair, and climb onto her mother Elena’s lap. After the heartbreak of losing their first baby, the Villarreals have watched in amazement as Evelyn has crawled, walked, and talked. “It was just a miracle. Every milestone was like a celebration. We opened a bottle of wine for every little thing she did,” Milan says. © 2017 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24280 - Posted: 11.02.2017

By LISA SANDERS, M.D. “Mom?” the middle-aged man asked. He recognized the voice, but the words were muffled and strange. I’ll be right over, he said into the phone. The 15-minute drive from his small Connecticut town to his mother’s seemed to last forever. Had she had a stroke? She was 94, and though she’d always been healthy, at her age, anything could happen. He burst into her tidy brick home to find her sitting in the living room, waiting. Her eyes were bright but scared, and her voice was just a whisper. He helped her to his car, then raced to the community hospital a couple of towns over. The doctors in the emergency room were also worried about a stroke. Her left eyelid hung lower across her eye than her right. She was seeing double, she told them. And the left side of her mouth and tongue felt strangely heavy, making it hard to speak. Initial blood tests came back normal; so did the CT scan of her brain. It wasn’t clear what was wrong with the patient, so she was transferred to nearby Yale New Haven Hospital. Dr. Paul Sanmartin, a resident in the second year of his neurology training, met the patient early the next morning. He’d already heard about her from the overnight resident: a 94-year-old woman with the sudden onset of a droopy eyelid, double vision and difficulty speaking, probably due to a stroke. As he entered the room, he realized he wasn’t sure what 94 was supposed to look like, but this woman looked much younger. She did have a droopy left lid, but her eyes moved in what looked to him to be perfect alignment, and her speech, though quiet, was clear. The patient’s story was also different from what he expected. She had macular degeneration and had been getting shots in her left eye for more than a decade. Her last injection was nearly two weeks earlier, and she’d had double vision and the droopy eyelid on and off ever since. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24111 - Posted: 09.26.2017

By Kerry Grens The rare, severe effects of Zika infection in adults may go beyond Guillain-Barre syndrome. Doctors in Brazil report today in JAMA Neurology that among a group of hospitalized patients, those with the virus sometimes presented with other neurological problems—namely, an inflamed nervous system. The physicians tracked 40 patients who came to a hospital in Rio de Janeiro between December 2015 and May 2016 for acute neuroinflammation. Among them, 35 turned out to have been infected with Zika, and within this group, 27 had Guillain-Barre syndrome, which causes debilitating paralysis. Five patients had encephalitis, or inflammation of the brain, two had inflamed spinal cords, and one had nerve inflammation. Such symptoms are thought to indicate “post-infectious syndromes, where you have a viral infection, you clear the infection by mounting an antibody response, and the antibodies actually attack parts of the central and peripheral nervous system, causing these neurological symptoms,” Richard Temes, director of the Center for Neurocritical Care at North Shore University Hospital in Manhasset, New York, tells HealthDay. He was not involved in this study. Zika infection in adults is typically not dangerous, and many people won’t develop symptoms at all. Doctors have noticed an uptick in Guillain-Barre syndrome among those who have caught the virus. The authors note in their study that admissions to their hospital for both Guillain-Barre syndrome and encephalitis rose after May 2014, when the Zika outbreak hit Brazil.

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23960 - Posted: 08.15.2017

By Diana Kwon Like humans, some golden retrievers develop Duchenne muscular dystrophy (DMD), a hereditary muscle wasting condition that begins early in life. Using gene therapy, scientists were able to restore muscle function in dogs with the disease, according to a study published today (July 25) in Nature Communications. Researchers injected microdystrophin, a shortened version of the dystrophin gene that individuals with DMD lack, into 12 dogs with the disease. The treatment led to improved muscle function in those animals for more than two years. “This preclinical study demonstrates the safety and efficacy of microdystrophin, and makes it possible to consider developing a clinical trial in patients,” study coauthor Caroline Le Guiner of the Université de Nantes in France, says in a statement. “Indeed, this is the first time that it has been possible to treat the whole body of a large-sized animal with this protein.” Scientists have also used CRISPR to correct the disease-causing mutations in mouse models of DMD and in the cells of a human patient with the condition. “This [study] is very encouraging, as current treatments for muscular dystrophy are merely palliative and patients are under constant medical care throughout their life,” John Counsell, a research associate at University College London who was not involved in the study, in a statement published by the Science Media Center. “Further preclinical trials will be required to show that this treatment can be effective in patients.” © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23883 - Posted: 07.27.2017

By Aylin Woodward Keep your head up. Today, navigating the urban jungle can be challenging, with uneven sidewalks and errant kerbs presenting obstacles to easy walking. So why do we rarely trip up even though we hardly ever give walking our full attention? It seems that all we need is a brief glimpse of what’s coming next on the road in front of us, just one step ahead of time, to keep up upright. Humans have a unique kind of locomotion – we’re bipedal, meaning we move around on two legs rather than four. Scientists are still struggling to unravel the mystery behind our shift to two legs – for instance, some suggest it freed up our hands to carry food. Others point out that our human gait is much more energetically efficient. Our walking style exploits external forces like gravity and inertia to use as little muscular energy as possible so that we actually fall forward onto the lifted foot with each step. Jonathan Samir Matthis at the University of Texas at Austin wanted to know how we aim and control this forward motion – particularly since the way ahead is rarely level and obstacle-free. “We have to be much more careful about where we place our feet than we would if we had four legs on the ground,” he says. “Because if we do it wrong, there’s serious consequences like breaking your leg.” © Copyright New Scientist Ltd.

Related chapters from BN8e: 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: 23872 - Posted: 07.25.2017

By Bob Grant Prosthetic limbs are rejected by amputees’ bodies at a rate of about 20 percent. Researchers at MIT are seeking to reduce that number, using an amputation procedure that encourages increased feedback between muscles, tendons, and the nervous system so that an artificial limb might stimulate them in a more natural way—giving patients a better sense of proprioception, or where their limb is in space. The key to the surgical technique, demonstrated in rats so far, is to emulate the normal agonist-antagonist pairing of muscles (think biceps and triceps) at the amputation site so that the muscles and nerves surrounding a prosthetic can sense and transmit proprioceptive information about the artificial limb and how much force is being applied to it. The researchers published their work today (May 31) in Science Robotics. “We’re talking about a dramatic improvement in patient care,” Hugh Herr, an MIT professor of media arts and sciences and a coauthor of the study, said in a statement. “Right now there’s no robust neural method for a person with limb amputation to feel proprioceptive positions and forces applied to the prosthesis. Imagine how that would completely hinder one’s ability to move, to successfully balance, or to manipulate objects.” Herr, himself a double-amputee, and his team operated on seven rats, cutting through muscles and nerves in their hind legs. The researchers then grafted on paired muscles, wiring them up to severed nerves. After healing for four months, the rats’ new muscles were contracting and relaxing in tandem, as in naturally paired muscles, and sending electrical signals that reflected the amplitude of the artificial stimulation Herr and his colleagues applied. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23693 - Posted: 06.02.2017

By LISA SANDERS, M.D. The woman woke to the sound of her 57-year-old husband sobbing. They’d been married for 30 years, and she had never heard him cry before. “I hurt so much,” he wailed. “I have to go back to the hospital.” The symptoms started two weeks earlier. One afternoon, coming home from his job as a carpenter, he felt hot and tired. He shook with shivers even though the day was warm. He drank a cup of tea and went to bed. The next day he felt fine, until the end of the day, when he felt overwhelmed by the heat and chills again. The day after that was the same. When he woke one morning and saw that his body was covered with pale pink dots — his arms, his face, his chest and thighs — he started to worry. His wife took him to the Griffin Hospital emergency room in Derby, Conn. The first doctor who saw him thought he probably had Lyme disease. Summer had just started, and he’d already seen a lot of cases. He sent the patient home with an antibiotic and steroid pills for the rash. The man took the medications but didn’t get any better. Soon everything started to hurt. His muscles, his joints and his back felt as if he’d been beaten. He dragged himself back to the E.R. He was given pain pills. A few days later, he went to the E.R. a third time and was given more pain meds. After waking up crying, he went yet again, and this time, the doctors admitted him. By then the patient had had several blood tests, which showed no sign of Lyme or other tick-borne diseases. A CT scan was equally uninformative. The next day, the man was walking to the bathroom when his legs gave out and he fell down. The doctor in charge of his care came and examined him once again. The man looked fit and healthy, despite the now-bright-red rash, but his legs were extremely weak. If the doctor applied even light pressure to the raised leg, it sagged back down to the bed. And his feet felt numb. He had a sensation of tingling in his hands, as if they had gone to sleep. That was how the weakness and numbness in his legs started, he told the doctor. And the next day, his hands were so weak he had to use both just to drink a cup of water. © 2017 The New York Times Company

Related chapters from BN8e: 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: 23644 - Posted: 05.22.2017

By Paul Taylor One of the bummers of getting older, as most baby boomers can attest, is that the list of stuff you don’t do as well as you once did keeps getting longer. Bennett Beach, 67, can measure his decline with a stopwatch. Three hours, 27 minutes, 56 seconds: That’s the difference between his best time in the Boston Marathon (2:27:26) and his worst (5:55:22). On April 17, he’ll be running the famous race once again. If he completes the course in less than six hours, he will have officially finished his 50th consecutive Boston Marathon. No one has ever done that. Nor, as far as he knows, will any of his 32,000 fellow racers be coping, as he is, with the rare and debilitating neurological movement disorder known as task-specific dystonia. Whenever he strides, Beach’s left leg gets hijacked by erratic signals from his brain. His walk is nearly normal, but for the past 15 years he has been running with a severe limp. His pursuit of the milestone has been fueled in roughly equal measure by antithetical parts — an Ahab-grade obsession mixed with an older-but-wiser acceptance of his body’s limits. “If someone had told me 30 years ago I’d be struggling to finish this race in six hours, I’d have said, ‘Spare me.’ Now I’m grateful.” Beach is a marathoner by demeanor: quiet, unassuming, self-effacing, iron-willed. And by body type: 5-foot-7, 125 pounds. He played all sports as a kid, distinguishing himself at none: “I just didn’t have the size or strength.” As a senior in prep school, he happened upon a radio broadcast of the Boston Marathon. “It was 30 degrees, it was sleeting, and these guys were out there running 26 miles,” he remembers. “Just the sort of bizarre, crazy thing I was drawn to. I already knew I’d be in Boston the next year, so I decided I’d give it a shot.” © 1996-2017 The Washington Post

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23471 - Posted: 04.10.2017

Sarah Jane Tribble In response to outrage from patients and lawmakers, Marathon Pharmaceuticals has delayed the launch of an $89,000 drug for Duchenne muscular dystrophy. The company had announced the annual list price for Emflaza, which is a steroid, after the Food and Drug Administration approved the drug Thursday. Emflaza is approved as an orphan drug, which means it is intended to treat a rare disease. Duchenne is an inherited disorder that causes muscles to become weak. There is no cure for the condition, which mainly affects boys, but some drugs, including Emflaza, are used to lessen symptoms. For years, many American patients have imported deflazacort, the generic version of Emflaza, for about $1,200 a year. But because the medicine wasn't approved in the U.S., the cost of the medicine wasn't typically covered by insurers. That contrast in price between became a flash point Monday as Sen. Bernie Sanders, I-Vt., and Rep. Elijah Cummings, D-Md., sent a letter to Marathon on Monday morning demanding answers about the $89,000 price for a drug that isn't new. It has been used routinely by Duchenne patients in the U.S. since at least 2005. "We believe Marathon is abusing our nation's 'orphan drug' program, which grants companies seven years of market exclusivity to encourage research into new treatments for rare diseases — not to provide companies like Marathon with lucrative market exclusivity rights for drugs that have been available for decades," Sanders and Cummings wrote. Marathon said FDA approval would help more patients get the drug. © 2017 npr

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23234 - Posted: 02.15.2017

Valerie Piro The alarm goes off at 4:30 a.m. Groggy, I turn on the lamp on my night stand and try to sit up. I put my right hand on the wall next to my bed to steady myself, and push my left into the bed. Right away, my abs and back seize up and my legs spasm and kick out straight, forcing me back down onto the bed. Clearly my body thinks it is too early to get up, but I don’t have time to argue with it. I have to get physical therapy out of the way so I can be on time for my medieval history class. After I sit up, I place my hands under my right knee and clasp them together as I bring my knee up and closer to my chest. I reach out to my right foot and cross its heel over my left thigh so that I can plant my heel on the bed. I hug my right leg against my torso and chest and feel a stretch in my lower back and butt. I repeat this on my other side and then proceed to stretch each ankle. Paralysis requires maintenance. I then hop toward the foot of my bed, where my commode chair sits. I set both feet on the footrests as best I can, grab the armrest on the far side of the chair with my left hand, and, using my right hand to drive down into my bed, lift myself onto the commode wheelchair, and wheel to the bathroom. I emerge at 5:35 a.m. I transfer now into a wheelchair whose dimensions are friendly toward my Functional Electrical Stimulation (F.E.S.) cycle — something like a gym exercise bike, without the seat. I pull some milk out of the mini-fridge and pour it over a bowl of cereal. I eat while checking and answering email. At 6:30 it’s time to start cycling. I put two small rectangular electrodes on my left shin muscles, and then two on my right, connect them to the cycle, then strap in my legs and feet. Then two more electrodes then two more, and so on, until most of my lower body is tapped and wired. After I turn on the tablet that’s attached to the cycle, I choose from one of several preset programs to start my workout. Within a couple of minutes, electrical shocks are pulsing into my legs, causing them to contract into pedaling. Imagine pedaling a bicycle uphill for an hour; this is my workout. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23081 - Posted: 01.11.2017

By KATIE THOMAS The Food and Drug Administration has approved the first drug to treat patients with spinal muscular atrophy, a savage disease that, in its most severe form, kills infants before they turn 2. “This is a miracle — seriously,” Dr. Mary K. Schroth, a lung specialist in Madison, Wis., who treats children who have the disease, said of the approval, which was made last week. “This is a life-changing event, and this will change the course of this disease.” Dr. Schroth has previously worked as a paid consultant to Biogen, which is selling the drug. The drug, called Spinraza, will not come cheap — and, by some estimates, will be among the most expensive drugs in the world. Biogen, which is licensing Spinraza from Ionis Pharmaceuticals, said this week that one dose will have a list price of $125,000. That means the drug will cost $625,000 to $750,000 to cover the five or six doses needed in the first year, and about $375,000 annually after that, to cover the necessary three doses a year. Patients will presumably take Spinraza for the rest of their lives. The pricing could put the drug in the cross hairs of lawmakers and other critics of high drug prices, and perhaps discourage insurers from covering it. High drug prices have attracted intense scrutiny in the last year, and President-elect Donald J. Trump has singled them out as an important issue. “We believe the Spinraza pricing decision is likely to invite a storm of criticism, up to and including presidential tweets,” Geoffrey C. Porges, an analyst for Leerink Partners, said in a note to investors on Thursday. Mr. Porges said the price could lead some insurers to balk or to limit the drug to patients who are the most severely affected, such as infants, even though the F.D.A. has approved Spinraza for all patients with the condition. © 2016 The New York Times Company

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23040 - Posted: 12.31.2016