Chapter 11. Motor Control and Plasticity

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By RONI CARYN RABIN A. Parkinsonism refers to a group of movement abnormalities — such as stiffness, slowness, shuffling of the feet and often tremor — that are classic features of Parkinson’s disease but that can also be caused by medications and other disorders with overlapping symptoms, said Dr. Michael S. Okun, a neurologist and the national medical director of the Parkinson’s Foundation. He said that he makes no assumptions about the cause of parkinsonism “until I see the patient and pinpoint the diagnosis.” Determining the cause of parkinsonism involves asking a series of questions, starting with, “Do we think this is regular Parkinson’s disease?” said Dr. Okun, who is also co-director of the Center for Movement Disorders and Neurorestoration at the University of Florida College of Medicine in Gainesville. Though a diagnosis of Parkinson’s disease strikes fear in patients, Dr. Okun said that the illness, a neurodegenerative brain disorder caused by the loss of dopamine-containing neurons and other cells, progresses slowly in many people and generally responds well to drugs that replenish dopamine in the brain. Some patients whose parkinsonism is not caused by Parkinson’s disease also respond to these drugs, but the medications are most effective for people with Parkinson’s disease, Dr. Okun said. It’s important to rule out other potential causes of parkinsonism, he said. The condition can be triggered by antipsychotic medications that affect dopamine levels in the brain, as well as by other drugs, including stimulants like amphetamines and cocaine. Discontinuing the drugs may stop the symptoms over time, though not always. Parkinsonism may also be caused by repeated injuries to the head, exposure to various toxins or brain lesions. Once doctors rule out Parkinson’s disease, they must consider several other serious neurological disorders. The three most common ones are multiple system atrophy, a degenerative disorder also referred to as Shy-Drager syndrome, which may or may not respond well to Parkinson’s medications; progressive supranuclear palsy, or PSP, which also may respond to high doses of drugs that replace dopamine in the brain; and corticobasal degeneration (CBD). Patients with a form of dementia called Lewy body dementia may also exhibit symptoms of parkinsonism, which may or may not respond to dopamine. Various other movement disorders, called ataxias or dystonias, also may display features of parkinsonism. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 24335 - Posted: 11.17.2017

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.

Keyword: Movement Disorders; Genes & Behavior
Link ID: 24280 - Posted: 11.02.2017

By Jessica Hamzelou Can you catch Alzheimer’s disease? Fear has been growing that the illness might be capable of spreading via blood transfusions and surgical equipment, but it has been hard to find any evidence of this happening. Now a study has found that an Alzheimer’s protein can spread between mice that share a blood supply, causing brain degeneration, and suggesting that the disease may transmissible in a similar way to Creutzfeldt-Jacob Disease (CJD). We already know from CJD that misfolded proteins can spread brain diseases. Variant CJD can spread through meat products or blood transfusions infected with so-called prion proteins, for example. Like CJD, Alzheimer’s also involves a misfolded protein called beta-amyloid. Plaques of this protein accumulate in the brains of people with the illness, although we still don’t know if the plaques cause the condition, or are merely a symptom. There has been evidence that beta-amyloid may spread like prions. Around 50 years ago, many people with a growth disorder were treated with growth hormone taken from cadavers. Many of the recipients went on to develop CJD, as these cadavers turned out to be carrying prions. But decades later, it emerged in postmortems that some of these people had also developed Alzheimer’s plaques, despite being 51 or younger at the time. The team behind this work suggested investigating whether beta-amyloid was spreading via blood products or surgical instruments, just as they can spread prions. © Copyright New Scientist Ltd

Keyword: Alzheimers; Prions
Link ID: 24266 - Posted: 10.31.2017

A new study published in the journal Neuron sheds light on the normal function of LRRK2, the most common genetic cause for late-onset Parkinson’s disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For more than 10 years, scientists have known that mutations in the LRRK2 gene can lead to Parkinson’s disease, yet both its role in the disease and its normal function in the brain remain unclear. In a study in mice, researchers have now found that LRRK is necessary for the survival of dopamine-containing neurons in the brain, the cells most affected by Parkinson’s. Importantly, this finding could alter the design of treatments against the disease. “Since its discovery, researchers have been trying to define LRRK2 function and how mutations may lead to Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “The findings in this paper emphasize the importance of understanding the normal role for genes associated with neurodegenerative disorders.” LRRK2 is found along with a closely related protein, LRRK1, in the brain. A mutation in LRRK2 alone can eventually produce Parkinson’s disease symptoms and brain pathology in humans as they age. In mice, however, LRRK2 loss or mutation does not lead to the death of dopamine-producing neurons, possibly because LRRK1 plays a complementary or compensatory role during the relatively short, two-year mouse lifespan.

Keyword: Parkinsons
Link ID: 24254 - Posted: 10.28.2017

By GRETCHEN REYNOLDS Do brains trump brawn? A remarkable new study of how the human body prioritizes its inner workings found that if you intensely think at the same time as you intensely exercise, your performance in both thinking and moving can worsen. But your muscles’ performance will decline much more than your brain’s will, the study found. The results raise interesting questions about the roles that our body’s wide-ranging abilities may have played in the evolution of humans and also whether a hard workout is the ideal time to be cogitating. Compared to almost all other animals, we humans have disproportionately large brains for our size. Our supersized cranial contents probably provided an advantage during our evolution as a species. Smart creatures presumably could have outwitted predators and outmaneuvered prey, keeping themselves fed, uneaten and winners in the biological sweepstakes to pass on their genes. But most other species eschewed developing similarly outsized brains during evolution, because large brains carry a hefty metabolic cost. Brains are extraordinarily hungry organs, requiring, ounce for ounce, more calories to sustain their operations than almost any other tissue, and these caloric demands rise when the brain is hard at work. Thinking demands considerable bodily fuel. In order to feed and maintain these large brains, early humans’ bodies had to make certain trade-offs, most evolutionary biologists agree. Our digestive systems shrank during evolution, for one thing, since food processing is also metabolically ravenous. But whether a similar trade-off occurred with our muscles has remained in doubt. Muscles potentially provided another route to survival during our species’ early days. With sufficient brawn, animals, including people, could physically overpower prey and sprint from danger. © 2017 The New York Times Company

Keyword: Attention
Link ID: 24243 - Posted: 10.26.2017

Jules Montague Steve Thomas and I are talking about brain implants. Bonnie Tyler’s Holding Out For a Hero is playing in the background and for a moment I almost forget that a disease has robbed Steve of his speech. The conversation breaks briefly; now I see his wheelchair, his ventilator, his hospital bed. Steve, a software engineer, was diagnosed with ALS (amyotrophic lateral sclerosis, a type of motor neurone disease) aged 50. He knew it was progressive and incurable; that he would soon become unable to move and, in his case, speak. He is using eye-gaze technology to tell me this (and later to turn off the sound of Bonnie Tyler); cameras pick up light reflection from his eye as he scans a screen. Movements of his pupils are translated into movements of a cursor through infrared technology and the cursor chooses letters or symbols. A speech-generating device transforms these written words into spoken ones – and, in turn, sentences and stories form. Eye-gaze devices allow some people with limited speech or hand movements to communicate, use environmental controls, compose music, and paint. That includes patients with ALS – up to 80% have communication difficulties, cerebral palsy, strokes, multiple sclerosis and spinal cord injuries. It’s a far cry from Elle editor-in-chief Jean-Dominique Bauby, locked-in by a stroke in 1995, painstakingly blinking through letters on an alphabet board. His memoir, written at one word every two minutes, later became a film, The Diving Bell and the Butterfly. Although some still use low-tech options (not everyone can meet the physical or cognitive requirements for eye-gaze systems; occasionally, locked-in patients can blink but cannot move their eyes), speech-to-text and text-to-speech functionality on smartphones and tablets has revolutionised communication. © 2017 Guardian News and Media Limited

Keyword: Robotics
Link ID: 24200 - Posted: 10.16.2017

Victoria Lorrimar Michael Burdett The idea of dangerous, inhumane artificial intelligence taking over the world is familiar to many of us, thanks to cautionary tales such as the Matrix and Terminator franchises. But what about the more sympathetic portrayals of robots? The benevolence of Arnold Schwarzenegger’s Terminator character in the later movies of the franchise may have been the exception in older portrayals of AI, but human-like machines are often represented more positively in contemporary films. Think of Ex Machina, Chappie or A.I. Artificial Intelligence. This shift is very likely representative of a wider shift in how we think about these technologies in reality. Blade Runner 2049, long-anticipated sequel to the original 1982 Blade Runner film, is a part of this shift. The ability of science fiction to inspire technological innovation is well-known. A lot of science fiction writers are scientists and technologists (Arthur C Clarke and Geoffrey Landis are two examples), and ideas from science fiction have sparked more serious scientific research (touch screens and tablet computers are common examples). But science fiction serves other purposes too. It can be a tool for exploring the social and ethical implications of technologies being developed now – a fictional laboratory for testing possible futures. It can also prepare us to deal with certain technologies as they arise in the real world. © 2010–2017, The Conversation US, Inc.

Keyword: Consciousness; Robotics
Link ID: 24160 - Posted: 10.07.2017

By GRETCHEN REYNOLDS Because we can never have enough reasons to keep exercising, a new study with mice finds that physical activity not only increases the number of new neurons in the brain, it also subtly changes the shape and workings of these cells in ways that might have implications for memory and even delaying the onset of dementia. As most of us have heard, our brains are not composed of static, unchanging tissue. Instead, in most animals, including people, the brain is a dynamic, active organ in which new neurons and neural connections are created throughout life, especially in areas of the brain related to memory and thinking. This process of creating new neurons, called neurogenesis, can be altered by lifestyle, including physical activity. Many past studies have shown that in laboratory rodents, exercise doubles or even triples the number of new cells produced in adult animals’ brains compared to the brains of animals that are sedentary. But it has not been clear whether the new brain cells in active animals are somehow different from comparable new neurons in inactive animals or if they are just more numerous. That question has long interested scientists at the Laboratory of Neurosciences at the National Institute on Aging, who have been examining how running alters the brains and behavior of lab animals. Last year, in an important study published in NeuroImage, the researchers found for the first time that young brain cells in adult mice that spent a month with running wheels in their cages did seem to be different from those in animals that did not run. For the experiment, the scientists injected a modified rabies vaccine into the animals, where it entered the nervous system and brain. They then tracked and labeled connections between brain cells and learned that compared to the sedentary animals’ brain cells, the runners’ newborn neurons had more and longer dendrites, the snaky tendrils that help to connect the cells into the neural communications network. They also found that more of these connections led to portions of the brain that are important for spatial memory, which is our internal map of where we have been and how we got there. © 2017 The New York Times Company

Keyword: Neurogenesis; Development of the Brain
Link ID: 24145 - Posted: 10.04.2017

By Dan Stark I used to tell people considering deep brain stimulation — which involves the surgical implantation of electrodes into the brain — that it gave the typical Parkinson’s sufferer perhaps 10 years of relief, during which the symptoms would be relatively minor. The bet — this is, after all, brain surgery that carries some risk of serious adverse results — would be that sometime during that decade, researchers would come up with a real solution. In other words, DBS was a way to buy time. Still, 10 years is no small period, particularly for those who have no other hope. My experience is typical. I had DBS just under 12 years ago. Things went so well that I became a huge fan of the procedure. But DBS works on only some Parkinson’s symptoms. (Drooling, for example, is not affected.) For slightly more than a decade, DBS performed wonders on me, eliminating the shakes that had accompanied my attempts to beat back Parkinson’s symptoms with medicine alone. But because DBS masks the symptoms while not affecting the underlying disease, in the end it will fail the Parkinson’s patient. For me, the failure was in the form of a one-two punch. The first blow was self-inflicted. In April, one of the batteries powering my neural implants died. That was my fault; one should monitor the batteries and replace them in advance. Because I hadn’t, I got a taste of what life would be like without the stimulators. © 1996-2017 The Washington Post

Keyword: Parkinsons
Link ID: 24132 - Posted: 10.02.2017

By GRETCHEN REYNOLDS For most of us, temptations are everywhere, from the dessert buffet to the online shoe boutique. But a new study suggests that exercise might be a simple if unexpected way to increase our willpower and perhaps help us to avoid making impulsive choices that we will later regret. Self-control is one of those concepts that we all recognize and applaud but do not necessarily practice. It requires forgoing things that entice us, which, let’s face it, is not fun. On the other hand, lack of self-control can be consequential for health and well-being, often contributing to problems like weight gain, depression or money woes. Given these impacts, scientists and therapists have been interested in finding ways to increase people’s self-restraint. Various types of behavioral therapies and counseling have shown promise. But such techniques typically require professional assistance and have for the most part been used to treat people with abnormally high levels of impulsiveness. There have been few scientifically validated options available to help those of us who might want to be just a little better at resisting our more devilish urges. So for the new study, which was published recently in Behavior Modification, a group of researchers at the University of Kansas in Lawrence began wondering about exercise. Exercise is known to have considerable psychological effects. It can raise moods, for example, and expand people’s sense of what they are capable of doing. So perhaps, the researchers speculated, exercise might alter how well people can control their impulses. To find out, the scientists decided first to mount a tiny pilot study, involving only four men and women. © 2017 The New York Times Company

Keyword: Obesity; Attention
Link ID: 24119 - Posted: 09.28.2017

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

Keyword: Movement Disorders
Link ID: 24111 - Posted: 09.26.2017

By Nathaniel P. Morris A growing trend in medicine has doctors prescribing visits to parks for their patients. A pediatrician named Robert Zarr at Unity Health Care in Washington, D.C., has worked with the National Park Service and other institutions to create DC Park Rx, an initiative that helps health care providers prescribe activity in outdoor spaces to patients. And National Geographic recently highlighted the rise of this practice in Vermont, where doctors are now prescribing thousands of visits to state parks. In the last several years park prescription programs have spread nationwide, from Maine to California, South Dakota to New Mexico. Proponents of these programs promote outdoor activity as a means of tackling chronic medical conditions like obesity, high blood pressure and type 2 diabetes. But park prescriptions also hold considerable promise for patients suffering from mental health issues. A large body of evidence suggests that exposure to nature may promote mental well-being. A 2010 meta-analysis of 10 studies including over 1,200 participants found people who exercised in green environments demonstrated significant improvements in mood and self-esteem. A 2011 systematic review looked at 11 trials that compared indoor and outdoor activity, finding that exercise in natural settings was “associated with greater feelings of revitalization and positive engagement, decreases in tension, confusion, anger and depression, and increased energy.” Another recent review of studies found activity in natural environments correlated with reductions in negative emotions like sadness, anger and fatigue. © 2017 Scientific American,

Keyword: Depression
Link ID: 24065 - Posted: 09.15.2017

By Helen Thomson DON’T mind the gap. A woman has reached the age of 24 without anyone realising she was missing a large part of her brain. The case highlights just how adaptable the organ is. The discovery was made when the woman was admitted to the Chinese PLA General Hospital of Jinan Military Area Command in Shandong Province complaining of dizziness and nausea. She told doctors she’d had problems walking steadily for most of her life, and her mother reported that she hadn’t walked until she was 7 and that her speech only became intelligible at the age of 6. Doctors did a CAT scan and immediately identified the source of the problem – her entire cerebellum was missing (see scan, above). The space where it should be was empty of tissue. Instead it was filled with cerebrospinal fluid, which cushions the brain and provides defence against disease. The cerebellum – sometimes known as the “little brain” – is located underneath the two hemispheres. It looks different from the rest of the brain because it consists of much smaller and more compact folds of tissue. It represents about 10 per cent of the brain’s total volume but contains 50 per cent of its neurons. Although it is not unheard of to have part of your brain missing, either congenitally or from surgery, the woman joins an elite club of just nine people who are known to have lived without their entire cerebellum. A detailed description of how the disorder affects a living adult is almost non-existent, say doctors from the Chinese hospital, because most people with the condition die at a young age and the problem is only discovered on autopsy (Brain, doi.org/vh7). © Copyright New Scientist Ltd.

Keyword: Development of the Brain
Link ID: 24056 - Posted: 09.12.2017

Laura Sanders The brain chemical missing in Parkinson’s disease may have a hand in its own death. Dopamine, the neurotransmitter that helps keep body movements fluid, can kick off a toxic chain reaction that ultimately kills the nerve cells that make it, a new study suggests. By studying lab dishes of human nerve cells, or neurons, derived from Parkinson’s patients, researchers found that a harmful form of dopamine can inflict damage on cells in multiple ways. The result, published online September 7 in Science, “brings multiple pieces of the puzzle together,” says neuroscientist Teresa Hastings of the University of Pittsburgh School of Medicine. The finding also hints at a potential treatment for the estimated 10 million people worldwide with Parkinson’s: Less cellular damage occurred when some of the neurons were treated early on with antioxidants, molecules that can scoop up harmful chemicals inside cells. Study coauthor Dimitri Krainc, a neurologist and neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and colleagues took skin biopsies from healthy people and people with one of two types of Parkinson’s disease, inherited or spontaneously arising. The researchers then coaxed these skin cells into becoming dopamine-producing neurons. These cells were similar to those found in the substantia nigra, the movement-related region of the brain that degenerates in Parkinson’s. |© Society for Science & the Public 2000 - 2017.

Keyword: Parkinsons
Link ID: 24049 - Posted: 09.08.2017

A test that involves drawing a spiral on a sheet of paper could be used to diagnose early Parkinson's disease. Australian researchers have trialled software that measures writing speed and pen pressure on the page. Both are useful for detecting the disease, which causes shaking and muscle rigidity. The Melbourne team said the test could be used by GPs to screen their patients after middle age and to monitor the effect of treatments. The study, published in Frontiers of Neurology, involved 55 people - 27 had Parkinson's and 28 did not. Speed of writing and pen pressure while sketching are lower among Parkinson's patients, particularly those with a severe form of the disease. Image copyright RMIT University Image caption Treatment options are effective only when the disease is diagnosed early In the trial, a tablet computer with special software took measurements during the drawing test and was able to distinguish those with the disease, and how severe it was. Poonam Zham, study researcher from RMIT University, said: "Our aim was to develop an affordable and automated electronic system for early-stage diagnosis of Parkinson's disease, which could be easily used by a community doctor or nursing staff." The system combines pen speed and pressure into one measurement, which can be used to tell how severe the disease is. David Dexter, deputy research director at Parkinson's UK, said current tests for the disease were not able to accurately measure how advanced someone's condition was. "This can impact on the ability to select the right people for clinical research, which is essential to develop new and better treatments for Parkinson's. "This new test could provide a more accurate assessment by measuring a wider range of features that may be affected by Parkinson's, such as co-ordination, pressure, speed and cognitive function." He added that the test could be a "stepping stone" to better clinical trials for Parkinson's. © 2017 BBC.

Keyword: Parkinsons
Link ID: 24042 - Posted: 09.07.2017

By Mitch Leslie When people with asthma have trouble breathing, they may reach for an inhaler containing salbutamol, a drug that expands the airways. Salbutamol may have another beneficial effect—protecting against Parkinson’s disease. Individuals who inhaled the highest doses of salbutamol were about half as likely to develop the devastating neurological condition as those who didn’t take the drug, a study reveals. “I’m sure it’s going to be a landmark paper,” says neurologist Joseph Jankovic of Baylor College of Medicine in Houston, Texas, who wasn’t involved in the research. In Parkinson’s disease, gobs of the protein α-synuclein accumulate in certain brain cells and may kill them. Scientists have tried to craft drugs that speed the elimination of the protein or prevent it from clumping. Neurologist and genomicist Clemens Scherzer of Harvard Medical School in Boston and colleagues decided to try a different strategy. “We wanted to find a drug that could turn down the production of α-synuclein,” he says. To identify promising compounds, the team grew human nerve cells in the lab and tested whether more than 1100 medications, vitamins, dietary supplements, and other molecules altered their output of α-synuclein. Three of the drugs that cut the protein’s production, including salbutamol, work by stimulating the b2-adrenoreceptor—a molecule on some body cells that triggers a variety of effects, including relaxing the airways. The researchers found that these drugs appear to alter how tightly the DNA containing the α-synuclein gene coils, and thus whether the gene is active. © 2017 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 24023 - Posted: 09.01.2017

Ewen Callaway Japanese researchers report promising results from an experimental therapy for Parkinson’s disease that involves implanting neurons made from ‘reprogrammed’ stem cells into the brain. A trial conducted in monkeys with a version of the disease showed that the treatment improved their symptoms and seemed to be safe, according to a report published on 30 August in Nature1. The study’s key finding — that the implanted cells survived in the brain for at least two years without causing any dangerous effects in the body — provides a major boost to researchers’ hopes of testing stem-cell treatments for Parkinson’s in humans, say scientists. Jun Takahashi, a stem-cell scientist at Kyoto University in Japan who led the study, says that his team plans to begin transplanting neurons made from induced pluripotent stem (iPS) cells into people with Parkinson’s in clinical trials soon. The research is also likely to inform several other groups worldwide that are testing different approaches to treating Parkinson’s using stem cells, with trials also slated to begin soon. Parkinson’s is a neurodegenerative condition caused by the death of cells called dopaminergic neurons, which make a neurotransmitter called dopamine in certain areas of the brain. Because dopamine-producing brain cells are involved in movement, people with the condition experience characteristic tremors and stiff muscles. Current treatments address symptoms of the disease but not the underlying cause. © 2017 Macmillan Publishers Limited,

Keyword: Parkinsons; Stem Cells
Link ID: 24019 - Posted: 08.31.2017

By Mo Costandi Voluntary movements are one of the brain’s main “outputs,” yet science still knows very little about how networks of neurons plan, initiate and execute them. Now, researchers from Columbia University and the Champalimaud Center for the Unknown in Lisbon, Portugal, say they have discovered an “activity map” that the brain uses to guide animals’ movements. The findings, published Wednesday in Neuron, could advance our understanding of how the brain learns new movements—and of what goes wrong in related disorders such as Parkinson's disease. Movements are controlled and coordinated by multiple brain structures including the primary motor cortex. Located at the back of the frontal lobe, it contains cells whose long fibers extend down through the spinal cord, where they contact “secondary” motor neurons that signal the body muscles. A set of deep brain structures called the basal ganglia are also critical for movement, as evidenced by their degeneration in conditions such as Parkinson’s. One component of the basal ganglia, called the striatum, receives information about possible actions from the motor cortex and is thought to be involved in selecting, preparing and executing the appropriate commands before they are sent to the body. Earlier research had shown that signals leave the striatum along one of two distinct pathways: one that facilitates movement, and another that suppresses it. A number of more recent studies show that both pathways are active during motion, however, suggesting that they do not act by simply sending “stop” and “go” signals. And although it has long been suspected that different groups of neurons in the striatum represent distinct actions, exactly how they might do so has remained unclear. © 2017 Scientific American

Keyword: Parkinsons; Brain imaging
Link ID: 24016 - Posted: 08.31.2017

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.

Keyword: Movement Disorders
Link ID: 23960 - Posted: 08.15.2017

By GRETCHEN REYNOLDS Some types of exercise may be better than others at blunting appetite and potentially aiding in weight management, according to an interesting new study of workouts and hunger. It finds that pushing yourself during exercise affects appetite, sometimes in surprising ways. As anyone who has begun an exercise program knows, the relationships between exercise, appetite, weight control and hunger are complex and often counterintuitive. The arithmetic involved seems straightforward. You burn calories during exercise and, over time, should drop pounds. But the reality is more vexing. In both scientific studies and the world inhabited by the rest of us, most people who start exercising lose fewer pounds than would be expected, given the number of calories they are burning during workouts. Many people even gain weight. The problem with exercise as a weight-loss strategy seems to be in large part that it can make you hungry, and many of us wind up consuming more calories after a workout than we torched during it, a biological response that has led some experts and frustrated exercisers to conclude that exercise by itself — without strict calorie reduction — is useless for shedding pounds. But much of the past research into exercise and appetite has concentrated on walking or other types of relatively short or light activities. Some scientists have begun to wonder whether exercise that was physically taxing, either because it was prolonged or intense, might affect appetite differently than more easeful exercise. So for the new study, which was published recently in the Journal of Endocrinology, scientists from Loughborough University in Britain and other institutions who have been studying exercise and appetite for years recruited 16 healthy, fit young men. (They did not include women because this was a small, pilot study, the authors say, and controlling for the effects of women’s menstrual cycles would have been difficult.) © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23934 - Posted: 08.09.2017