By Jack Tamisiea An elephant’s trunk has 40,000 muscles and weighs more than a Burmese python. The appendage is strong enough to uproot a tree, yet sensitive enough to suction up fragile tortilla chips. But how does an elephant’s brain help accomplish these feats of dexterity? That has been difficult to study, according to Michael Brecht, a neuroscientist at the Humboldt University of Berlin. Weighing in excess of 10 pounds, the elephant’s brain degrades quickly after death and is a hassle to store. “I tend to think that the big animals are a bit neglected because we don’t do enough work on big brains,” Dr. Brecht said. Dr. Brecht and his colleagues were fortunate enough to gain access to a trove of elephant brains from animals that had died of natural causes or were euthanized for health reasons and ended up either frozen or in a fixative substance at the Leibniz Institute for Zoo and Wildlife Research in Berlin. In a study published Wednesday in the journal Science Advances, Dr. Brecht and his colleagues reported that elephants had more facial neurons than any other land mammal, which might contribute to trunk dexterity and other anatomical abilities. The study also helped to pinpoint major differences between the neural wirings of African savanna elephants and Asian elephants. Using the brains of four Asian elephants and four African savanna elephants, the researchers homed in on the facial nucleus, a bundle of neurons concentrated in the brainstem and hooked up to facial nerves. In mammals, these neurons serve as the control center for facial muscles. They’re in command whenever you wrinkle your nose, purse your lips or raise your eyebrows. They also help elephants employ their trunks. The researchers divided the facial nucleus into regions of neurons that controlled the elephant’s ears, lips and trunk. African elephants sported 63,000 facial neurons, while their Asian cousins had 54,000. The only mammals with more are dolphins, which pack nearly 90,000 facial neurons into their sensitive snouts. While his team expected both African savanna and Asian elephants to possess massive stores of facial neurons, Dr. Brecht said the discrepancy between the two species was noteworthy. © 2022 The New York Times Company

Keyword: Evolution; Pain & Touch
Link ID: 28533 - Posted: 10.28.2022

By Jackie Rocheleau For people haunted by recurring nightmares, untroubled sleep would be a dream come true. Now in a small experiment, neuroscientists have demonstrated a technique that, for some, may chase the bad dreams away. Enhancing the standard treatment for nightmare disorder with a memory-boosting technique cut down average weekly nightmares among a few dozen people from three to near zero, researchers report online October 27 in Current Biology. “The fact that they could actually make a big difference in the frequency of those nightmares is huge,” says Gina Poe, a neuroscientist at UCLA who wasn’t involved in the study. People with nightmare disorder fear the night not for the monsters under the bed, but the monsters in their dreams. Frequent, terrifying dreams disturb sleep and even affect well-being in waking life. The go-to nightmare disorder treatment is imagery rehearsal therapy, or IRT. In this treatment, patients reimagine nightmares with a positive spin, mentally rehearsing the new story line while awake. It reduces nightmares for most but fails for nearly a third of people. To boost IRT’s power, neuroscientist Sophie Schwartz of the University of Geneva and her colleagues leveraged a learning technique called targeted memory reactivation, or TMR. In this technique, a person focuses on learning something while a sound plays, and that same cue plays again during sleep. Experiencing the cue during sleep, which is important for memory storage, may reactivate and strengthen the associated memory (SN: 10/3/19). In the new study, the researchers gave 36 people with nightmare disorder training in IRT, randomly assigning half of them to rehearse their revised nightmares in silence. The other half rehearsed while a short piano chord, the TMR cue, played every 10 seconds for five minutes. © Society for Science & the Public 2000–2022.

Keyword: Sleep
Link ID: 28532 - Posted: 10.28.2022

By Nicola Jones What color is a tree, or the sky, or a sunset? At first glance, the answers seem obvious. But it turns out there is plenty of variation in how people see the world — both between individuals and between different cultural groups. A lot of factors feed into how people perceive and talk about color, from the biology of our eyes to how our brains process that information, to the words our languages use to talk about color categories. There’s plenty of room for differences, all along the way. For example, most people have three types of cones — light receptors in the eye that are optimized to detect different wavelengths or colors of light. But sometimes, a genetic variation can cause one type of cone to be different, or absent altogether, leading to altered color vision. Some people are color-blind. Others may have color superpowers. Our sex can also play a role in how we perceive color, as well as our age and even the color of our irises. Our perception can change depending on where we live, when we were born and what season it is. To learn more about individual differences in color vision, Knowable Magazine spoke with visual neuroscientist Jenny Bosten of the University of Sussex in England, who wrote about the topic in the 2022 Annual Review of Vision Science. This conversation has been edited for length and clarity. How many colors are there in the rainbow? Physically, the rainbow is a continuous spectrum. The wavelengths of light vary smoothly between two ends within the visible range. There are no lines, no sharp discontinuities. The human eye can discriminate far more than seven colors within that range. But in our culture, we would say that we see seven color categories in the rainbow: red, orange, yellow, green, blue, indigo and violet. That’s historical and cultural. © 2022 Annual Reviews

Keyword: Vision
Link ID: 28531 - Posted: 10.28.2022

Elizabeth Pennisi Think of the chattiest creatures in the animal kingdom and songbirds, dolphins, and—yes—humans probably come to mind. Turtles probably don’t register. But these charismatic reptiles also communicate using a large repertoire of clicks, snorts, and chortles. Now, by recording the “voices” of turtles and other supposedly quiet animals, scientists have concluded that all land vertebrate vocalizations—from the canary’s song to the lion’s roar—have a common root that dates back more than 400 million years. The findings imply animals began to vocalize very early in their evolutionary history—even before they possessed well-developed ears, says W. Tecumseh Fitch, a bioacoustician at the University of Vienna who was not involved with the work. “It suggests our ears evolved to hear these vocalizations.” Several years ago, University of Arizona evolutionary ecologist John Wiens and his graduate student Zhuo Chen started looking into the evolutionary roots of acoustic communication—basically defined as the sounds animals make with their mouths using their lungs. Combing the scientific literature, the duo compiled a family tree of all the acoustic animals known at the time, eventually concluding such soundmaking abilities arose multiple times in vertebrates between 100 million and 200 million years ago. But Gabriel Jorgewich-Cohen, an evolutionary biologist at the University of Zürich, noticed an oversight: turtles. Though Wiens and Chen had found that only two of 14 families of turtles made sounds, he was finding a lot more. He spent 2 years recording 50 turtle species in the act of “speaking.”

Keyword: Hearing; Evolution
Link ID: 28530 - Posted: 10.28.2022

By Erika Check Hayden Weeks after Valeria Schenkel took an experimental drug named after her, the daily seizures that had afflicted her from birth became less frequent. But the drug caused fluid to build up in her brain, and a year later, she died at age 3. The drug was given to only one other child, and she experienced the same side effect and nearly died last year. The drug contained snippets of genetic material tailor-made to turn off the mutated gene causing the extremely rare form of epilepsy that these children were born with. A handful of researchers and nonprofit organizations have raised millions of dollars to make these treatments, known as antisense drugs, for at least 19 children and adults with severe diseases that are too rare to garner interest from pharmaceutical companies. The treatments have helped some of these patients, raising hopes that the personalized approach might one day save thousands of lives. But the brain side effect, known as hydrocephalus, reported on Sunday at the American Neurological Association meeting in Chicago, is a blow for the niche medical field that has made rapid progress over the past five years. Hydrocephalus happens when too much fluid fills cavities in the brain, increasing pressure on brain tissue and risking lethal damage if untreated. “I think it’s worth saying: No question that encountering hydrocephalus has been a setback, sobering and important,” said Dr. Timothy Yu, the neurologist and genetics researcher at Boston Children’s Hospital who developed the drug, known as valeriasen. But traditional drug companies, he added, are not helping patients with thousands of rare, untreatable and rapidly progressing diseases that cause death and severe disabilities. Personalized genetic treatments may be their only hope. “We have to learn as much as we can from each and every one, because they’re just so incredibly valuable in every sense,” Dr. Yu said. Scientists first imagined creating “antisense oligonucleotide” drugs — pieces of custom-made DNA or RNA designed to correct for genetic errors in cells — in the 1960s. But it took decades to make stable and effective versions of such drugs. © 2022 The New York Times Company

Keyword: Epilepsy; Development of the Brain
Link ID: 28529 - Posted: 10.28.2022

By Hannah Thomasy Ned and Sunny stretch out together on the warm sand. He rests his head on her back, and every so often he might give her an affectionate nudge with his nose. The pair is quiet and, like many long-term couples, they seem perfectly content just to be in each other’s presence. The couple are monogamous, which is quite rare in the animal kingdom. But Sunny and Ned are a bit scalier that your typical lifelong mates — they are shingleback lizards that live at Melbourne Museum in Australia. In the wild, shinglebacks regularly form long-term bonds, returning to the same partner during mating season year after year. One lizard couple in a long-term study had been pairing up for 27 years and were still going strong when the study ended. In this way, the reptiles are more like some of the animal kingdom’s most famous long-term couplers, such as albatrosses, prairie voles and owl monkeys, and they confound expectations many people have about the personalities of lizards. “There’s more socially going on with reptiles than we give them credit for,” said Sean Doody, a conservation biologist at the University of South Florida. Social behavior in reptiles has been largely overlooked for decades, but a handful of dedicated scientists have begun unraveling reptiles’ cryptic social structures. With the help of camera traps and genetic testing, scientists have discovered reptiles living in family groups, caring for their young and communicating with each other in covert ways. And they aren’t only doing this because they love lizards. Currently, one in five reptile species are threatened with extinction; researchers say learning more about reptile sociality could be crucial for conservation. Humans have a long history of animosity toward reptiles, and influential twentieth century scientists added to the idea of reptiles as cold, unintelligent beasts. In the mid-1900s, Paul MacLean, a neuroscientist at Yale and then the National Institute of Mental Health, began developing the triune brain hypothesis. He theorized that the human brain contained three parts: the reptilian R-complex, which governed survival and basic instinctual behaviors; the paleomammalian complex, which controlled emotional behavior; and the neomammalian cortex, which was responsible for higher functions like problem-solving and language. © 2022 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 28528 - Posted: 10.26.2022

By Jan Claassen, Brian L. Edlow A medical team surrounded Maria Mazurkevich’s hospital bed, all eyes on her as she did … nothing. Mazurkevich was 30 years old and had been admitted to New York–Presbyterian Hospital at Columbia University on a blisteringly hot July day in New York City. A few days earlier, at home, she had suddenly fallen unconscious. She had suffered a ruptured blood vessel in her brain, and the bleeding area was putting tremendous pressure on critical brain regions. The team of nurses and physicians at the hospital’s neurological intensive care unit was looking for any sign that Mazurkevich could hear them. She was on a mechanical ventilator to help her breathe, and her vital signs were stable. But she showed no signs of consciousness. Mazurkevich’s parents, also at her bed, asked, “Can we talk to our daughter? Does she hear us?” She didn’t appear to be aware of anything. One of us (Claassen) was on her medical team, and when he asked Mazurkevich to open her eyes, hold up two fingers or wiggle her toes, she remained motionless. Her eyes did not follow visual cues. Yet her loved ones still thought she was “in there.” She was. The medical team gave her an EEG—placing sensors on her head to monitor her brain’s electrical activity—while they asked her to “keep opening and closing your right hand.” Then they asked her to “stop opening and closing your right hand.” Even though her hands themselves didn’t move, her brain’s activity patterns differed between the two commands. These brain reactions clearly indicated that she was aware of the requests and that those requests were different. And after about a week, her body began to follow her brain. Slowly, with minuscule responses, Mazurkevich started to wake up. Within a year she recovered fully without major limitations to her physical or cognitive abilities. She is now working as a pharmacist. © 2022 Scientific American,

Keyword: Consciousness; Brain imaging
Link ID: 28527 - Posted: 10.26.2022

Nina Lakhani The mystery behind the astronomical rise in neurological disorders like Parkinson’s disease and Alzheimer’s could be caused by exposure to environmental toxins that are omnipresent yet poorly understood, leading doctors warn. At a conference on Sunday, the country’s leading neurologists and neuroscientists will highlight recent research efforts to fill the gaping scientific hole in understanding of the role environmental toxins – air pollution, pesticides, microplastics, forever chemicals and more – play in increasingly common diseases like dementias and childhood developmental disorders. Humans may encounter a staggering 80,000 or more toxic chemicals as they work, play, sleep and learn – so many that it is almost impossible to determine their individual effects on a person, let alone how they may interact or the cumulative impacts on the nervous system over a lifespan. Some contact with environmental toxins is inevitable given the proliferation of plastics and chemical pollutants, as well as America’s hands off regulatory approach, but exposure is unequal. In the US, communities of color, Indigenous people and low income families are far more likely to be exposed to a myriad of pollutants through unsafe housing and water, manufacturing and agricultural jobs, and proximity to roads and polluting industrial plants, among other hazards. It’s likely genetic makeup plays a role in how susceptible people are to the pathological effects of different chemicals, but research has shown higher rates of cancers and respiratory disease in environmentally burdened communities. © 2022 Guardian News & Media Limited

Keyword: Alzheimers; Parkinsons
Link ID: 28526 - Posted: 10.26.2022

By David Grimm “Whooo’s a good boy?” “Whooo’s a pretty kitty?” When it comes to communicating with our pets, most of us can’t help but talk to them like babies. We pitch our voices high, extend our vowels, and ask short, repetitive questions. Dogs seem to like this. They’re far more likely to pay attention to us when we use this “caregiver speech,” research has shown. Now, scientists have found the same is true for cats, though only when their owner is talking. The work adds evidence that cats—like dogs—may bond with us in some of the same ways infants do. “It’s a fascinating study,” says Kristyn Vitale, an animal behaviorist and expert on cat cognition at Unity College, who was not involved with the work. “It further supports the idea that our cats are always listening to us.” Charlotte de Mouzon had a practical reason for getting into this line of research. An ethologist at Paris Nanterre University, she had previously been a cat behaviorist, consulting with owners on how to solve everything from litter box problems to aggressive behavior. “Sometimes people would ask me, ‘What’s the scientific evidence behind your approaches?’” she says. “I was frustrated that there were no studies being done on cat behavior in France.” So, she began a Ph.D. and was soon studying cat-human communication. As a first step, de Mouzon confirmed what most cat owners already know: We dip into “baby talk” when we address our feline friends–a habit de Mouzon is guilty of herself. “What’s up, my little ones?” she finds herself asking in a high-pitched voice when greeting her two kitties, Mila and Shere Khan. But do cats, like dogs, actually respond more to this “cat-directed speech”? To find out, de Mouzon recruited 16 cats and their owners—students at the Alfort National Veterinary School just outside of Paris. Because cats can be challenging to work with, de Mouzon studied them on feline-friendly turf, converting a common room in the students’ dormitory into a makeshift animal behavior lab filled with toys, a litter box, and places to hide.

Keyword: Animal Communication; Language
Link ID: 28525 - Posted: 10.26.2022

By Elisabeth Egan BEVERLY HILLS, Calif. — When I pictured Matthew Perry, the actor frequently known as Chandler Bing, I saw him on the tangerine couch at Central Perk or seated on one of the twin recliners in the apartment he shared with Joey Tribbiani. In September, after arriving at his 6,300-square-foot rental house and being ushered through a driveway gate by his sober companion, I sat across from Perry, who perched on a white couch in a white living room, a world away from “Friends,” the NBC sitcom that aired for 10 seasons and catapulted all six of its stars into fame, fortune and infinite memes. Instead of the foosball table where Chandler, Joey, Monica, Phoebe, Rachel and Ross gathered, nudging each other through the first chapters of adulthood, Perry, 53, had a red felt pool table that looked untouched. There was plenty of light in the house, but not a lot of warmth. I have watched every episode of “Friends” three times — in prime time, on VHS and on Netflix — but I’m not sure I would have recognized Perry if I’d seen him on the street. If he was an ebullient terrier in those 1990s-era Must See TV days — as memorable for his full-body comedy as he was for the inflection that made “Can you BE any more [insert adjective]” the new “Gag me with a spoon” — he now seemed more like an apprehensive bulldog, with the forehead furrows to match. As his former co-star Lisa Kudrow confesses in the foreword to his memoir, “Friends, Lovers and the Big Terrible Thing,” the first question people ask about “Friends” is often “How’s Matthew Perry doing?” Perry answers that question in the book, which Flatiron will publish on Nov. 1, by starkly chronicling his decades-long cage match with drinking and drug use. His addiction led to a medical odyssey in 2018 that included pneumonia, an exploded colon, a brief stint on life support, two weeks in a coma, nine months with a colostomy bag, more than a dozen stomach surgeries, and the realization that, by the time he was 49, he had spent more than half of his life in treatment centers or sober living facilities. © 2022 The New York Times Company

Keyword: Drug Abuse
Link ID: 28524 - Posted: 10.26.2022

WASHINGTON — A massive recall of millions of sleep apnea machines has stoked anger and frustration among patients, and U.S. officials are weighing unprecedented legal action to speed a replacement effort that is set to drag into next year. Sound-dampening foam in the pressurized breathing machines can break down over time, leading users to potentially inhale tiny black particles or hazardous chemicals while they sleep, manufacturer Philips warned in June 2021. Philips initially estimated it could repair or replace the units within a year. But with the recall expanding to more than 5 million devices worldwide, the Dutch company now says the effort will stretch into 2023. That's left many patients to choose between using a potentially harmful device or trying risky remedies, including removing the foam themselves, buying second-hand machines online or simply going without the therapy. The devices are called continuous positive airway pressure, or CPAP, machines. They force air through a mask to keep passageways open during sleep. Untreated sleep apnea can cause people to stop breathing hundreds of times per night, leading to dangerous drowsiness and increased heart attack risk. The problem is more common in men than women, with estimates ranging from 10% to 30% of adults affected. Most patients are better off using a recalled device because the risks of untreated sleep apnea still outweigh the potential harms of the disintegrating foam, physicians say. But doctors have been hard pressed to help patients find new machines, which generally cost between $500 and $1,000, and were already in short supply due to supply chain problems. © 2022 npr

Keyword: Sleep
Link ID: 28523 - Posted: 10.26.2022

by Carey Gillam and Aliya Uteuova For decades, Swiss chemical giant Syngenta has manufactured and marketed a widely used weed-killing chemical called paraquat, and for much of that time the company has been dealing with external concerns that long-term exposure to the chemical may be a cause of the incurable brain ailment known as Parkinson’s disease. Syngenta has repeatedly told customers and regulators that scientific research does not prove a connection between its weedkiller and the disease, insisting that the chemical does not readily cross the blood-brain barrier, and does not affect brain cells in ways that cause Parkinson’s. But a cache of internal corporate documents dating back to the 1950s reviewed by the Guardian suggests that the public narrative put forward by Syngenta and the corporate entities that preceded it has at times contradicted the company’s own research and knowledge. And though the documents reviewed do not show that Syngenta’s scientists and executives accepted and believed that paraquat can cause Parkinson’s, they do show a corporate focus on strategies to protect product sales, refute external scientific research and influence regulators. In one defensive tactic, the documents indicate that the company worked behind the scenes to try to keep a highly regarded scientist from sitting on an advisory panel for the US Environmental Protection Agency (EPA). The agency is the chief US regulator for paraquat and other pesticides. Company officials wanted to make sure the efforts could not be traced back to Syngenta, the documents show. And the documents show that insiders feared they could face legal liability for long-term, chronic effects of paraquat as long ago as 1975. One company scientist called the situation “a quite terrible problem” for which “some plan could be made … ”

Keyword: Parkinsons; Neurotoxins
Link ID: 28522 - Posted: 10.22.2022

Ewen Callaway Set on a rocky outcrop in southern Siberia, Chagyrskaya Cave might not look like much. But for one family of Neanderthals, it was home. For the first time, researchers have identified a set of closely related Neanderthals: a father and his teenage daughter and two other, more-distant relatives. The discovery of the family — reported on 19 October in Nature1 — and seven other individuals (including a pair of possible cousins from another clan) in the same cave, along with two more from a nearby site, represents the largest ever cache of Neanderthal genomes. The findings also suggest that Neanderthal communities were small, and that females routinely left their families to join new groups. Gleaning insights into kinship and social structure is new territory for ancient-genome studies, which have typically focused on broader population history, says Krishna Veeramah, a population geneticist at Stonybrook University in New York. “The fact that we can do this with Neanderthals is incredible.” Buried treasure Set on the banks of the Charysh River in the foothills of the Altai mountains, Chagyrskaya is 100 kilometres west of Denisova Cave, an archaeological treasure trove in which humans, Neanderthals, Denisovans (and at least one Neanderthal–Denisovan hybrid) all lived intermittently over some 300,000 years2,3. Excavations of Chagyrskaya, however, have so far revealed only Neanderthal remains, dated to between 50,000 to 60,000 years ago, and characteristic stone tools. In 2020, a genome sequence from a female Neanderthal from Chagyrskaya suggested she belonged to population distinct from those that occupied Denisova Cave much earlier4. To study the cave’s inhabitants in greater depth, a team of researchers led by palaeogeneticist Laurits Skov and population geneticist Benjamin Peter at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted DNA from 17 other ancient-human remains from Chagyrskaya, as well as several from a nearby cave, called Okladnikov. © 2022 Springer Nature Limited

Keyword: Evolution
Link ID: 28521 - Posted: 10.22.2022

By Fenit Nirappil A national shortage of Adderall has left patients who rely on the pills for attention-deficit/hyperactivity disorder scrambling to find alternative treatments and uncertain whether they will be able to refill their medication. The Food and Drug Administration announced the shortage last week, saying that one of the largest producers is experiencing “intermittent manufacturing delays” and that other makers cannot keep up with demand. Some patients say the announcement was a belated acknowledgment of a reality they have faced for months — pharmacies unable to fill their orders and anxiety about whether they will run out of a medication needed to manage their daily lives. Experts say it is often difficult for patients to access Adderall, a stimulant that is tightly regulated as a controlled substance because of high potential for abuse. Medication management generally requires monthly doctor visits. There have been other shortages in recent years. “This one is more sustained,” said Timothy Wilens, an ADHD expert and chief of child and adolescent psychiatry at Massachusetts General Hospital who said access issues stretch back to spring. “It’s putting pressure on patients, and it’s putting pressure on institutions that support the patients.” Erik Gude, a 28-year-old chef who lives in Atlanta, experiences regular challenges filling his Adderall prescription, whether it’s pharmacies not carrying generic versions or disputes with insurers. He has been off the medication for a month after his local pharmacy ran out.

Keyword: ADHD; Drug Abuse
Link ID: 28520 - Posted: 10.22.2022

Kate Siber Sharon Maxwell spent much of her life trying to make herself small. Her family put her on her first diet when she was 10. Early on Saturday mornings, she and her mother would drive through the empty suburban streets of Hammond, Ind., to attend Weight Watchers meetings. Maxwell did her best at that age to track her meals and log her points, but the scale wasn’t going down fast enough. So she decided to barely eat anything on Fridays and take laxatives that she found in the medicine cabinet. Food had long been a fraught subject in the Maxwell household. Her parents were also bigger-bodied and dieted frequently. They belonged to a fundamentalist Baptist megachurch where gluttony was seen as a sin. To eat at home was to navigate a labyrinth of rules and restrictions. Maxwell watched one time as her mother lost 74 pounds in six months by consuming little more than carrot juice (her skin temporarily turned orange). Sometimes her father, seized with a new diet idea, abruptly ransacked shelves in the kitchen, sweeping newly forbidden foods into the trash. Maxwell was constantly worried about eating too much. She started to eat alone and in secret. She took to chewing morsels and spitting them out. She hid food behind books, in her pockets, under mattresses and between clothes folded neatly in drawers. Through Maxwell’s teenage years and early 20s, eating became even more stressful. Her thoughts constantly orbited around food: what she was eating or not eating, the calories she was burning or not burning, the size of her body and, especially, what people thought of it. Her appearance was often a topic of public interest. When she went grocery shopping for her family, other customers commented on the items in her cart. “Honey, are you sure you want to eat that?” one person said. Other shoppers offered unsolicited advice about diets. Strangers congratulated her when her cart was filled with vegetables. As she grew older, people at the gym clapped and cheered for her while she worked out. “People would say: ‘Go! You can lose the weight!’” she says. While eating in public, other diners offered feedback — and still do to this day — on her choices, a few even asking if she wanted to join their gym. Some would call her names: Pig, Fatty. Sometimes people told her she was brave for wearing shorts, while others said she should cover up. She was always aware, whether she wanted to be or not, of how others viewed her body. © 2022 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 28519 - Posted: 10.19.2022

By Sandra G. Boodman For years Carter Caldwell had adamantly rejected doctors’ recommendations that he consider surgery to treat the frequent, uncontrolled seizures that were ravaging his brain. Caldwell, who had developed epilepsy when he was 28, regarded the operation that involved removing a portion of his brain as too big a risk — particularly because doctors weren’t sure what was causing the seizures and couldn’t pinpoint their location. Instead the Philadelphia business executive had organized his life to minimize certain foreseeable hazards: He lived downtown and didn’t drive. He didn’t push his toddler’s stroller. When taking the train he stood at the back of the platform — nowhere near the tracks in case he suddenly collapsed. His colleagues at work knew about his condition. But that calculus changed abruptly in November 2014. Caldwell, accompanied by his wife, Connie, and their 3-year-old son, was atop a hill at Pennsylvania’s Valley Forge National Historical Park posing for photos for a holiday card. Without warning he began an awkward shuffling walk that signified the onset of a seizure. Then he lost consciousness and fell head first down a rocky 15-foot embankment before landing at the edge of a stream. “Thankfully,” he said, “I didn’t roll into the stream.” He spent the next 2 1/2 weeks in a nearby hospital where a plastic surgeon performed multiple operations on his broken jawbone, lacerated cheek and shattered eye socket. “I remember him saying, ‘I can’t believe this happened in front of my family,’ ” recalled his longtime neurologist John R. Pollard, formerly associate director of the epilepsy center at the University of Pennsylvania. Pollard had warned Caldwell that his intractable seizures, which had proved resistant to numerous medications, placed him at risk for sudden death or serious injury. In September 2015 a successful operation unmasked the very unusual cause of Caldwell’s seizures, a culprit experts had long suspected but had been unable to definitively identify.

Keyword: Epilepsy; Emotions
Link ID: 28518 - Posted: 10.19.2022

By Jyoti Madhusoodanan Q: I recently started taking an S.S.R.I. antidepressant, but I have been confused about whether it’s safe to drink alcohol. Some internet sources say it’s fine, others say to avoid drinking completely. Help! For many health care providers who treat anxiety and depression, the concern about whether it’s safe — or even advised — to drink alcohol while taking an antidepressant is a common one. “Patients tell me all the time, ‘I’m going to be drinking with friends tonight, so I skipped a dose,’” said Dr. Sarah Ramsay Andrews, a psychiatrist at the Johns Hopkins University School of Medicine. But skipping a dose is never a good idea, said Dr. Jody Glance, an addiction medicine specialist at the University of Pittsburgh Medical Center Western Behavioral Health — even if you’re going out for cocktails with friends. “When people stop taking their medicines for a day or two, they often don’t resume, and that can lead to a relapse of anxiety or depression.” Besides, she added, how safe it is to drink while on antidepressants depends on the kind of antidepressant you’re taking — and for most people taking selective serotonin reuptake inhibitors (or S.S.R.I.s), an occasional drink likely won’t do much harm. There are, however, caveats to keep in mind. S.S.R.I. medications — which include citalopram (Celexa), sertraline (Zoloft) and escitalopram (Lexapro) — are the most commonly prescribed class of antidepressants. They are typically used to help treat depression, and can also be effective for other conditions like anxiety, obsessive compulsive disorder, certain phobias and even premenstrual dysphoric disorder. They work by increasing the levels of the brain chemical serotonin — which is thought to influence your mood and emotions, among other things — by blocking its removal after it carries messages in the brain. But unlike many other medications used to treat mood disorders — like the anxiety medication alprazolam (Xanax) or the tricyclic antidepressant amitriptyline (Elavil) — S.S.R.I.s are less likely to interact with alcohol than other kinds of drugs, Dr. Glance said. © 2022 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 28517 - Posted: 10.19.2022

Nicola Davis Science correspondent Playing sounds while you slumber might help to strengthen some memories while weakening others, research suggests, with experts noting the approach might one day help people living with traumatic recollections. Previous work has shown that when a sound is played as a person learns an association between two words, the memory of that word association is boosted if the same sound is played while the individual sleeps. Now researchers have found fresh evidence the approach could also be used to weaken such memories. “We can an actually induce forgetting of specific material whilst people are asleep,” said Dr Aidan Horner, co-author of the study from the University of York. Advertisement Writing in the journal Learning & Memory, Horner and colleagues report how 29 participants were shown pairs of words on a computer screen, one of which was an object word, such as bicycle, while the other was either a place word, such as office, or a person, such as David Beckham. The process was repeated for 60 different object words, and in the course of the process both possible pairings were shown, resulting in 120 associations. As the pairs flashed up, participants heard the object word being spoken out loud. The team tested the participants on a subset of the associations, presenting them with one of the words and asking them to select a paired word from a list of six options. Participants then spent a night in the team’s sleep laboratory. Once they had entered a particular sleep state – as judged by electrodes placed on their heads – they were played audio of 30 of the object words. The team tested participants on the word associations the next day. The results reveal participants’ ability to recall the first word they had learned to pair with an object word was boosted if audio of the latter was played as they slept, compared with if it was not played. However, their ability to recall the second word they learned to associate with the same object decreased relative to the audio-free scenario. © 2022 Guardian News & Media Limited

Keyword: Sleep; Learning & Memory
Link ID: 28516 - Posted: 10.19.2022

McKenzie Prillaman A twist on functional magnetic resonance imaging (fMRI) offers a multi-fold improvement in its time sensitivity, better enabling it to unveil the fine-scale dynamics underlying mental processes. Researchers published the results on 13 October in Science1. Can brain scans reveal behaviour? Bombshell study says not yet A standard fMRI technique measures brain activity indirectly, by tracking increases in blood flow in regions where neurons are suddenly consuming more oxygen. This signal, however, can lag behind neuronal activity by 1 second, which dampens time sensitivity — the speedy cells take mere milliseconds to send messages to one another. Jang-Yeon Park, an MRI physicist at Sungkyunkwan University in Suwon, South Korea, set out to enhance fMRI’s temporal precision to track neuronal activity on the order of milliseconds. He and his colleagues accomplished this by changing the software of a high-intensity MRI scanner to acquire data every 5 milliseconds — about 8 times faster than what the standard technique can capture — and applying frequent, repetitive stimulation to animals they were testing. This suppressed the slower-paced blood oxygenation signal, making it possible to observe faster-paced brain activity. The researchers named their technique direct imaging of neuronal activity, or DIANA. In the study, an anaesthetized mouse inside an MRI scanner received a minor electric shock to its face every 200 milliseconds. Between shocks, the machine acquired data from one tiny region of the mouse’s brain every 5 milliseconds. It moved on to a new area after the next electric shock. After the software stitched everything together, the process produced a head-on image of one full slice of the brain, capturing neuronal activity over a 200-millisecond time period. (Spatial resolution was 0.22 millimetres, which is standard for high-intensity MRI.) During the scan, the facial stimulation activated a part of the brain that processes sensory inputs, causing the region to light up with a signal. The researchers found that this ‘DIANA response’ happened at the same time that neurons fired off signals, or ‘spiked’ — activity that was measured separately, using a surgically inserted probe. Furthermore, the team was able to trace the DIANA signal through a brain circuit as groups of neurons sequentially triggered each other. © 2022 Springer Nature Limited

Keyword: Brain imaging
Link ID: 28515 - Posted: 10.15.2022

By Lisa Sanders, M.D. “What just happened?” The 16-year-old girl’s voice was flat and tired. “I think you had a seizure,” her mother answered. Her daughter had asked to be taken to the pediatrician’s office because she hadn’t felt right for the past several weeks — not since she had what looked like a seizure at school. And now she’d had another. “You’re OK now,” the mother continued. “It’s good news because it means that maybe we finally figured out what’s going on.” To most people, that might have been a stretch — to call having a seizure good news. But for the past several years, the young woman had been plagued by headaches, episodes of dizziness and odd bouts of profound fatigue, and her mother embraced the possibility of a treatable disorder. The specialists she had taken her daughter to see attributed her collection of symptoms to the lingering effect of the many concussions she suffered playing sports. She had at least one concussion every year since she was in the fourth grade. Because of her frequent head injuries, her parents made her drop all her sports. Even when not on the playing field, the young woman continued to fall and hit her head. The headaches and other symptoms persisted long after each injury. She saw several specialists who agreed that she had what was called persistent post-concussive syndrome — symptoms caused either by a severe brain injury or, in her case, repeated mild injuries. She should get better with time and patience, the girl and her mother were told. And yet her head pounded and she retreated to her darkened room several times a week. She did everything her doctors suggested: She got plenty of sleep, rested when she was tired and tried to be patient. But she still got headaches, still got dizzy. She found it harder and harder to pay attention. For the past couple of years, it had even started to affect her grades. © 2022 The New York Times Company

Keyword: Epilepsy; Attention
Link ID: 28514 - Posted: 10.15.2022