Links for Keyword: Movement Disorders

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By Christine Hauser Health authorities in the United States said this week that they were investigating an unusual spike in cases of a rare condition that causes limb paralysis and severe muscle weakness in children. Since mid-September, six cases of the condition, acute flaccid myelitis, in children under 10 years old have been reported to the Minnesota Department of Health, the agency said. Another two possible cases are pending confirmation, officials said. The number of cases of the illness, also known as A.F.M., is the highest in the state since 2014, when there were three reported cases, the health authorities said. Minnesota typically records one case of A.F.M. each year, and some years it does not have any at all, the department said. Officials have not found a specific cause for the illness. On Tuesday, the health authorities said three children suspected to have A.F.M. were being treated at UPMC Children’s Hospital of Pittsburgh. Officials in Colorado said this week that they were investigating a viral infection outbreak among children that included 14 cases of A.F.M. this year. The Centers for Disease Control and Prevention says it has seen an increasing number of people across the United States with the serious condition in the past four years. A.F.M. affects the nervous system and causes, mostly in children, paralysis similar to polio. The signs include sudden muscle weakness in the arms or legs; neck weakness or stiffness; a drooping face or eyelids; difficulty swallowing; and slurred speech, health officials say. Parents usually notice the child’s loss of the use of an arm or a leg. That was the case with Orville Young, a 4-year-old boy in Minnesota who lost mobility in his right arm and had difficulty sitting up and moving his legs. © 2018 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 25562 - Posted: 10.11.2018

Anna Azvolinsky When you move only your right arm, there’s neural activity in both the left and right sides of the brain, researchers report today (October 8) in The Journal of Neuroscience. Recent animal and human studies have hinted that moving muscle on only one side of the body resulted in neural activity from the same side—or ipsilateral—part of the brain. But the data haven’t been convincing enough to completely erase the idea that only the left side of the brain is responsible for movement on the right side of the body or vice versa. The new study shows the ipsilateral brain activity encodes detailed arm movement information including position, speed, and velocity. The results could one day be used to help improve recovery therapies for patients with brain injuries. “This is an important contribution to our understanding of how the brain controls arm movement because it reveals a greater role of ipsilateral brain activity than previously recognized,” writes Nathan Crone, a professor of neurology who runs a cognitive neurophysiology lab at Johns Hopkins University in Maryland and was not involved in the research, in an email to The Scientist. In the study, Eric Leuthardt, professor of neurosurgery, engineering, and neuroscience at Washington University in St. Louis, and his colleagues enlisted four patients with epilepsy who were to undergo surgery and who had electrodes implanted for a week under the skull. The electrodes were placed directly onto the cortex of the patients’ brain cortex regions, including the primary motor cortex—responsible for coordinating voluntary muscle movements. The patients volunteered to perform three-dimensional, individual arm motions while the researchers recorded neural activity from the implanted electrodes. The team then used machine learning to derive speed, velocity, and position information on each movement—gathering data on fine motor movements that cannot be easily captured using noninvasive techniques such as functional magnetic resonance imaging (fMRI). © 1986 - 2018 The Scientist.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25561 - Posted: 10.11.2018

Laura Sanders With the help of a spine stimulator and intensive training, a formerly paralyzed man can command his legs to step again. This achievement, described online September 24 in Nature Medicine, inches researchers closer to restoring movement to paraplegic people. The therapy allows 29-year-old Jered Chinnock to control his leg movements with his thoughts. “This is highly significant,” study coauthor Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minn., said in a news briefing on September 20. A snowmobile wreck left Chinnock paralyzed, unable to move or feel sensations below the chest. His initial rehabilitation focused on acclimating to life in a wheelchair. But three years after the accident, he enrolled in an aggressive study designed to get him moving. Surgeons implanted a stimulator that zaps nerve cells on the spinal cord below the site of Chinnock’s injury. With the stimulator on, therapists led Chinnock through exercises to reactivate muscles and nerves. Over two weeks of training with the stimulator, he could stand and, while lying on his side, make voluntary steplike movements. Those results were published last year in Mayo Clinic Proceedings. Now, after 43 weeks of intense rehabilitation, Chinnock has made even greater strides. He can step on a treadmill on his own, and, with assistance and a walker, can step across the ground. Over the course of one training session, he was able to travel 102 meters, about the length of an American football field, the researchers report. Because he required assistance, researchers describe Chinnock’s motion as “independent stepping” rather than walking. That’s because, in clinical terms, walking describes “a highly coordinated activity in terms of balance, strength and adaptation to the environment,” said Lee’s coauthor Kristin Zhao, also of the Mayo Clinic. |© Society for Science & the Public 2000 - 2018.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25491 - Posted: 09.25.2018

by Marvin M. Lipman, ‘I thought I had Parkinson’s disease!” the 65-year-old stock analyst exclaimed. Over the past six months, her handwriting had deteriorated to the point that she was having difficulty signing checks. Because a good friend of hers had recently received a diagnosis of Parkinson’s disease, she feared the worst. I began to suspect that her concern was groundless when I noticed that both of her hands shook and that she had a barely noticeable to-and-fro motion of her head — two signs that are uncommon in Parkinson’s disease. And as she walked toward the examining room, her gait was normal and her arms swung freely — hardly the stiff, hesitant shuffle so often seen with Parkinson’s. The exam turned up none of the other cardinal manifestations of Parkinson’s: the typical masklike facial expression; the slowed, monotonous speech pattern; and the ratchet-like sensation the examiner feels when alternately flexing and extending the patient’s arm. Moreover, her hand tremors seemed to improve at rest and worsen when asked to do the “finger to nose” test. The diagnosis was unmistakable: She had essential tremor, a nervous-system problem that causes unintentional shaking, most often starting in the hands. © 1996-2018 The Washington Post

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25486 - Posted: 09.25.2018

Marcy Cuttler · CBC News Janaya Chekowski-McKenzie was born with the odds against her. On the day she arrived in 2009, she was non-responsive, and she spent a month in hospital with a lung infection. At three months, she had a seizure. Janaya needed hormone replacements to grow and doctors determined she had underdeveloped optic nerves. In spite of these early difficulties, the Beaumont, Alta., youngster has grown up to be a sassy, funny, bright girl with a lion's mane of curly-brown hair. When Janaya started complaining of worsening headaches last January, her mother, Amanda Chekowski, thought it was yet another medical hurdle to overcome. Instead, doctors told her Janaya had a rare, incurable form of brain cancer called diffuse intrinsic pontine glioma, or DIPG. Hearing the news, Chekowski and her family were stunned. They had to figure out how to explain this to an eight-year-old in terms she would understand. Initially, they made a bit of a joke of it. Janaya was told that "we found a booger in your brain that's not supposed to be there and we're going to try to shrink it," said Chekowski. The truth is very different. DIPG is a cancer that targets kids, and thus far, none have survived. But doctors around the world are trying to change that. ©2018 CBC/Radio-Canada.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25416 - Posted: 09.05.2018

Laurel Hamers Gene editing can reverse muscular dystrophy in dogs. Using CRISPR/Cas9 in beagle puppies, scientists have fixed a genetic mutation that causes muscle weakness and degeneration, researchers report online August 30 in Science. Corrections to the gene responsible for muscular dystrophy have been made before in mice and human muscle cells in dishes, but never in a larger mammal. The results, though preliminary, bring scientists one step closer to making such treatments a reality for humans, says study coauthor Eric Olson, a molecular biologist at the University of Texas Southwestern Medical Center in Dallas. Duchenne muscular dystrophy is a rare but severe, progressive disease that affects mostly boys and men. People with the disease, which is just one of many types of muscular dystrophy, rarely live past their 20s, usually dying of heart failure. An estimated 300,000 people worldwide suffer from the condition. The disease can be caused by any number of mutations to the gene that makes the protein dystrophin, which is essential for muscle structure and function. The mutations, which are often clustered in one particular region of the gene, usually stop production of the protein. Gene editing targeting that region could correct for these mutations’ effects, restoring protein production. Researchers injected two 1-month-old beagle puppies with a mutation in this hot spot with different doses of a virus carrying the gene-editing machinery. The team then measured dystrophin levels in different muscles after eight weeks. |© Society for Science & the Public 2000 - 201

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25403 - Posted: 08.31.2018

by Lynn Peterson Mobley We started our ascent of Italy’s Stromboli volcano at dusk, as the Tyrrhenian Sea darkened behind us. It was a long, steady trek upward, but not an exhausting one. At the crater’s rim, with fountains and bombs of glowing lava exploding into the night sky, we soon forgot the effort it had taken to get there. Going down, however, was unforgettably harder. The trail through the deep black sand blanketing the massive cone was impossible to follow by the paltry light of our helmet lamps. I had never witnessed my athletic husband struggle before. He stumbled down the mountain for two hours with borrowed walking sticks, falling more than once. We had been hiking along the Volcano Route: Vesuvius, Amalfi’s Trail of the Gods, Vulcano, Etna. Robert was a fit 70-year-old then, never sick in his life. But after Stromboli, things weren’t quite the same. Back in Rome for a few days before our flight home, he was aware of weakness in his feet and lower legs. His shoes slapped the sidewalks as if they were too big. It took forever to get back to our hotel after a day of sightseeing. He was tired, yes, but this was different. Later that year, in 2010, he was diagnosed with a disease that we had never heard of, and that he shared with millions of other Americans: peripheral neuropathy, or PN. As we were to learn, the nervous system is composed of two parts. The brain and spinal cord make up the central nervous system, while the nerves running from them form the peripheral nervous system. PN encompasses damage to the nerves that deliver messages to or from the brain. Damage to the sensory nerves can mean tingling or numbness in the hands, feet and legs; damage to motor nerves that control the muscles causes loss of strength and balance; damage to the autonomic nervous system, which regulates automatic functions, affects things such as heart rate, blood pressure, bladder control and digestion, along with a host of other involuntary responses. © 1996-2018 The Washington Post

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25186 - Posted: 07.09.2018

By Meredith Wadman Roughly once a day in the United States, a child is born with a fatal genetic disorder that destroys motor neurons in the brain stem and spinal cord. In its worst and most common form, spinal muscular atrophy (SMA) kills children when they are still toddlers, as their respiratory muscles fail. But 18 months ago, the Food and Drug Administration approved a first, promising treatment: a drug that restores production of a key protein missing in SMA. Now, SMA advocacy groups and members of Congress are urging Secretary of Health and Human Services (HHS) Alex Azar to recommend that all 4 million infants born in the United States each year be tested for SMA. They argue that affected children should be identified and treated when the new drug likely helps the most—before neurons die. By law, Azar faces an 8 July deadline, but such deadlines have been missed in the past. And although an advisory panel voted in February in favor of screening all newborns, some of its experts dissented. They noted that key studies of the new treatment—a drug called nusinersen (marketed as Spinraza by Biogen of Cambridge, Massachusetts)—are still ongoing, involve small numbers of children, and are unpublished. But delay "would be a tragedy for children born in the interim who may benefit from screening because they will miss the window for receiving treatment when it is most effective," 14 members of the House of Representatives wrote to Azar last month, urging speedy approval. An HHS spokesperson says Azar is "still reviewing this important issue." © 2018 American Association for the Advancement of Science.

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 25156 - Posted: 06.29.2018

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 BN: 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 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 BN: 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 BN: 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 BN: 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 BN: Chapter 11: Motor Control and Plasticity; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 14: Attention and Higher Cognition
Link ID: 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 BN: 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 BN: 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 BN: 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 BN: 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 BN: 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 BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 23960 - Posted: 08.15.2017