Chapter 5. The Sensorimotor System

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National Institutes of Health scientists have used human skin cells to create what they believe is the first cerebral organoid system, or “mini-brain,” for studying sporadic Creutzfeldt-Jakob disease (CJD). CJD is a fatal neurodegenerative brain disease of humans believed to be caused by infectious prion protein. It affects about 1 in 1 million people. The researchers, from NIH’s National Institute of Allergy and Infectious Diseases (NIAID), hope the human organoid model will enable them to evaluate potential therapeutics for CJD and provide greater detail about human prion disease subtypes than the rodent and nonhuman primate models currently in use. Human cerebral organoids are small balls of human brain cells ranging in size from a poppy seed to a small pea. Their organization, structure, and electrical signaling are similar to brain tissue. Because these cerebral organoids can survive in a controlled environment for months, nervous system diseases can be studied over time. Cerebral organoids have been used as models to study Zika virus infection, Alzheimer’s disease, and Down syndrome. In a new study published in Acta Neuropathologica Communications, scientists at NIAID’s Rocky Mountain Laboratories discovered how to infect five-month-old cerebral organoids with prions using samples from two patients who died of two different CJD subtypes, MV1 and MV2. Infection took about one month to confirm, and the scientists monitored the organoids for changes in health indicators, such as metabolism, for more than six months. By the end of the study, the scientists observed that seeding activity, an indication of infectious prion propagation, was present in all organoids exposed to the CJD samples. However, seeding was greater in organoids infected with the MV2 sample than the MV1 sample. They also reported that the MV1-infected organoids showed more damage than the MV2-infected organoids.

Keyword: Prions; Development of the Brain
Link ID: 26331 - Posted: 06.15.2019

By Carl Zimmer Last week, ladybugs briefly took over the news cycle. Meteorologists at the National Weather Service were looking over radar images in California on the night of June 4 when they spotted what looked like a wide swath of rain. But there were no clouds. The meteorologists contacted an amateur weather-spotter directly under the mysterious disturbance. He wasn’t getting soaked by rain. Instead, he saw ladybugs. Everywhere. Radar apparently had picked up a cloud of migrating ladybugs spread across 80 miles, with a dense core ten miles wide floating 5,000 feet to 9,000 feet in the air. As giant as the swarm was, the meteorologists lost track of it. The ladybugs disappeared into the night. Compared to other animal migrations, the migrations of insects are a scientific mystery. It’s easy to spot a herd of wildebeest making its way across the savanna. Insects, even in huge numbers, move from place to place without much notice. One day you look around, and ladybugs are everywhere. “The migrations themselves are totally invisible,” said Jason Chapman, an ecologist at the University of Exeter in Britain. Dr. Chapman and his colleagues are using radar to bring insect migrations to light. The scientists help run a unique network of small radar stations in southern England designed to scan the sky 24 hours a day, spotting insects flying overhead. “These radars are fantastic,” said Dr. Chapman. “We have a lot of information about every individual insect that flies over overhead, including a measure of the shape and a measure of their size.” © 2019 The New York Times Company

Keyword: Animal Migration
Link ID: 26329 - Posted: 06.14.2019

By Sarah Baird Few topics occupy pregnant women’s minds in the months leading up to birth more than devising a plan for pain management during labor. In the United States, the options during delivery have long been pretty limited. On one side of the dichotomy is a completely unmedicated childbirth, where visualization and breathing techniques offer a mind-over-matter approach to labor pain. On the other side, epidurals are the pain-eliminating gold standard — but can come with plenty of trade-offs. Across the world, though, nitrous oxide (yes, “laughing gas”) has long been standard — dating back to the turn-of-the-century — in delivery rooms, allowing women to help mitigate the pain of labor while remaining present and, perhaps best of all, maintaining their sense of control. Now, this low-stakes form of delivery room relief is finally taking hold in the United States as women seek out a wider range of options for their birthing experience. Nitrous oxide is a blend of 50 percent nitrous and 50 percent oxygen that women are able to self-administer during labor by holding a face mask over their nose and mouth and breathing deeply. (The 50/50 ratio is a set concentration and cannot be raised or lowered, unlike the dialed system in a dentist’s office which can be increased up to 70 percent nitrogen.) The option, unlike other types of pain relief, requires no I.V., does not limit mobility and will not slow contractions. The effects of nitrous kick in within 30 to 50 seconds of beginning inhalation, providing a very different form of pain management than other methods available. “It’s been described as a dissociative effect, so it reduces anxiety related to pain and kind of disassociates [women] from their pain,” said Kelly Curlee, R.N., director of inpatient nursing at Texas Health Cleburne in Cleburne, Tex. “Pain breeds fear, fear breeds pain. That’s kind of a cycle that nitrous helps break.” © 2019 The New York Times Company

Keyword: Pain & Touch
Link ID: 26319 - Posted: 06.10.2019

Patti Neighmond Jeannine, who is 37 and lives in Burbank, Calif., has endured widespread pain since she was 8. She has been examined by dozens of doctors, but none of their X-rays, MRIs or other tests have turned up any evidence of physical injury or damage. Over the years, desperate for relief, she tried changing her diet, wore belts to correct her posture and exercised to strengthen muscles. Taking lots of ibuprofen helped, she says, but doctors warned her that taking too much could cause gastric bleeding. Nothing else eased her discomfort. On a pain scale of 0 to 10, her pain ranged from "7 to 9, regularly," she says. Around 50 million Americans suffer from chronic pain. Most of us think of pain as something that arises after a physical injury, accident or damage from an illness or its treatment. But researchers are learning that, in some people, there can be another source of chronic pain. Repeated exposure to psychological trauma, or deep anxiety or depression — especially in childhood — can leave a physical imprint on the brain that can make some people, like Jeannine, more vulnerable to chronic pain, scientists say. (We are not using her last name for reasons of privacy.) Jeannine was eventually diagnosed with fibromyalgia — a condition characterized by widespread pain throughout the body, among other symptoms. The cause is unknown and likely varies from person to person. The pain Jeannine experienced was physical. She'd feel "lightning bolts, kind of going up through my shoulders to my neck to my head," she says. Other times, she'd suddenly experience the shooting pain of sciatica in her legs, and she often suffered from a "grinding pain" in her hips. "I would feel like I can't walk anymore — it was just so very painful to walk." © 2019 npr

Keyword: Pain & Touch
Link ID: 26316 - Posted: 06.10.2019

By: Karen Moxon, Ph.D., Ignacio Saez, Ph.D., and Jochen Ditterich, Ph.D. Technology that is sparking an entirely new field of neuroscience will soon let us simply think about something we want our computers to do and watch it instantaneously happen. In fact, some patients with severe neurological injury or disease are already reaping the benefits of initial advances by using their thoughts to signal and control robotic limbs. This brain-computer interface (BCI) idea is spawning a new area of neuroscience called cognitive neuroengineering that holds the promise of improving the quality of life for everyone on the planet in unimaginable ways. But the technology is not yet ready for prime time. There are three basic aspects of BCIs—recording, decoding, and operation, and progress will require refining all three. BCI works because brain activity generates a signal—typically an electrical field—that can be recorded through a dedicated device, which feeds it to a computer whose analysis software (i.e., a decoding algorithm) “translates” the signal to a simple command. This command signal operates a computer or other machine. The resulting operation can be as simple as moving a cursor on a screen, for which the command need contain just X and Y coordinates, or as complex as controlling a robotic arm, which requires information about position, orientation, speed, rotation, and more. Recent work from University of Pittsburgh has shown that subjects with amyotrophic lateral sclerosis (ALS) can control a complex robot arm—having it pick up a pitcher and pour water into a glass—just by thinking about it. The downside is that it is necessary to surgically implant recording microelectrodes intothe brain and that, most importantly, such electrodes are not reliable for more than a few years. © 2019 The Dana Foundation.

Keyword: Robotics; ALS-Lou Gehrig's Disease
Link ID: 26306 - Posted: 06.06.2019

By Frances Cronin Health reporter Alison Cameron, from Dorset, was 17 when she had appendicitis and went into hospital. "I had my appendix out and I remember I came round out of the anaesthetic screaming, the pain was something else." It was the start of a "horrendous" three years of investigation before "they came to the conclusion through a process of elimination, it was nerve damage". Over the next 30 years, Alison had more than 50 injections, known as cryoblocks, to freeze the site of her abdominal pain, but none of them stopped the pain for more than six months. This left her needing high doses of painkillers which left her unable to eat or drink - and she ended up on a feeding tube which led to her losing weight, and her health deteriorating. But she says she always tried to stay positive, which was instilled in her by her mum. "No matter how bad things have been, I've always been able to find a positive at the end of the day. That isn't saying that I didn't have some very, very low moments. "I miscarried seven times - six of which were definitely down to the pain. So not only have I paid the price - but also those potential lives." She managed to have two children in the gaps between treatment, and now has three grandchildren. The eldest burst into tears the first time she saw Alison without an eating tube, "as that, for her, wasn't normal granny". Five years ago, a cryoblock caused a collapsed lung, and Alison was referred to consultant neurosurgeon Girish Vajramani at the University Hospital Southampton. "Alison is one of the most challenging patients I have ever known," he says. "She had undergone 50 cryoblocks over 30 years, which is unprecedented, and resulted in her referral to me when this proved too dangerous." © 2019 BBC

Keyword: Pain & Touch
Link ID: 26299 - Posted: 06.05.2019

By Cara Giaimo If you’ve ever taken a big bite of wasabi, you know what comes next: a painful zing that creeps over your whole scalp. You aren’t the only animal that feels this way. The condiment’s sinus-burning kick comes from a chemical compound called allyl isothiocyanate, or AITC, that actively damages proteins within cells. Flies and flatworms shun it, as do mice and wolf spiders. “Practically every animal you look at will avoid AITC,” said Gary Lewin, a molecular physiologist at the Max Delbrück Center for Molecular Medicine in Berlin. But there is one exception. In a paper published Thursday in Science, scientists including Dr. Lewin showed that the highveld mole rat, a rodent found in South Africa, is entirely impervious to the substance. The study “demonstrates the power of studying naturally occurring differences in pain sensitivity,” said Ewan St. John Smith, a neurobiologist at the University of Cambridge, who was not involved in the research. The work could eventually lead to more effective pain treatment in humans. The scientists didn’t originally set out to find a wasabi aficionado. They were simply hoping to compare how several mole rat species respond to things that cause pain. Years ago, Dr. Lewin and others discovered that naked mole rats — pink, bucktoothed creatures known for their uncanny longevity, insectlike social cultures and blasé attitude toward oxygen — aren’t sensitive to acid or capsaicin, the compound that gives peppers their burn. To see whether their close relatives shared these traits, they exposed nine species of mole rat to a few pain agents. The naked mole rats didn’t react well to AITC. Neither did most of the other species the group studied, including the humans administering the trials. © 2019 The New York Times Company

Keyword: Pain & Touch
Link ID: 26282 - Posted: 05.31.2019

By Jan Hoffman Opening statements in the country’s first trial over whether a pharmaceutical company is liable for the opioid crisis began as a battle between fire and ice: Lawyers for Oklahoma, a state brought to its knees by addiction and overdose deaths, heatedly accused Johnson & Johnson of creating a deadly demand for the drugs, while the company coolly responded that it had acted responsibly and lawfully in its quest to offer relief to chronic pain patients. The trial, heard by a judge without a jury but livestreamed to the public, is being closely watched not only by those affected by prescription opioid addiction, but also by lawyers in almost 1,900 similar federal and state cases nationwide. Two other defendants who manufacture opioids settled with Oklahoma — Purdue Pharma will pay $270 million, Teva Pharmaceuticals, $85 million — leaving only J & J on trial. The state directly confronted what many legal experts have predicted will be the highest hurdle in the case: connecting one manufacturer of opioids to the cascading harms wrought by the entire industry. J & J pushed back hard, arguing that the state itself looked the other way as its own drug review board and prescription monitoring program for years neglected to swoop down on sources of diverted opioids. In addition, it said, Oklahoma could not tie any death directly to the company’s products — Duragesic, a fentanyl patch, and Nucynta, an opioid pill it no longer makes. “You hear about pill mills,” said Larry D. Ottaway, the lead counsel for a J & J subsidiary, Janssen Pharmaceuticals. “You don’t hear about patch mills.” Indeed both sides introduced what are sure to be their signature earworms, themes that will be echoed throughout the trial, estimated to take about two months. © 2019 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 26275 - Posted: 05.29.2019

Ashley Yeager The US Food and Drug Administration has approved a new treatment for a rare childhood disorder that costs $2.125 million for single dose—the most expensive medicine on the market. The medicine is designed to treat spinal muscular atrophy (SMA), a condition driven by defects in the SMN1 gene, which causes afflicted babies to lose muscle control. The illness affects about 400 babies in the US each year and kills those with the most common form of the disease in just a few years. The new treatment is a gene therapy that uses genetically modified viruses to deliver healthy copies of the SMN1 gene to patients’ cells so they can generate a protein that helps the babies develop normally. In tests of the treatment, babies who received it by 6 months of age didn’t have as severe muscle problems as those who didn’t get the drug. Infants getting the drug after six months also didn’t lose muscle control, but they suffered irreversible damage. Babies who got the treatment the earliest were the healthiest, according to the Associated Press. “We saw just remarkable results for these kids,” David Lennon tells NPR. Lennon is the president of AveXis, the company, owned by Novartis that developed the drug, called Zolgensma. It is only the second FDA-approved gene therapy designed to treat a genetic disorder. While the success of the treatment is being celebrated, the price tag is taking heat. “It's absolutely stunning,” Peter Bach, who studies health policy at Memorial Sloan Kettering Cancer Center in New York, tells NPR. The drug’s price tag, he says, drains resources from society, and it’s not alone. © 1986–2019 The Scientist

Keyword: Movement Disorders; Muscles
Link ID: 26274 - Posted: 05.29.2019

By Anna Groves | Bipolar patients are seven times more likely to develop Parkinson’s disease, according to a new study. Though the news may be disheartening to those suffering from the already-trying condition, the link might also lead to clues about the causes behind the two conditions. Parkinson’s is a complex disease associated with a gradual decline in dopamine levels produced by neurons, or brain cells. It eventually leads to impaired movements and other bodily functions. The causes are unknown, and there is no cure. Bipolar disorder, also known as manic-depressive illness, is characterized by episodic fluctuations in mood, concentration or energy levels. Its causes are also unknown, though some bipolar-associated genes have been identified. Researchers are still figuring out how brain structure and function changes under the disease. Previous research has linked Parkinson’s with depression. So when the authors of the new study, most of whom are practicing physicians, noticed some of their bipolar patients developing Parkinson’s, they wondered if there was a connection. The study, out today in Neurology, was led by Huang Mao-Hsuan, who practices in the department of psychiatry at Taipei Veterans General Hospital. The researchers compared data from two groups of adults in the Taiwan National Health Insurance Research Database. Members of one group — over 56,000 individuals — were diagnosed with bipolar disorder between 2001 and 2009. The other — 225,000 individuals — had never been diagnosed with the disorder. No one in either cohort had received a Parkinson’s diagnosis and all the patients were over 20. And researchers ensured the two groups had similar ages, socioeconomic status, and other traits that might influence health.

Keyword: Parkinsons; Schizophrenia
Link ID: 26264 - Posted: 05.23.2019

By Jane E. Brody One of the most widely prescribed prescription drugs, gabapentin, is being taken by millions of patients despite little or no evidence that it can relieve their pain. In 2006, I wrote about gabapentin after discovering accidentally that it could counter hot flashes. The drug was initially approved 25 years ago to treat seizure disorders, but it is now commonly prescribed off-label to treat all kinds of pain, acute and chronic, in addition to hot flashes, chronic cough and a host of other medical problems. The F.D.A. approves a drug for specific uses and doses if the company demonstrates it is safe and effective for its intended uses, and its benefits outweigh any potential risks. Off-label means that a medical provider can legally prescribe any drug that has been approved by the Food and Drug Administration for any condition, not just the ones for which it was approved. This can leave patients at the mercy of what their doctors think is helpful. Thus, it can become a patient’s job to try to determine whether a medication prescribed off-label is both safe and effective for their particular condition. This is no easy task even for well-educated doctors, let alone for desperate patients in pain. Two doctors recently reviewed published evidence for the benefits and risks of off-label use of gabapentin (originally sold under the trade name Neurontin) and its brand-name cousin Lyrica (pregabalin) for treating all kinds of pain. (There is now also a third drug, gabapentin encarbil, sold as Horizant, approved only for restless leg syndrome and postherpetic neuralgia, which can follow a shingles outbreak.) © 2019 The New York Times Company

Keyword: Pain & Touch; Drug Abuse
Link ID: 26253 - Posted: 05.21.2019

Jon Hamilton When Sterling Witt was a teenager in Missouri, he was diagnosed with scoliosis. Before long, the curvature of his spine started causing chronic pain. It was "this low-grade kind of menacing pain that ran through my spine and mostly my lower back and my upper right shoulder blade and then even into my neck a little bit," Witt says. The pain was bad. But the feeling of helplessness it produced in him was even worse. "I felt like I was being attacked by this invisible enemy," Witt says. "It was nothing that I asked for, and I didn't even know how to battle it." So he channeled his frustration into music and art that depicted his pain. It was "a way I could express myself," he says. "It was liberating." Witt's experience is typical of how an unpleasant sensation can become something much more complicated, scientists say. "At its core, pain is just something that hurts or makes you say ouch," says Karen Davis, a senior scientist at the Krembil Brain Institute in Toronto. "Everything else is the outcome of the pain, how it then impacts your emotions, your feelings, your behaviors." The ouch part of pain begins when something — heat, certain chemicals or a mechanical force — activates special nerve endings called nociceptors. © 2019 npr

Keyword: Pain & Touch
Link ID: 26249 - Posted: 05.20.2019

Sarah Boseley Health editor A drug that could prolong the lives of children with a rare muscle-wasting disease has been approved by the NHS in England after lengthy negotiations with the manufacturer over the high price. Spinraza could help between 600 and 1,200 children and adults in England and Wales who have the genetic condition spinal muscular atrophy (SMA). It affects the nerves in the spinal cord, making muscles weaker and causing problems with movement, breathing and swallowing. It can shorten the life expectancy of babies and toddlers. The drug can slow the progress of the disease but the company making the drug, Biogen, was asking for a high price, that effectively amounted to more than £400,000 for a year of good quality life, according to the National Institute for Health and Care Excellence (Nice), which assesses value for money. Nice said there was limited data on its long-term effectiveness and turned it down last August, to the distress of affected families. Simon Stevens, the NHS England chief executive, said agreement had been reached and children would shortly get Spinraza, the market name of the drug nusinursen. “This promising treatment has the potential to be life changing for children and their families,” said Stevens. “The NHS has now reached one of the most comprehensive deals in the world, which allows us to assess real-world evidence of its long-term benefits. © 2019 Guardian News & Media Limited

Keyword: Movement Disorders; Muscles
Link ID: 26235 - Posted: 05.15.2019

By Gretchen Reynolds A need and desire to be in motion may have been bred into our DNA before we even became humans and could have helped to guide the evolution of our species, according to a fascinating new study of the genetics of physical activity. The study uses big data and sophisticated genetic analyses to determine that some of the gene variants associated with how much and whether people move seem to have joined our ancestors’ genome hundreds of thousands of years ago, making them integral to human existence and well-being and raising interesting questions about what that means today, when most humans are sedentary. There has been evidence for some time that whether and how much people and other animals move depends to some extent on family history and genetics. Past twin studies and genome-wide association studies — which scan genomes looking for snippets of DNA shared by individuals who also share certain traits — suggest that about 50 percent of physical activity behavior in people may depend on genes. Our tendency to move or not is different from our innate aerobic fitness. Someone could be born with a large inherited endurance capacity and no interest at all in leaving the couch, or vice versa. Little has been known, though, about when any of the gene variants associated with moving became integrated into the human genome, and that question matters. Many of the most common chronic illnesses and conditions in people today, including Type 2 diabetes, obesity, heart disease, osteoarthritis and others, are associated with being inactive. But some other species, including chimps, which share much of our DNA, retain robust good health even when they move relatively little. © 2019 The New York Times Company

Keyword: Genes & Behavior
Link ID: 26234 - Posted: 05.15.2019

By Meredith Wadman The data behind the promising trial of a drug that blocks the production of a mutant protein that causes brain damage in people with Huntington disease—an inherited and ultimately fatal neurological disorder—were published today in The New England Journal of Medicine, giving an official imprimatur to news that first electrified the community of patients with the disease 17 months ago. The results, originally announced in December 2017, were published alongside an editorial that called the trial “pathbreaking.” The new paper reports that the drug, a short stretch of synthetic DNA called HTTRx that blocks the production of the mutant protein huntingtin, is safe in humans; no serious adverse events were reported by the 46 people who participated in the trial. (Last summer, Science wrote in depth about the first participant, Michelle Dardengo.) The results also provide details behind the source of excitement about the trial: that HTTRx reduced levels of huntingtin in the cerebrospinal fluid (CSF) that bathes the spinal cord—a proxy, it is hoped, for what is happening in the brain—by amounts that had reversed Huntington-like motor and cognitive symptoms in mice. And the reductions in the mutant protein in the CSF of patients were dose-dependent: Through a range of dosing levels, the bigger the dose, the more the reduction of the mutant protein. © 2019 American Association for the Advancement of Science

Keyword: Huntingtons; Prions
Link ID: 26217 - Posted: 05.07.2019

By Gabrielle Emanuel and Katie Thomas BOSTON — A federal jury on Thursday found the top executives of Insys Therapeutics, a company that sold a fentanyl-based painkiller, guilty of racketeering charges in a rare criminal prosecution that blamed corporate officials for contributing to the nation’s opioid epidemic. The jury, after deliberating for 15 days, issued guilty verdicts against the company’s founder, the onetime billionaire John Kapoor, and four former executives, finding they had conspired to fuel sales of its highly potent drug, Subsys, by not only bribing doctors to prescribe their product but also by misleading insurers about patients’ need for the drug. The verdict against Insys executives is a sign of the accelerating effort to hold pharmaceutical and drug distribution companies and their executives and owners accountable in ways commensurate with the devastation wrought by the prescription opioid crisis. More than 200,000 people have overdosed on such drugs in the past two decades. Federal authorities last month for the first time filed felony drug trafficking charges against a major pharmaceutical distributor, Rochester Drug Cooperative, and two former executives, accusing them of shipping tens of millions of oxycodone pills and fentanyl products to pharmacies that were distributing drugs illegally. And the state attorneys general of Massachusetts and New York have recently sued not just Purdue Pharma, the maker of OxyContin, but also members of the Sackler family who own the company — and who have largely escaped personal legal penalties for the company’s role in the epidemic, culpability they deny. © 2019 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 26209 - Posted: 05.04.2019

By Jocelyn Kaiser WASHINGTON, D.C.—A new gene therapy treatment has had striking results in nine boys born with myotubular myopathy (MTM), a rare disease that causes extreme muscle weakness often from birth. All of the boys have better neuromuscular function, most can sit on their own, and four are now breathing without ventilators. As videos of their improvements were shown here on 1 May at the annual meeting of the American Society of Gene & Cell Therapy (ASGCT), the audience broke out in applause. The results, the first of their kind for this rare disease, cap a year of early signs of success in using gene therapy for inherited muscle diseases. As far as muscle function is concerned, the boys “have gone from nothing to something,” says principal investigator Perry Shieh, a neurologist at the University of California, Los Angeles. “Time will tell how much that something will be.” The patients in the new study have X-linked MTM, caused by a defect in a gene called MTM1 that encodes an enzyme, myotubularin. Skeletal muscles need the enzyme to develop and function. Boys with the disease have low muscle tone and, in many cases, can barely breathe or move on their own; most require a ventilator and feeding tube. Half of patients die by 18 months, and few live past age 10. In the trial, sponsored by Audentes Therapeutics, a gene therapy company in San Francisco, California, nine boys between 8 months and 6 years old with X-linked MTM received an intravenous (IV) infusion of many trillions of particles of a harmless virus, called an adeno-associated virus. The viruses were designed to carry a good copy of the MTM1 gene into the boys’ muscle cells. The gene, a free-floating piece of DNA, could then trigger the cell’s proteinmaking machinery to produce myotubularin. Three patients had serious side effects that may have been related to the therapy, such as heart inflammation, but all were treatable. © 2019 American Association for the Advancement of Science

Keyword: Movement Disorders; Muscles
Link ID: 26204 - Posted: 05.03.2019

By Rahul Desikan What is it like to be locked into your body, to be alive but not living? I’m dying — fast. My lungs are at 20 percent of vital capacity and it’s a matter of time before the nerves supplying my breathing muscles degenerate. I have a rapid form of ALS — amyotrophic lateral sclerosis, or Lou Gehrig’s disease. Two years ago, I was running around with my kids, hiking with my wife. All that is over. My body no longer moves. I cannot talk — my only voice is the one in my head, telling me over and over that I am going to die. Soon. I can’t even breathe for myself anymore — I am tethered to a ventilator that breathes for me. I don’t want you to feel sorry for me. At all. It is just ironic, this new, condensed life of mine. I went into medicine to take care of patients with brain diseases. Now, I have one of the diseases that I study. Even with this lethal disease, I continue to find neurology fascinating and beautiful. I wish you knew the old me. ALS has completely destroyed my body and parts of my brain. The new version has stripped me of control over regulating my emotions. I laugh and cry inappropriately during movies, and even during conversations. The cognitive parts of my brain are still working perfectly fine so I’m able to get through the day. But because swallowing has become increasingly difficult, eating and drinking are a battle: continuous bouts of choking, vomiting, crying, sweating, drooling — until finally, it goes through. It is not a pretty picture. What is it like to be locked in? When I swallow, I imagine my childhood in India — driving with my parents and sister in our sky-blue Maruti minivan through the wide roads of New Delhi, relishing my grandmother’s sambar, a savory soup of lentils and vegetables. In my mind, I am always in Boston where I lived for 15 years during college and then medical school and for my doctorate in neurobiology. In my mind, which is all I have left, I am playing house music records at Satellite Records in the Back Bay or trying the Persian eggplant dish at Lala Rokh with my wife or going out with my friends to River Gods or the Enormous Room in Central Square. I am so good at imagining the old me that I see, taste, hear, touch everything. And relive every single detail. © 1996-2019 The Washington Post

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26183 - Posted: 04.29.2019

By Jane E. Brody I was packing up at the end of a family vacation in Florida when my back went into an excruciating spasm unrelieved by a fistful of pain medication. As my twin sons, then 8 years old, wheeled me through the airport, one of them suggested, “Mom, if you think about something else, it won’t hurt so much.” At the time, I failed to appreciate the wisdom of his advice. Now, four decades later, a sophisticated distraction technique is being used to help patients of all ages cope with pain, both acute and chronic. The method, called Virtual Reality Therapy, goes beyond simple distraction, as might result from watching television. Rather, it totally immerses the patient in an entertaining, relaxing, interactive environment that so occupies the brain, it has no room to process pain sensations at the same time. “It’s not just a distraction — it’s like an endogenous narcotic providing a physiological and chemical burst that causes you to feel good,” said Jeffrey I. Gold, director of the pediatric pain management clinic at Children’s Hospital Los Angeles. “It’s different from reading a book or playing with a toy. It’s a multisensory experience that engages a person’s attention on a much deeper level.” Virtual Reality Therapy is the new kid on the block for pain management, now gradually growing in use as the opioid epidemic continues to soar and the price of the needed equipment has plummeted. VR, as it is called, has been most widely and successfully used so far to help children and adults weather acute pain, as can accompany an IV insertion or debridement of burns. But it can also enhance the effectiveness of established techniques like physical therapy, hypnosis and cognitive behavioral therapy to treat debilitating chronic pain. © 2019 The New York Times Company

Keyword: Pain & Touch; Attention
Link ID: 26182 - Posted: 04.29.2019

Lisa Wehrstedt Researchers in Philadelphia revealed last week that tastebuds also bear odour-detecting proteins, calling into question the idea that smell and taste come together in the brain to produce flavour. According to Dr Mehmet Hakan Ozdener, his findings open up the possibility of using smells to trick us into healthier eating, for example by adding a low-concentration odour to food to make it taste sweeter and thereby reduce sugar intake. It is believed that we all experience a form of motion-induced blindness while driving at night, when the red lights of the cars in front temporarily disappear if we move our eyes to the oncoming traffic. This phenomenon, where the brain ignores or discards visual information when it is placed in front of a moving background, was first observed in the lab in 1965. First described in 1976, the McGurk effect is a connection between hearing and vision in speech perception. When the auditory component of a syllable is paired with the visual component of another, this can lead to the perception of a third sound. Research conducted by the University of Oxford in 2013 suggests that the sight of cutlery and the perception of its size, weight, shape and colour have an effect on how we determine flavour, suggesting that the brain makes judgments on food even before it goes in our mouths. Yoghurt, for example, tastes sweeter on a white spoon than it does on a black spoon. © 2019 Guardian News & Media Limited

Keyword: Chemical Senses (Smell & Taste); Vision
Link ID: 26180 - Posted: 04.29.2019