Chapter 5. The Sensorimotor System

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Amy Fleming Taking a stroll with Shane O’Mara is a risky endeavour. The neuroscientist is so passionate about walking, and our collective right to go for walks, that he is determined not to let the slightest unfortunate aspect of urban design break his stride. So much so, that he has a habit of darting across busy roads as the lights change. “One of life’s great horrors as you’re walking is waiting for permission to cross the street,” he tells me, when we are forced to stop for traffic – a rude interruption when, as he says, “the experience of synchrony when walking together is one of life’s great pleasures”. He knows this not only through personal experience, but from cold, hard data – walking makes us healthier, happier and brainier. We are wandering the streets of Dublin discussing O’Mara’s book, In Praise of Walking, a backstage tour of what happens in our brains while we perambulate. Our jaunt begins at the grand old gates of his workplace, Trinity College, and takes in the Irish famine memorial at St Stephen’s Green, the Georgian mile, the birthplace of Francis Bacon, the site of Facebook’s new European mega-HQ and the salubrious seaside dwellings of Sandymount. O’Mara, 53, is in his element striding through urban landscapes – from epic hikes across London’s sprawl to more sedate ambles in Oxford, where he received his DPhil – and waxing lyrical about science, nature, architecture and literature. He favours what he calls a “motor-centric” view of the brain – that it evolved to support movement and, therefore, if we stop moving about, it won’t work as well. © 2020 Read It Later, Inc.

Keyword: Depression
Link ID: 27364 - Posted: 07.15.2020

For every cell in the body there comes a time when it must decide what it wants to do for the rest of its life. In an article published in the journal PNAS, National Institutes of Health researchers report for the first time that ancient viral genes that were once considered “junk DNA” may play a role in this process. The article describes a series of preclinical experiments that showed how some human endogenous retrovirus (HERV-K) genes inscribed into chromosomes 12 and 19 may help control the differentiation, or maturation, of human stem cells into the trillions of neurons that are wired into our nervous systems. The experiments were performed by researchers in a lab led by Avindra Nath, M.D., clinical director, at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Over the course of evolution, the human genome has absorbed thousands of human endogenous retrovirus genes. As a result, nearly eight percent of the DNA that lines our chromosomes includes remnants of these genes. Although once thought to be inactive, or “junk”, recent studies have shown that these genes may be involved in human embryonic development, the growth of some tumors, and nerve damage during multiple sclerosis. Previously, researchers in Dr. Nath’s lab showed that amyotrophic lateral sclerosis (ALS) may be linked to activation of the HERV-K gene. In this study, led by Tongguang (David) Wang, M.D., Ph.D., staff scientist at NINDS, the team showed that deactivation of the gene may free stem cells to become neurons. The researchers performed most of their experiments on blood cells, drawn from healthy volunteers at the NIH’s Clinical Center, that they genetically transformed into induced pluripotent stem cells, which can then turn into any cell type in the body. Surprisingly, they found that the surfaces of the stem cells were lined with high levels of HERV-K, subtype HML-2, an envelope protein, that viruses often use to latch onto and infect cells. These proteins progressively disappeared as the cells were served two rounds of “cocktails.” One round nudged the cells into an intermediate, neural stem cell state followed by a second round that pushed the cells into finally becoming neurons.

Keyword: ALS-Lou Gehrig's Disease ; Development of the Brain
Link ID: 27359 - Posted: 07.14.2020

By Laura Sanders Exercise’s power to boost the brain might require a little help from the liver. A chemical signal from the liver, triggered by exercise, helps elderly mice keep their brains sharp, suggests a study published in the July 10 Science. Understanding this liver-to-brain signal may help scientists develop a drug that benefits the brain the way exercise does. Lots of studies have shown that exercise helps the brain, buffering the memory declines that come with old age, for instance. Scientists have long sought an “exercise pill” that could be useful for elderly people too frail to work out or for whom exercise is otherwise risky. “Can we somehow get people who can’t exercise to have the same benefits?” asks Saul Villeda, a neuroscientist at the University of California, San Francisco. Villeda and colleagues took an approach similar to experiments that revealed the rejuvenating effects of blood from young mice (SN: 5/5/14). But instead of youthfulness, the researchers focused on fitness. The researchers injected sedentary elderly mice with plasma from elderly mice that had voluntarily run on wheels over the course of six weeks. After eight injections over 24 days, the sedentary elderly mice performed better on memory tasks, such as remembering where a hidden platform was in a pool of water, than elderly mice that received injections from sedentary mice. Comparing the plasma of exercised mice with that of sedentary mice showed an abundance of proteins produced by the liver in mice that ran on wheels. The researchers closely studied one of these liver proteins produced in response to exercise, called GPLD1. GPLD1 is an enzyme, a type of molecular scissors. It snips other proteins off the outsides of cells, releasing those proteins to go do other jobs. Targeting these biological jobs with a molecule that behaves like GPLD1 might be a way to mimic the brain benefits of exercise, the researchers suspect. © Society for Science & the Public 2000–2020.

Keyword: Learning & Memory; Development of the Brain
Link ID: 27358 - Posted: 07.11.2020

By Jocelyn Kaiser It’s well established that exercise can sharpen the mind: People and mice who work out do better on cognitive tests, and elderly people who are physically active reduce their risk of dementia. Now, in a surprising finding, researchers report that blood from a mouse that exercises regularly can perk up the brain of a “couch potato” mouse. This effect, traced to a specific liver protein in the blood, could point the way to a drug that confers the brain benefits of exercise to an old or feeble person who rarely leaves a chair or bed. “Can your brain think that you exercised, from just something in your blood?” asks aging researcher Saul Villeda of the University of California, San Francisco (UCSF), who led the rodent research. The study grew out of research in Villeda’s lab and others suggesting blood from a young mouse can rejuvenate the brain and muscles of an old mouse. Some teams have since claimed to find specific proteins that explain the benefits of this “young blood.” Graduate student Alana Horowitz and postdoc Xuelai Fan in Villeda’s group wondered whether exercise—not just youth—could confer similar benefits via the blood. It was easy to enough to test: Put a wheel in a cage full of mice, and the mostly inactive animals will run for miles at night. The researchers collected blood from elderly or middle-aged mice that had an exercise wheel in their cage for 6 weeks and then transfused this blood into old mice without a wheel in their cage. Couch potato mice receiving this blood eight times over 3 weeks did nearly as well on learning and memory tests, such as navigating through a maze, as the exercising mice. A control group of couch potatoes receiving blood from similarly old, nonexercising mice saw no boost. The rodents getting the blood from the active mice also grew roughly twice as many new neurons in the hippocampus, a brain region involved in learning and memory, Villeda’s team reports today in Science. That change is comparable to what’s seen in rodents that directly exercise. © 2020 American Association for the Advancement of Science.

Keyword: Alzheimers; Development of the Brain
Link ID: 27357 - Posted: 07.11.2020

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 Angie Voyles Askham Toddlers with autism have unusually strong connections between sensory areas of the brain, according to a new study1. And the stronger the connections, the more pronounced a child’s autism traits tend to be. Overconnectivity in sensory areas may get in the way of an autistic child’s brain development, says lead investigator Inna Fishman, associate research professor at San Diego State University in California. “Their brain is busy with things it shouldn’t be busy with.” The findings add to a complicated field of research on brain connectivity and autism, which has shown weakened connectivity between some brain areas, strengthened connectivity between others, or no difference in connectivity at all. Previous brain-imaging studies have found that babies and toddlers with autism have altered connectivity in various brain areas and networks, including sensory areas. But most of these data come from ‘baby sibs’ — the younger siblings of autistic children, who are about 20 times more likely to have autism than the general population. “A lot of our early knowledge is from these high-risk samples of infant siblings,” says Benjamin Yerys, assistant professor of psychology in psychiatry at the University of Pennsylvania, who was not involved with the study. “If their behaviors and genetics are different, then all of this early brain work may also be different.” By contrast, the new work focused on autistic children who were newly diagnosed. “There are very, very few studies focused on this age, right around the time the diagnosis can be made,” says Christine Wu Nordahl, associate professor at the University of California, Davis MIND Institute. “I think that is the major strength of the study.” © 2020 Simons Foundation

Keyword: Autism
Link ID: 27345 - Posted: 07.06.2020

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

By William Schwalbe More than three years ago, I came down with a mysterious illness I thought might be a flu, but turned out to be something entirely different. My blizzard of symptoms began innocuously in November 2016 with terribly cold feet. So cold that even when I got under the covers with a hot water bottle between them, and they were warm to the touch, they still felt like painful ice-blocks. At other times, I had the equally unpleasant sensation that my feet and shins were burning or already burnt. A few weeks later, I started to experience intense throbbing pain in all my toes, as if someone had seconds before stomped on them with heavy boots, which made walking or standing difficult. Often my legs were so heavy that I could barely move them. Occasionally, my feet turned bright red. And every few hours came shooting pains, electric shocks that traveled up my legs. In my 55 years on earth, I’d never felt pain like that — except when a dentist drilled without Novocain. All the symptoms increased at night, so sleep became elusive. I wound up sticking my feet outside the covers because even a sheet brushing against them proved too painful to bear. Before long, the same panoply of pains had moved to my hands and then arms — and occasionally my face and stomach. Heat made the symptoms worse; cold and damp made them much worse. But often these pains flared for no discernible reason. Totally unrelated, or so I thought, were other things that began to go wrong with me over the next few months: I often found myself pouring with sweat from my forehead, but became unable to sweat on my legs and arms; I lost all the hair on my lower legs; I was increasingly faint and dizzy, with my heart racing whenever I changed position or had a shower; and I was experiencing a fatigue and bone-pain so profound that every few hours I needed to stop whatever I was doing and lie down on the floor. © 1996-2020 The Washington Post

Keyword: Pain & Touch
Link ID: 27334 - Posted: 06.29.2020

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 Tessa van Leeuwen, Rob van Lier Have you ever considered what your favorite piece of music tastes like? Or the color of Tuesday? If the answer is yes, you might be a synesthete. For people with synesthesia, ordinary sensory events, such as listening to music or reading text, elicit experiences involving other senses, such as perceiving a taste or seeing a color. Synesthesia is not to be confused with common metaphors — such as saying someone ‘sees red’ to describe anger. Instead, synesthetic associations are perceptual, highly specific and idiosyncratic, and typically stable beginning in childhood. And many types exist: A taste can have a shape, a word can have a color, the months of the year may be experienced as an array around the body. In the general population, the phenomenon is relatively rare: Only 2 to 4 percent of people have it. But as much as 20 percent of people with autism experience synesthesia1,2. Why would two relatively rare conditions occur together so often? Over the past few years, researchers have found that people with synesthesia or autism share many characteristics. Synesthetes often have sensory sensitivities and attention differences, as well as other autism traits3,4. The two conditions also share brain connectivity patterns and possibly genes, suggesting they have common biological underpinnings. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27304 - Posted: 06.17.2020

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

Ashley Yeager It had been seven weeks since I’d touched another human being. Arms outstretched, I walked quickly toward my dad, craving his embrace. In the instant before we touched, we paused, our minds probably running quick, last-minute calculations on the risk of physical contact. But, after turning our faces away from each other and awkwardly shuffling closer, we finally connected. Wrapped in my dad’s bear hug, I momentarily forgot we were in the midst of the worst global crisis I have ever experienced. “Touch is the most powerful safety signal of togetherness,” says Steve Cole, a psychiatrist and biobehavioral scientist at the University of California, Los Angeles. Like more than 35 million other Americans, I live alone, and with the guidelines of physical distancing set by the Centers for Disease Control and Prevention, I hadn’t been getting close to anyone to avoid being infected with (or potentially spreading) SARS-CoV-2, the virus that causes COVID-19. I’d been working, thankfully, at home and staying connected with friends and family through Zoom and Skype, but those virtual interactions were no replacement for being with loved ones in person. “When we get lonely and isolated our brainstem recognizes that suddenly we are in insecure territory and flips on a bunch of fight-or-flight stress responses without us even knowing it,” Cole says. “There’s all sorts of things in our social world that lead us to calculate that we are either safe or unsafe. You can think of physical touch, supportive and affectionate touch, as the most fundamental signal that you’re with somebody who cares about you . . . a fundamental signal of safety and well-being.” © 1986–2020 The Scientist.

Keyword: Pain & Touch; Stress
Link ID: 27259 - Posted: 05.21.2020

Sirin Kale Alice,* a 31-year-old director from London, has been breaking the coronavirus lockdown rules. “I almost don’t want to tell you this,” she says, lowering her voice. Her violation? Once a week, Alice, who lives alone, walks to the end of her garden to meet her best friend Lucy.* There, with the furtiveness of a street drug deal, Lucy hugs her tightly. Alice struggles to let her go. “You just get that rush of feeling better,” Alice says. “Like it’s all OK.” Aside from Lucy’s hugs, Alice hasn’t been touched by another person since March 15, which is when she went into a self-imposed lockdown, a week before the official government advice to self-isolate. “I’ve found it really hard,” she says. “I am a huggy person. You start to notice it after a while. I miss it.” She feels guilty about her surreptitious hugs. “I feel like I can’t tell my other friends about it,” Alice says. “There’s a lot of shaming going on. I know we aren’t meant to. But I am so grateful to her for checking in on me. It gives me such a lift.” Alice is experiencing the neurological phenomenon of "skin hunger," supercharged by the coronavirus pandemic. Skin hunger is the biological need for human touch. It’s why babies in neonatal intensive care units are placed on their parent’s naked chests. It’s the reason prisoners in solitary confinement often report craving human contact as ferociously as they desire their liberty. © 2020 Condé Nast.

Keyword: Emotions; Pain & Touch
Link ID: 27240 - Posted: 05.08.2020

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