Chapter 11. Motor Control and Plasticity

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Ian Sample Science editor Doctors may be missing signs of serious and potentially fatal brain disorders triggered by coronavirus, as they emerge in mildly affected or recovering patients, scientists have warned. Neurologists are on Wednesday publishing details of more than 40 UK Covid-19 patients whose complications ranged from brain inflammation and delirium to nerve damage and stroke. In some cases, the neurological problem was the patient’s first and main symptom. The cases, published in the journal Brain, revealed a rise in a life-threatening condition called acute disseminated encephalomyelitis (Adem), as the first wave of infections swept through Britain. At UCL’s Institute of Neurology, Adem cases rose from one a month before the pandemic to two or three per week in April and May. One woman, who was 59, died of the complication. A dozen patients had inflammation of the central nervous system, 10 had brain disease with delirium or psychosis, eight had strokes and a further eight had peripheral nerve problems, mostly diagnosed as Guillain-Barré syndrome, an immune reaction that attacks the nerves and causes paralysis. It is fatal in 5% of cases. “We’re seeing things in the way Covid-19 affects the brain that we haven’t seen before with other viruses,” said Michael Zandi, a senior author on the study and a consultant at the institute and University College London Hospitals NHS foundation trust. “What we’ve seen with some of these Adem patients, and in other patients, is you can have severe neurology, you can be quite sick, but actually have trivial lung disease,” he added. “Biologically, Adem has some similarities with multiple sclerosis, but it is more severe and usually happens as a one-off. Some patients are left with long-term disability, others can make a good recovery.” © 2020 Guardian News & Media Limited

Keyword: Stroke; Movement Disorders
Link ID: 27354 - Posted: 07.08.2020

Sherry H-Y. Chou Aarti Sarwal Neha S. Dangayach The patient in the case report (let’s call him Tom) was 54 and in good health. For two days in May, he felt unwell and was too weak to get out of bed. When his family finally brought him to the hospital, doctors found that he had a fever and signs of a severe infection, or sepsis. He tested positive for SARS-CoV-2, the virus that causes COVID-19 infection. In addition to symptoms of COVID-19, he was also too weak to move his legs. When a neurologist examined him, Tom was diagnosed with Guillain-Barre Syndrome, an autoimmune disease that causes abnormal sensation and weakness due to delays in sending signals through the nerves. Usually reversible, in severe cases it can cause prolonged paralysis involving breathing muscles, require ventilator support and sometimes leave permanent neurological deficits. Early recognition by expert neurologists is key to proper treatment. We are neurologists specializing in intensive care and leading studies related to neurological complications from COVID-19. Given the occurrence of Guillain-Barre Syndrome in prior pandemics with other corona viruses like SARS and MERS, we are investigating a possible link between Guillain-Barre Syndrome and COVID-19 and tracking published reports to see if there is any link between Guillain-Barre Syndrome and COVID-19. Some patients may not seek timely medical care for neurological symptoms like prolonged headache, vision loss and new muscle weakness due to fear of getting exposed to virus in the emergency setting. People need to know that medical facilities have taken full precautions to protect patients. Seeking timely medical evaluation for neurological symptoms can help treat many of these diseases. © 2010–2020, The Conversation US, Inc.

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27353 - Posted: 07.08.2020

Jon Hamilton The same process that causes dew drops to form on a blade of grass appears to play an important role in Alzheimer's disease and other brain diseases. The process, known as phase transition, is what allows water vapor to condense into liquid water, or even freeze into solid ice. That same sort of process allows brain cells to constantly reorganize their inner machinery. But in degenerative diseases that include amyotrophic lateral sclerosis, frontotemporal dementia and Alzheimer's, the phase transitions inside neurons seem to go awry, says Dr. J. Paul Taylor, a neurogeneticist at St. Jude Children's Research Hospital in Memphis, and an investigator with the Howard Hughes Medical Institute. This malfunctioning prompts the interior of the cell to become too viscous, Taylor says. "It's as if you took a jar of honey [and] left it in the refrigerator overnight." In this sticky environment, structures that previously could nimbly disassemble and move around become "irreversibly glommed together," says Clifford Brangwynne, a professor of chemical and biological engineering at Princeton University and an investigator with the Howard Hughes Medical Institute. "And when they're irreversibly stuck like that, they can no longer leave to perform functions elsewhere in the cell." That glitch seems to allow toxins to begin to build up in and around these dysfunctional cells, Taylor says — including the toxins associated with Alzheimer's and other neurodegenerative diseases. The science behind this view of brain diseases has emerged only in the past decade. In 2009, Brangwynne was part of a team that published a study showing that phase transitions are important inside cells — or at least inside the reproductive cells of worms. © 2020 npr

Keyword: ALS-Lou Gehrig's Disease ; Alzheimers
Link ID: 27351 - Posted: 07.08.2020

By Gretchen Reynolds When we start to lift weights, our muscles do not strengthen and change at first, but our nervous systems do, according to a fascinating new study in animals of the cellular effects of resistance training. The study, which involved monkeys performing the equivalent of multiple one-armed pull-ups, suggests that strength training is more physiologically intricate than most of us might have imagined and that our conception of what constitutes strength might be too narrow. Those of us who join a gym — or, because of the current pandemic restrictions and concerns, take up body-weight training at home — may feel some initial disappointment when our muscles do not rapidly bulge with added bulk. In fact, certain people, including some women and most preadolescent children, add little obvious muscle mass, no matter how long they lift. But almost everyone who starts weight training soon becomes able to generate more muscular force, meaning they can push, pull and raise more weight than before, even though their muscles may not look any larger and stronger. Scientists have known for some time that these early increases in strength must involve changes in the connections between the brain and muscles. The process appears to involve particular bundles of neurons and nerve fibers that carry commands from the brain’s motor cortex, which controls muscular contractions, to the spinal cord and, from there, to the muscles. If those commands become swifter and more forceful, the muscles on the receiving end should respond with mightier contractions. Functionally, they would be stronger. But the mechanics of these nervous system changes have been unclear. Understanding the mechanics better could also have clinical applications: If scientists and doctors were to better understand how the nervous system changes during resistance training, they might be better able to help people who lose strength or muscular control after a stroke, for example, or as a result of aging or for other reasons. © 2020 The New York Times Company

Keyword: Muscles
Link ID: 27350 - Posted: 07.08.2020

By Gretchen Reynolds When we start to lift weights, our muscles do not strengthen and change at first, but our nervous systems do, according to a fascinating new study in animals of the cellular effects of resistance training. The study, which involved monkeys performing the equivalent of multiple one-armed pull-ups, suggests that strength training is more physiologically intricate than most of us might have imagined and that our conception of what constitutes strength might be too narrow. Those of us who join a gym — or, because of the current pandemic restrictions and concerns, take up body-weight training at home — may feel some initial disappointment when our muscles do not rapidly bulge with added bulk. In fact, certain people, including some women and most preadolescent children, add little obvious muscle mass, no matter how long they lift. But almost everyone who starts weight training soon becomes able to generate more muscular force, meaning they can push, pull and raise more weight than before, even though their muscles may not look any larger and stronger. Scientists have known for some time that these early increases in strength must involve changes in the connections between the brain and muscles. The process appears to involve particular bundles of neurons and nerve fibers that carry commands from the brain’s motor cortex, which controls muscular contractions, to the spinal cord and, from there, to the muscles. If those commands become swifter and more forceful, the muscles on the receiving end should respond with mightier contractions. Functionally, they would be stronger. © 2020 The New York Times Company

Keyword: Movement Disorders; Learning & Memory
Link ID: 27343 - Posted: 07.02.2020

Ruth Williams Turning off just one factor in the brain’s astrocyte cells is sufficient to convert them into neurons in live mice, according to a paper published in Nature today (June 24) and one this spring by another research team in Cell. By flipping this cellular identity switch, researchers have, to some extent, been able to reverse the neuron loss and motor deficits caused by a Parkinson’s-like illness. Not everyone is entirely convinced by the claims. “I think this is very exciting work,” says Pennsylvania State University’s Gong Chen of the Nature paper. It reaffirms that “using the brain’s internal glial cells to regenerate new neurons is a really new avenue for the treatment of brain disorders,” he continues. Chen, who is also based at Jinan University and is the chief scientific officer for NeuExcell—a company developing astrocyte-to-neuron conversion therapies—has performed such conversions in the living mouse brain by a different method but was not involved in the new study. In Parkinson’s disease, dopaminergic neurons within the brain’s substantia nigra—a region in the midbrain involved in movement and reward—gradually die. This results in a deterioration of motor control, characterized by tremors and other types of dyskinesia, with other faculties such as cognition and mood sometimes affected too, especially at later stages of the disease. While treatments to boost diminishing dopamine levels, such as the drug levodopa, can ameliorate symptoms, none can stop the underlying disease process that relentlessly eats away at the patient’s neurological functions and quality of life. © 1986–2020 The Scientist.

Keyword: Parkinsons; Glia
Link ID: 27324 - Posted: 06.26.2020

As we open computers to connect with each other remotely, motor neurons in our spinal cord are opening synaptic pathways to connect with our muscles physically. We rarely think about these electrical signals passing back and forth between computers or our neurons and muscles, until those signals are lost. Kennedy’s disease, a neuromuscular degenerative disease, affects 1 in 40,000 men every year. Little progress has been made in understanding its biological basis since it was identified in the 1960s, but one promising lead may be a family of proteins known as neurotrophic factors. MSU scientists Cynthia Jordan, professor in the College of Natural Science Neuroscience Program, and Katherine Halievski, former Ph.D. student in Jordan’s Lab and lead author, published a benchmark study in the Journal of Physiology describing the key role of one of these proteins in Kennedy’s disease: Brain-Derived Neurotrophic Factor (BDNF). “There were stories that neurotrophic factors could slow down neurodegenerative diseases, but where they fell short was really understanding how they slow down the disease,” Jordan explained. “Where this paper and Katherine’s work stand alone is in using classic neuroscience techniques to understand how BDNF improved neuromuscular function at the cellular level.” Motor neurons are cells that carry signals from the brain to every muscle in the body — fast twitch muscles that perform quick, high impact movements such as jumping, and slow-twitch muscles that sustain long contractions such as standing. At each step in the pathway — from the neuron, along the synaptic pathway and to the muscle — BDNF supports the process, giving both neurons and muscles what they need to connect, survive and thrive. © Michigan State University

Keyword: Movement Disorders; Hormones & Behavior
Link ID: 27320 - Posted: 06.24.2020

Jon Hamilton A neurologist who encased his healthy right arm in a pink fiberglass cast for two weeks has shown how quickly the brain can change after an injury or illness. Daily scans of Dr. Nico Dosenbach's brain showed that circuits controlling his immobilized arm disconnected from the body's motor system within 48 hours. But during the same period, his brain began to produce new signals seemingly meant to keep those circuits intact and ready to reconnect quickly with the unused limb. Dosenbach, an assistant professor at Washington University School of Medicine in St. Louis, repeated the experiment on two colleagues (their casts were purple and blue) and got the same result. In all three people, the disconnected brain circuits quickly reconnected after the cast was removed. The study, published online in the journal Neuron, shows that "within a few days, we can rearrange some of the most fundamental, most basic functional relationships of the brain," Dosenbach says. It suggests it is possible to reverse brain changes caused by disuse of a limb after a stroke or brain injury. The results of the study appear to support the use of something called constraint-induced movement therapy, or CIMT, which helps people – usually children — regain the use of a disabled arm or hand by constraining the other, healthy limb with a sling, splint or cast. Previous studies of CIMT have produced mixed results, in part because they focused on brain changes associated with increased use of a disabled arm, Dosenbach says. "We looked at the effect of actually not using an arm because we thought that was a much more powerful intervention," he says. © 2020 npr

Keyword: Stroke
Link ID: 27311 - Posted: 06.19.2020

By Sam Roberts Oleh Hornykiewicz, a Polish-born pharmacologist whose breakthrough research on Parkinson’s disease has spared millions of patients the tremors and other physical impairments it can cause, died on May 27 in Vienna. He was 93. His death was confirmed by his longtime colleague, Professor Stephen J. Kish of the University of Toronto, where Professor Hornykiewicz (pronounced whor-nee-KEE-eh-vitch) taught from 1967 until his retirement in 1992. Professor Hornykiewicz was among several scientists who were considered instrumental in first identifying a deficiency of the neurotransmitter dopamine as a cause of Parkinson’s disease, and then in perfecting its treatment with L-dopa, an amino acid found in fava beans. The Nobel laureate Dr. Arvid Carlsson and his colleagues had earlier shown that dopamine played a role in motor function. Drawing on that research, Professor Hornykiewicz and his assistant, Herbert Ehringer, discovered in 1960 that the brains of patients who had died of Parkinson’s had very low levels of dopamine. He persuaded another one of his collaborators, the neurologist Walther Birkmayer, to inject Parkinson’s patients with L-dopa, the precursor of dopamine, which could cross the barrier between blood vessels and the brain and be converted into dopamine by enzymes in the body, thus replenishing those depleted levels. The treatment alleviated symptoms of the disease, and patients who had been bedridden started walking. The initial results of this research were published in 1961 and presented at a meeting of the Medical Society of Vienna. The “L-dopa Miracle,” as it was called, inspired Dr. Oliver Sacks’s memoir “Awakenings” (1973) and the fictionalized movie of the same name in 1990. © 2020 The New York Times Company

Keyword: Parkinsons
Link ID: 27299 - Posted: 06.13.2020

Sandra G. Boodman First she toppled off a ladder. Then Carol Hardy-Fanta tripped on a step outside her western Massachusetts home while gazing at her cellphone. Next she fell three times during a five-mile hike after catching her left foot on a rock or tree root. At first, Hardy-Fanta thought her repeated stumbles had a simple cause: She was distracted. But when she racked up more than 30 falls in a three-year period — some for no apparent reason — she repeatedly asked her doctors whether an undiagnosed medical problem might be causing her to “drop like a log.” The 10 doctors she consulted between 2016 and 2019 — four orthopedists, three neurologists, a rheumatologist, a podiatrist and her internist — reached disparate conclusions. One suggested she was clumsy. Others suspected her problem was primarily orthopedic or could find no clear explanation. It wasn't until September 2019 that a scan revealed what Hardy-Fanta had come to suspect — a diagnosis she said several of her doctors had brushed off. “These are the smartest people,” said Hardy-Fanta, now 71, whose husband is a Boston physician. “They really wanted to help” but appeared to be misled by her symptoms. “If someone’s falling that much, they should really pay attention.” The falls started in 2016, shortly after Hardy-Fanta and her husband sold their house in a Boston suburb and began splitting their time between a condo in the city and what she described as their “dream home” in the Berkshires. Hardy-Fanta had retired as director of a university think tank. Her fourth book on women and politics had just been published. She was in excellent health, which she regarded as a legacy from her mother, who remained mentally sharp and physically able until shortly before her death at age 100. Hardy-Fanta said she was looking forward to traveling with her husband and taking long bike rides along the scenic rural roads that snake through the Berkshires.

Keyword: Parkinsons
Link ID: 27216 - Posted: 04.27.2020

By E. Ray Dorsey, Todd Sherer, Michael S. Okun, Bastiaan R. Bloem The number of people with Parkinson’s disease more than doubled from 1990 to 2015 and could double again by 2040. An aging population alone does not account for this rise. Air pollution, metal production, certain industrial chemicals, and some synthetic pesticides are linked to Parkinson’s. Yet we are doing little to manage known risk factors. Neither our increased awareness of the disease nor our lengthening life spans can fully account for the upsurge in diagnoses that we now face. Our knowledge of another neurological disorder, multiple sclerosis, has increased too, and we have improved diagnostic tools for it. Rates for multiple sclerosis have indeed gone up, but that increase is nothing like the exponential rise of Parkinson’s (see figure below). As for aging, more people are, of course, living longer. For example, from 1900 to 2014, the number of individuals over age 65 in the United Kingdom increased about sixfold. However, over that same period, the number of deaths due to Parkinson’s disease increased almost three times faster. Parkinson’s disease is characterized by tremors, slowness in movement, stiffness, and difficulties with balance and walking. It can also cause a wide range of symptoms that are not visible—loss of smell, constipation, sleep disorders, and depression. Most people with Parkinson’s are diagnosed in their fifties or later. But it is not just a disease of the elderly. Up to 10 percent of those with the condition develop the disease in their forties or younger. © 2020 Sigma Xi, The Scientific Research Honor Society

Keyword: Parkinsons; Neurotoxins
Link ID: 27213 - Posted: 04.24.2020

Abby Olena Base editors, which convert one nucleotide to another without a double-strand DNA break, have the potential to treat diseases caused by mutant genes. One drawback, though, is that the DNA that encodes CRISPR base editors is long—too long to fit in the adeno-associated viruses (AAVs) most commonly used for gene therapy. In a study published in Molecular Therapy on January 13, researchers split the DNA encoding a base editor into two AAV vectors and injected them into a mouse model of inherited amyotrophic lateral sclerosis (ALS). The strategy disabled the disease-causing gene, improving the animals’ symptoms and prolonging their lives. “We’d like to be able to make gene editing tools that can fit inside an AAV vector. Unfortunately, some of the tools are so big that they can’t fit inside, so in this study, they were able to come up with a solution to that by using a split protein,” says David Segal, a biochemist at the University of California, Davis, who was not involved in the work. “It’s not the first time that that system has been used, but it’s the first time it’s been applied to this kind of base editor.” Pablo Perez-Pinera, a bioengineer at University of Illinois at Urbana-Champaign, and colleagues developed a strategy to split the base editor into two chunks. In a study published in 2019, they generated two different AAV vectors, each containing a portion of coding DNA for an adenine-to-thymine base editor. They also included sequences encoding so-called inteins—short peptides that when they are expressed within proteins stick together and cleave themselves out, a bit like introns in RNA. The researchers built the inteins into the vectors such that when the inteins produced by the two vectors dimerized, bringing the two base editor parts together, and then excised themselves, they left behind a full-length, functional base editor. © 1986–2020 The Scientist

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 27194 - Posted: 04.15.2020

By Denise Grady Year after year for two decades, Nancy Wexler led medical teams into remote villages in Venezuela, where huge extended families lived in stilt houses on Lake Maracaibo and for generations, had suffered from a terrible hereditary disease that causes brain degeneration, disability and death. Neighbors shunned the sick, fearing they were contagious. “Doctors wouldn’t treat them,” Dr. Wexler said. “Priests wouldn’t touch them.” She began to think of the villagers as her family, and started a clinic to care for them. “They are so gracious, so kind, so loving,” she said. Over time, Dr. Wexler coaxed elite scientists to collaborate rather than compete to find the cause of the disorder, Huntington’s disease, and she raised millions of dollars for research. Her work led to the discovery in 1993 of the gene that causes Huntington’s, to the identification of other genes that may have moderating effects and, at long last, to experimental treatments that have begun to show promise. Now, at 74, Dr. Wexler is facing a painful and daunting task that she had long postponed. She has decided it’s time to acknowledge publicly that she has the disease she’s spent her life studying and that killed her mother, uncles and grandfather. “There is such stigma, and such ostracization,” Dr. Wexler, a professor of neuropsychology at the College of Physicians and Surgeons at Columbia University, said in a lengthy interview. “I think it’s important to destigmatize Huntington’s and make it not as scary. Of course it is scary. Having a fatal disease is scary and I don’t want to trivialize that. But if I can say, I’m not stopping my life, I’m going to work, we’re still trying to find a cure, that would help. If I can do anything to take the onus off having this thing, I want to do it.” Among her greatest concerns are the thousands of Venezuelans from the families full of the disease, whose willingness to donate blood and skin samples, and the brains of deceased relatives, made it possible to find the gene. But they live in an impoverished region, and, Dr. Wexler said, they are still outcasts. The clinic that she and her colleagues opened has been shut down by Venezuela’s government. © 2020 The New York Times Company

Keyword: Huntingtons; Genes & Behavior
Link ID: 27110 - Posted: 03.10.2020

By Karen Weintraub At age 16, German Aldana was riding in the back seat of a car driven by a friend when another car headed straight for them. To avoid a collision, his friend swerved and hit a concrete pole. The others weren’t seriously injured, but Aldana, unbuckled, was tossed around enough to snap his spine just below his neck. For the next five years, he could move only his neck, and his arms a little. Right after he turned 21 and met the criteria, Aldana signed up for a research project at the University of Miami Miller School of Medicine near his home. Researchers with the Miami Project to Cure Paralysis carefully opened Aldana's skull and, at the surface of the brain, implanted electrodes. Then, in the lab, they trained a computer to interpret the pattern of signals from those electrodes as he imagines opening and closing his hand. The computer then transfers the signal to a prosthetic on Aldana's forearm, which then stimulates the appropriate muscles to cause his hand to close. The entire process takes 400 milliseconds from thought to grasp. A year after his surgery, Aldana can grab simple objects, like a block. He can bring a spoon to his mouth, feeding himself for the first time in six years. He can grasp a pen and scratch out some legible letters. He has begun experimenting with a treadmill that moves his limbs, allowing him to take steps forward or stop as he thinks about clenching or unclenching the fingers of his right hand. But only in the lab. Researchers had permission to test it only in their facility, but they’re now applying for federal permission to extend their study. The hope is that by the end of this year, Aldana will be able to bring his device home — improving his ability to feed himself, open doors and restoring some measure of independence.

Keyword: Robotics
Link ID: 27107 - Posted: 03.09.2020

By Kelly Servick Building a beautiful robotic hand is one thing. Getting it to do your bidding is another. For all the hand-shaped prostheses designed to bend each intricate joint on cue, there’s still the problem of how to send that cue from the wearer’s brain. Now, by tapping into signals from nerves in the arm, researchers have enabled amputees to precisely control a robotic hand just by thinking about their intended finger movements. The interface, which relies on a set of tiny muscle grafts to amplify a user’s nerve signals, just passed its first test in people: It translated those signals into movements, and its accuracy stayed stable over time. “This is really quite a promising and lovely piece of work,” says Gregory Clark, a neural engineer at the University of Utah who was not involved in the research. It “opens up new opportunities for better control.” Most current robotic prostheses work by recording—from the surface of the skin—electrical signals from muscles left intact after an amputation. Some amputees can guide their artificial hand by contracting muscles remaining in the forearm that would have controlled their fingers. If those muscles are missing, people can learn to use less intuitive movements, such as flexing muscles in their upper arm. These setups can be finicky, however. The electrical signal changes when a person’s arm sweats, swells, or slips around in the socket of the prosthesis. As a result, the devices must be recalibrated over and over, and many people decide that wearing a heavy robotic arm all day just isn’t worth it, says Shriya Srinivasan, a biomedical engineer at the Massachusetts Institute of Technology. © 2020 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 27095 - Posted: 03.05.2020

When the spinal cord is injured, the damaged nerve fibers — called axons — are normally incapable of regrowth, leading to permanent loss of function. Considerable research has been done to find ways to promote the regeneration of axons following injury. Results of a study performed in mice and published in Cell Metabolism suggests that increasing energy supply within these injured spinal cord nerves could help promote axon regrowth and restore some motor functions. The study was a collaboration between the National Institutes of Health and the Indiana University School of Medicine in Indianapolis. “We are the first to show that spinal cord injury results in an energy crisis that is intrinsically linked to the limited ability of damaged axons to regenerate,” said Zu-Hang Sheng, Ph.D., senior principal investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and a co-senior author of the study. Like gasoline for a car engine, the cells of the body use a chemical compound called adenosine triphosphate (ATP) for fuel. Much of this ATP is made by cellular power plants called mitochondria. In spinal cord nerves, mitochondria can be found along the axons. When axons are injured, the nearby mitochondria are often damaged as well, impairing ATP production in injured nerves. “Nerve repair requires a significant amount of energy,” said Dr. Sheng. “Our hypothesis is that damage to mitochondria following injury severely limits the available ATP, and this energy crisis is what prevents the regrowth and repair of injured axons.” Adding to the problem is the fact that, in adult nerves, mitochondria are anchored in place within axons. This forces damaged mitochondria to remain in place while making it difficult to replace them, thus accelerating a local energy crisis in injured axons.

Keyword: Regeneration
Link ID: 27091 - Posted: 03.04.2020

By Abdul-Kareem Ahmed “I use a spoon instead of a fork, so I spill less,” the patient said. “I eat sandwiches and hamburgers so I can use both hands to hold my food.” He was 73 and had suffered from essential tremor for the past decade. His hands would shake uncontrollably, more on the right than on the left, which would worsen if he tried using them. “I could still do crowns, but giving injections became impossible,” he said. His disease, gradual and grasping, had forced the Baltimore-area dentist into early retirement. The patient, who is not being named to protect his privacy, was going to undergo surgery to treat his tremor, which I was curious to observe. I headed to the MRI exam suite to meet him. Wearing a hospital gown, he sat at the edge of his bed, talking to the attending neurosurgeon. He was tall, and balder today than he usually was. As was required, he had shaved his head. Essential tremor is a neurological disease that can affect the torso, arms, neck, head or even voice. Medications are used to attenuate symptoms, but for many patients, these fail or are difficult to tolerate. “I don’t want to take medications forever,” he said. A particularity to this disease is social visibility. Like our patient, people with essential tremor tend to withdraw from society, feeling self-conscious about their inability to perform simple tasks. Dropping food, drinks or other objects is quickly noticed by others.

Keyword: Movement Disorders
Link ID: 27087 - Posted: 03.03.2020

Merrit Kennedy As doctors in London performed surgery on Dagmar Turner's brain, the sound of a violin filled the operating room. The music came from the patient on the operating table. In a video from the surgery, the violinist moves her bow up and down as surgeons behind a plastic sheet work to remove her brain tumor. The King's College Hospital surgeons woke her up in the middle of the operation in order to ensure they did not compromise parts of the brain necessary for playing the violin, such as parts that control precise hand movements and coordination. "We knew how important the violin is to Dagmar, so it was vital that we preserved function in the delicate areas of her brain that allowed her to play," Keyoumars Ashkan, a neurosurgeon at King's College Hospital, said in a press release. Turner, 53, learned that she had a slow-growing tumor in 2013. Late last year, doctors found that it had become more aggressive and the violinist decided to have surgery to remove it. In an interview with ITV News, Turner recalled doctors telling her, "Your tumor is on the right-hand side, so it will not affect your right-hand side, it will affect your left-hand side." "And I'm just like, 'Oh, hang on, this is my most important part. My job these days is playing the violin,' " she said, making a motion of pushing down violin strings with her left hand. Ashkan, an accomplished pianist, and his colleagues came up with a plan to keep the hand's functions intact. © 2020 npr

Keyword: Epilepsy; Movement Disorders
Link ID: 27054 - Posted: 02.20.2020

Scott Grafton When people ask me about the “mind-body connection,” I typically suggest walking on an icy sidewalk. Skip the yoga, mindfulness, or meditation, and head to the corner on a cold, windy, snowy day. Every winter, much of North America becomes exceedingly slippery with ice. Emergency rooms across the continent see a sharp uptick in fractured limbs and hips as people confidently trudge outside in such conditions, unveiling a profound disconnection between what people believe and what they can actually do with their bodies. One might think that a person could call on experience from years past to adjust their movement or provide a little insight or caution. But the truth is that the body forgets what it takes to stay upright in these perilous conditions. Why is there so much forgetting and relearning on an annual basis? We remember how to ride a bike. Why can’t we remember how to walk on ice? I attempt to answer this and other questions concerning the connection (or lack thereof) between motion in the mind and motion by the body in my new book, Physical Intelligence: The Science of How the Body and the Mind Guide Each Other Through Life. Pantheon, January 2020 Falling on ice reveals a delicate tradeoff that the brain must reconcile as it pilots the body. On the one hand, it needs to build refined motor programs to execute skills such as walking, running, and throwing. On the other hand, those programs can’t be too specific. There is a constant need to tweak motor plans to account for dynamic conditions. When I throw a backpack on, my legs don’t walk in the same way as they do without the pack: my stance widens, my stride shortens. Often, the tweaking needs to happen in moments. As I pick the pack up, I need to lean in or I could tip myself over. Just as importantly, as soon as I put it down, I need to forget I ever held it in the first place. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27001 - Posted: 01.28.2020

By Megan Schmidt Scientists say they’ve figured out what causes essential tremor, a common neurological disorder characterized by involuntary, rhythmic trembling that typically occurs in the hands. In a paper published in Science Translational Medicine this week, researchers at National Taiwan University and Columbia University Irving Medical Center discovered that people with essential tremor have abnormal connections among the neurons in their cerebellum, a region in the back of the brain that’s involved in the coordination of voluntary movement. Researchers say people with these abnormalities tend to generate overactive brain waves, or too much electrical activity, in this region of the brain, which is what fuels the tremors. In addition to pinpointing the roots of the disorder, the researchers say their work uncovered some new approaches that could potentially treat and diagnose essential tremor more effectively. Essential tremor is often mistaken for Parkinson’s disease, but there are some key distinctions that set these movement disorders apart. Parkinson’s, which is less common than essential tremor, is caused by the progressive loss of dopamine neurons in the midbrain, a small region of the brain that plays an important role in motor function. Essential tremor, as this new research reveals, is linked to abnormalities in the hindbrain — specifically, the cerebellum. © 2020 Kalmbach Media Co.

Keyword: Movement Disorders
Link ID: 26994 - Posted: 01.25.2020