Laura Sanders A teenager’s brain does not magically mature into its reasoned, adult form the night before his or her 18th birthday. Instead, aspects of brain development stretch into a person’s 20s — a protracted fine-tuning with serious implications for young people caught in the U.S. justice system, argues cognitive neuroscientist B.J. Casey of Yale University. In the May 22 Neuron, Casey describes the heartbreaking case of Kalief Browder, sent at age 16 to Rikers Island correctional facility in New York City after being accused of stealing a backpack. Unable to come up with the $3,000 bail, Browder spent three years in the violent jail before his case was ultimately dropped. About two-thirds of his time in custody was spent in solitary confinement — “a terrible place for a child to have to grow up,” Casey says. Two years after his 2013 release, Browder died from suicide. Casey uses the case to highlight how the criminal justice system — and the accompanying violence, stress and isolation (SN: 12/8/18, p. 11) that come with being incarcerated — can interfere with brain development in adolescents and children. Other recent stories of immigrant children being separated from their families and held in detention centers have raised similar concerns (SN Online: 6/20/18). Studies with lab animals and brain imaging experiments in people show that chronic stress and other assaults “impact the very brain circuitry that is changing so radically during adolescence,” Casey says. An abundance of science says that “the way we’re treating our young people is not the way to a healthy development.” |© Society for Science & the Public 2000 - 2019

Keyword: Development of the Brain; Stress
Link ID: 26262 - Posted: 05.23.2019

Ed Yong In 1996, a group of European researchers found that a certain gene, called SLC6A4, might influence a person’s risk of depression. It was a blockbuster discovery at the time. The team found that a less active version of the gene was more common among 454 people who had mood disorders than in 570 who did not. In theory, anyone who had this particular gene variant could be at higher risk for depression, and that finding, they said, might help in diagnosing such disorders, assessing suicidal behavior, or even predicting a person’s response to antidepressants. Back then, tools for sequencing DNA weren’t as cheap or powerful as they are today. When researchers wanted to work out which genes might affect a disease or trait, they made educated guesses, and picked likely “candidate genes.” For depression, SLC6A4 seemed like a great candidate: It’s responsible for getting a chemical called serotonin into brain cells, and serotonin had already been linked to mood and depression. Over two decades, this one gene inspired at least 450 research papers. But a new study—the biggest and most comprehensive of its kind yet—shows that this seemingly sturdy mountain of research is actually a house of cards, built on nonexistent foundations. Richard Border of the University of Colorado at Boulder and his colleagues picked the 18 candidate genes that have been most commonly linked to depression—SLC6A4 chief among them. Using data from large groups of volunteers, ranging from 62,000 to 443,000 people, the team checked whether any versions of these genes were more common among people with depression. “We didn’t find a smidge of evidence,” says Matthew Keller, who led the project. (c) 2019 by The Atlantic Monthly Group.

Keyword: Depression; Genes & Behavior
Link ID: 26261 - Posted: 05.22.2019

By Emily Willingham As anyone who’s dealt with substance addiction can tell you, breaking the physical intimacy with the drug isn’t always the most challenging part of treatment. People trying to avoid resurrecting their addiction also must grapple with reminders of it: the sights, sounds and people who were part of their addictive behaviors. These cues can trigger a craving for the drug, creating anxiety that steers them straight back into addiction for relief. The opioid epidemic in the United States has taken more than 300,000 lives, and support for people working to keep these drugs out of their orbit has become crucial. Methadone and buprenorphine, the current medical treatment options, help break the physical craving for opioids by targeting the same pathways that opioids use. Although these drugs can ease physical need, they don’t quiet the anxiety that environmental cues can trigger, leaving open a door to addiction reentry. The cannabis compound cannabidiol (CBD), a nonpsychoactive component of cannabis, might be the key to keeping that door locked. Researchers report that among people with opioid addiction, CBD dampens cue-triggered cravings and anxiety, along with reducing stress hormone levels and heart rate. The results were published May 21 in the American Journal of Psychiatry. “These findings provide support for an effect of cannabidiol on this process,” says Kathryn McHugh, assistant professor in the department of psychiatry at Harvard Medical School’s Division of Alcohol and Drug Abuse, who was not involved in the study. However, she cautions, the results are preliminary, and behavioral therapies are also quite effective at dimming the signal from cues. © 2019 Scientific American

Keyword: Drug Abuse; Depression
Link ID: 26260 - Posted: 05.22.2019

Carolyn Wilke Here’s a downer: Pessimism seems contagious among ravens. But positivity? Not so much. When ravens saw fellow birds’ responses to a disliked food, but not the food itself, their interest in their own food options waned, researchers report May 20 in the Proceedings of the National Academy of Sciences. The study suggests that the birds pick up on and even share negative emotions, the researchers say. Ravens are “very good problem solvers … but this paper’s really highlighting their social intelligence as well,” says Andrew Gallup, a psychologist at SUNY Polytechnic Institute in Utica, N.Y., who was not involved in the study. The work paints a richer picture of how the birds’ brains work, he says. Known for their smarts, ravens act in ways that suggest a capacity for empathy, such as by appearing to console a distressed comrade. Thomas Bugnyar, a cognitive ethologist at the University of Vienna, and his colleagues wanted to look into one building block of empathy — whether animals share emotions. To be able to feel for others, an animal needs to be able to feel like others, he says. But sizing up an animal’s mood is tricky. Scientists generally rely on behavioral or physiological cues to clue into a creature’s emotional state. More challenging is assessing how one animal’s mood might influence another’s: Similar actions appearing to stem from kindred emotions may just be mimicry. |© Society for Science & the Public 2000 - 2019

Keyword: Emotions; Evolution
Link ID: 26259 - Posted: 05.22.2019

By Kenneth Miller A model of Ben Barres’ brain sits on the windowsill behind his desk at Stanford University School of Medicine. To a casual observer, there’s nothing remarkable about the plastic lump, 3-D-printed from an MRI scan. Almost lost in the jumble of papers, coffee mugs, plaques and trophies that fill the neurobiologist’s office, it offers no hint about what Barres’ actual gray matter has helped to accomplish: a transformation of our understanding of brains in general, and how they can go wrong. Barres is a pioneer in the study of glia. This class of cells makes up 90 percent of the human brain, but gets far less attention than neurons, the nerve cells that transmit our thoughts and sensations at lightning speed. Glia were long regarded mainly as a maintenance crew, performing such unglamorous tasks as ferrying nutrients and mopping up waste, and occasionally mounting a defense when the brain faced injury or infection. Over the past two decades, however, Barres’ research has revealed that they actually play central roles in sculpting the developing brain, and in guiding neurons’ behavior at every stage of life. “He has made one shocking, revolutionary discovery after another,” says biologist Martin Raff, emeritus professor at University College London, whose own work helped pave the way for those advances. Recently, Barres and his collaborators have made some discoveries that may revolutionize the treatment of neurodegenerative ailments, from glaucoma and multiple sclerosis to Alzheimer’s disease and stroke. What drives such disorders, their findings suggest, is a process in which glia turn from nurturing neurons to destroying them. Human trials of a drug designed to block that change are just beginning.

Keyword: Glia; Learning & Memory
Link ID: 26258 - Posted: 05.22.2019

By Gretchen Reynolds Skipping breakfast before exercise might reduce how much we eat during the remainder of the day, according to a small but intriguing new study of fit young men. The study finds that the choice to eat or omit a meal before an early workout could affect our relationship to food for the rest of the day, in complicated and sometimes unexpected ways. Weight management is, of course, one of the great public — and private — health concerns of our time. But the role of exercise in helping people to maintain, lose or, in some instances, add pounds is problematic. Exercise burns calories, but in many past studies, people who begin a new exercise program do not lose as much weight as would be expected, because they often compensate for the energy used during exercise by eating more later or moving less. These compensations, usually subtle and unintended, indicate that our brains are receiving internal communiqués detailing how much energy we used during that last workout and, in response, sending biological signals that increase hunger or reduce our urge to move. Our helpful brains do not wish us to sustain an energy deficit and starve. Previous studies show that many aspects of eating and exercise can affect how much people compensate for the calories burned during exercise, including the type and length of the exercise and the fitness and weight of the exercisers. Skipping or consuming breakfast also can matter. When we eat a meal, our bodies rely on the carbohydrates in those foods as a primary source of energy. Some of those carbohydrates are stored in our bodies, but those internal stores of carbohydrates are small compared to the stores of fat. Some researchers believe that our brains may pay particular attention to any reductions in our carbohydrate levels and rush to replace them. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26257 - Posted: 05.22.2019

Ian Sample Science editor Male bonobos living with their mothers are three times more likely to father offspring, research suggests. Their mothers are so keen for them to father children that they usher them in front of promising partners, shield them from violent competitors and dash the chances of other males by charging them while they are at it. For a bonobo mother, it is all part of the parenting day, and analysis finds the hard work pays off. Males of the species that live with their mothers are three times more likely to father offspring than those whose mothers are absent. Martin Surbeck, a primatologist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, said: “We wanted to see if the mothers’ behaviour changes the odds of their sons’ success, and it does. The mothers have a strong influence on the number of grandchildren they get.” Bonobo mothers seize every opportunity to give their sons a leg-up. In bonobo society, the lower ranks tend to be gender balanced, but females dominate the top ranks. Many mothers have social clout and chaperone their sons to huddles with fertile females, ensuring them better chances to mate. “The mothers tend to be a social passport for their sons,” said Surbeck. © 2019 Guardian News & Media Limited

Keyword: Sexual Behavior; Evolution
Link ID: 26256 - Posted: 05.21.2019

Alison Abbott Pharmacologists gave mescaline a fair trial. In the early and mid-twentieth century, it seemed more than plausible that the fashionable hallucinogen could be tamed into a therapeutic agent. After all, it had profound effects on the human body, and had been used for centuries in parts of the Americas as a gateway to ceremonial spiritual experience. But this psychoactive alkaloid never found its clinical indication, as science writer Mike Jay explains in Mescaline, his anthropological and medical history. In the 1950s, the attention of biomedical researchers abruptly switched to a newly synthesized molecule with similar hallucinogenic properties but fewer physical side effects: lysergic acid diethylamide, or LSD. First synthesized by Swiss scientist Albert Hofmann in 1938, LSD went on to become a recreational drug of choice in the 1960s hippy era. And, like mescaline, it teased psychiatrists without delivering a cure. Jay traces the chronology of mescaline use. The alkaloid is found in the fast-growing San Pedro cactus (Echinopsis pachanoi) that towers above the mountainous desert scrub of the Andes, and the slow-growing, ground-hugging peyote cactus (Lophophora williamsii) native to Mexico and the southwestern United States. Archaeological evidence suggests that the use of these cacti in rites of long-vanished cultures goes back at least 5,000 years. © 2019 Springer Nature Publishing AG

Keyword: Drug Abuse; Depression
Link ID: 26255 - Posted: 05.21.2019

by C.L. Lynch Everyone knows that autism is a spectrum. People bring it up all the time. “My son is on the severe end of the autism spectrum.” “We’re all a little autistic– it’s a spectrum.” “I’m not autistic but I’m definitely ‘on the spectrum.'” If only people knew what a spectrum is… because they are talking about autism all wrong. Let’s use the visible spectrum as an example. As you can see, the various parts of the spectrum are noticeably different from each other. Blue looks very different from red, but they are both on the visible light spectrum. Red is not “more blue” than blue is. Red is not “more spectrum” than blue is. When people discuss colours, they don’t talk about how “far along” the spectrum a colour is. They don’t say “my walls are on the high end of the spectrum” or “I look best in colours that are on the low end of the spectrum.” But when people talk about autism they talk as if it were a gradient, not a spectrum at all. People think you can be “a little autistic” or “extremely autistic,” the way a paint colour could be a little red or extremely red. An image of a colour gradient moving from white to red. The lightest zone is labelled How people think the spectrum looks But autism isn’t that simple. Autism isn’t a set of defined symptoms that collectively worsen as you move “up” the spectrum.

Keyword: Autism
Link ID: 26254 - Posted: 05.21.2019

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

By Nathaniel Scharping | Don’t get a big head, your mother may have told you. That’s good advice, but it comes too late for most of us. Humans have had big heads, relatively speaking, for hundreds of thousands of years, much to our mothers’ dismay. Our oversize noggins are a literal pain during childbirth. Babies have to twist and turn as they exit the birth canal, sometimes leading to complications that necessitate surgery. And while big heads can be painful for the mother, they can downright transformative for babies: A fetus’ pliable skull deforms during birth like putty squeezed through a tube to allow it to pass into the world. This cranial deformation has been known about for a long time, but in a new study, scientists from France and the U.S. actually watched it happen using an MRI machine during labor. The images, published in a study in PLOS One, show how the skulls (and brains) of seven infants squished and warped during birth to pass through the birth canal. They also shine new light on how much our skulls change shape as we’re born. The researchers recruited pregnant women in France to undergo an MRI a few weeks before pregnancy and another in the minutes before they began to actually give birth. In total, seven women were scanned in the second stage of labor, when the baby begins to make its way out of the uterus. They were then rushed to the maternity ward to actually complete giving birth.

Keyword: Development of the Brain; Brain imaging
Link ID: 26252 - Posted: 05.20.2019

Before he was born, his parents knew their boy was in trouble. That was clear from what their doctors' saw in their baby's ultrasound. And tragically, the boy died when he was only ten months old. But in his short life, he left behind a valuable legacy by helping scientists understand a crucial type of brain cell. That's because — as it turned out — the child had none. "One of the things about being a pediatric geneticist is on any given day you can see a patient you could spend the rest of your life or your career thinking about," Dr. James Bennett told Quirks & Quarks host Bob McDonald. Dr. Bennett is a physician and researcher from Seattle Children's Hospital and assistant professor of pediatric genetics at the University of Washington. Devastating problems with brain development On the first day he met the child — the boy's very first day of life — Dr. Bennett said he could tell this baby needed a lot of support. The baby was having difficulty breathing, had an enlarged head as well as some very significant abnormalities of his brain. "Every single part of his brain was affected. There was no connection between the left side and the right side of his brain. And there was too much fluid on the brain — that the spaces that hold fluid around the brain were enlarged. And the white matter, which is the part of the brain that sort of connects the neurons — you can think of it as sort of the wires connecting things in the brain — was decreased and abnormal," said Dr. Bennett. Scientists had never seen a medical mystery like this before, so Dr. Bennett was determined to figure out what was wrong with the infant. He he undertook a "diagnostic odyssey" to identify the cause of this extremely rare condition. ©2019 CBC/Radio-Canada

Keyword: Development of the Brain; Glia
Link ID: 26251 - Posted: 05.20.2019

By John Horgan In a previous post I summarized my remarks at “Souls or Selfish Genes,” a conversation at Stevens Institute of Technology about religious versus scientific views of humanity. I represented the agnostic position and David Lahti, a biologist and philosopher at the City University of New York, a position more friendly to theism. Below is Lahti’s summary of his opening comments. –John Horgan I’ve been asked to deal with the question of “Souls vs. Selfish Genes”. And whereas I am sure this is a false dichotomy, I’m not quite sure how exactly to fit the two parts of the truth together. But I’ll give you a few thoughts I’ve had about it, which can at least start us off. First, selfish genes. This of course is a reference to Richard Dawkins’ 1976 book of the same name, which is a popular and sensational description of a revolution in our understanding of the way evolution by natural selection operates. Briefly, we discovered in the 1960s-70s that the organismic individual was generally the most important level at which natural selection operates, meaning that evolution by natural selection proceeds primarily via certain individuals in a population reproducing more successfully than others. In fact, this is too simplistic. Hamilton’s theory of kin selection showed that it’s actually below the level of the individual where we really have to concentrate in order to explain certain traits, such as the self-sacrificial stinging of bees and the fact that some young male birds help their mother raise her next brood instead of looking for a mate. Those individuals are not being as selfish as we might predict. © 2019 Scientific American

Keyword: Consciousness; Genes & Behavior
Link ID: 26250 - Posted: 05.20.2019

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

By Neuroskeptic | A paper in PNAS got some attention on Twitter recently. It’s called Childhood trauma history is linked to abnormal brain connectivity in major depression and in it, the authors Yu et al. report finding (as per the Significance Statement) A dramatic primary association of brain resting-state network (RSN) connectivity abnormalities with a history of childhood trauma in major depressive disorder (MDD). The authors go on to note that even though “the brain imaging took place decades after trauma occurrence, the scar of prior trauma was evident in functional dysconnectivity.” Now, I think that this talk of dramatic scarring is overblown, but in this case there’s also a wider issue with the use of a statistical method which easily lends itself to misleading interpretations – canonical correlation analysis (CCA). First, we’ll look at what Yu et al. did. In a sample of 189 unmedicated patients with depression, Yu et al. measured the resting-state functional connectivity of the brain using fMRI. They then analyzed this to give a total of 55 connection strengths for each individual. Each of these 55 measures reflects the functional coupling between two brain networks. For each patient, Yu et al. also administered questionnaires measuring personality, depression and anxiety symptoms, and history of trauma. These measures were then compressed into 4 clinical clusters, (i) anxious misery (ii) positive traits (iii) physical and emotional neglect or abuse, and (iv) sexual abuse.

Keyword: Depression; Development of the Brain
Link ID: 26248 - Posted: 05.20.2019

Hannah Devlin Science correspondent A mind-controlled hearing aid that allows the wearer to focus on particular voices has been created by scientists, who say it could transform the ability of those with hearing impairments to cope with noisy environments. The device mimics the brain’s natural ability to single out and amplify one voice against background conversation. Until now, even the most advanced hearing aids work by boosting all voices at once, which can be experienced as a cacophony of sound for the wearer, especially in crowded environments. Nima Mesgarani, who led the latest advance at Columbia University in New York, said: “The brain area that processes sound is extraordinarily sensitive and powerful. It can amplify one voice over others, seemingly effortlessly, while today’s hearing aids still pale in comparison.” This can severely hinder a wearer’s ability to join in conversations, making busy social occasions particularly challenging. Scientists have been working for years to resolve this problem, known as the cocktail party effect. The brain-controlled hearing aid appears to have cracked the problem using a combination of artificial intelligence and sensors designed to monitor the listener’s brain activity. The hearing aid first uses an algorithm to automatically separate the voices of multiple speakers. It then compares these audio tracks to the brain activity of the listener. Previous work by Mesgarani’s lab found that it is possible to identify which person someone is paying attention to, as their brain activity tracks the sound waves of that voice most closely. © 2019 Guardian News & Media Limited

Keyword: Hearing
Link ID: 26247 - Posted: 05.18.2019

By Dhruti Shah BBC News When Dani Donovan wanted to show her colleagues what life was like for her as someone diagnosed with Attention Deficit Hyperactivity Disorder (ADHD), she never thought her sketches would lead to a series of web comics with a celebrity fan base. The 28-year-old, who lives in Omaha, Nebraska, was diagnosed about a decade ago with ADHD and now hopes her comics will help others to understand the challenges for those with the condition. She told the BBC: "I'd just started a new job working in data visualisation, and it was the first time I was able to be really open about having ADHD and talk to my colleagues about what it's like. "We were telling stories and joking about how I always get off track while I'm telling stories, and I said that it's very much like having a sleepy train conductor running my train of thought. I had the idea for a flowchart, I posted it on Twitter and it took off immediately." Her graphic shows that when she hears non-ADHD storytelling, it involves a straight move from the start of a story to the end. Her storytelling, however, involves a pre-story prologue before moving to the start of the story, and then wandering through 'too many details', a side-story and losing her train of thought before reaching the end of the tale - and then apologising. However, as with all things that hit the internet - once it's let loose, be careful of memes and amendments. Dani's diagram was re-versioned by an unknown person who split the flowcharts and created a meme with 'How a normal person tells a story' taking the place of the 'Non-ADHD Storytelling' heading Dani had given her first flowchart, and 'How I tell a story' replacing the 'ADHD Storytelling' heading for the meandering flowchart. © 2019 BBC

Keyword: ADHD
Link ID: 26246 - Posted: 05.18.2019

Ruth Williams Sequencing the nuclear RNA of more than 100,000 individual postmortem brain cells from people with and without autism spectrum disorder indicates the types of genes dysregulated in the condition and the types of cells in which such dysregulation occurs. The results, reported in Science today (May 16), help narrow the focus of future ASD studies to the most likely molecular and cellular anomalies, say researchers. “It’s using the latest technology, it’s looking at the single cell level, and it validates and extends previous observations,” says autism researcher Daniel Geschwind of the University of California, Los Angeles, who was not involved in the research. “It takes the previous work and brings it to a level of resolution that we didn’t have before.” “This was an experiment that needed to be done,” adds geneticist Stephan Sanders of the University of California, San Francisco, writing in an email to The Scientist. “At the tissue level, it broadly replicates previous data in autism. Then, [it] provides a first look at which cell types are responsible for the differences.” ASD, which currently affects somewhere around 1 in 60 children in the United States, includes a broad range of conditions that are characterized by an impaired ability to communicate and interact socially. The heterogeneous nature of ASD has made studies of its molecular pathology difficult. Nevertheless, gene expression studies carried out on postmortem brain tissue from ASD patients have pointed to commonly affected pathways, including synapse function, says Dmitry Velmeshev, an author of the study and postdoc in the lab of neurologist Arnold Kriegstein, also an author. © 1986–2019 The Scientist

Keyword: Autism
Link ID: 26245 - Posted: 05.18.2019

By DAN HURLEY MAY 15, 2019 The piercing, high-pitched noises were first heard by a couple of recently arrived United States Embassy officials in Havana in late 2016, soon after Donald Trump was elected president. They heard the noises in their homes, in the city’s leafy western suburbs. If they moved to a different room, or walked outside, the noise stopped. The two officials said they believed that the sound was man-made, a form of harassment. Around the same time, they began to develop a variety of symptoms: headaches, fatigue, dizziness, mental fog, hearing loss, nausea. On Dec. 30, 2016, the Embassy’s chargé d’affaires, Jeffrey DeLaurentis, and his security chief, Anthony Spotti, were told what the men were experiencing. By then, a third Embassy worker who lived nearby also heard the sounds and began developing symptoms. DeLaurentis eventually sent the three for evaluation by an otolaryngologist at the University of Miami, who told them they had damage to their inner ears’ vestibular organs. Similar reports of sickness after hearing noises began trickling in from other diplomats in Havana. One of them, a foreign-service officer, told me he was awakened one morning in March by a screeching noise. “It paralyzed me,” he said. “When the sound occurred, I could not move. I couldn’t get up until it stopped.” In the days that followed, he felt extreme fatigue, heard a ringing in his ears, found himself making many mistakes at work and became sensitive to loud sounds and bright light. That month, DeLaurentis called a meeting of his senior staff to tell them what was going on. He insisted that they tell no one else — not even their families — which had the perverse effect of heightening the staff members’ anxiety rather than calming it. Within days, DeLaurentis felt compelled to call an open meeting of the American staff. More than 60 people crammed into the Embassy’s Sensitive Compartmented Information Facility — an inner sanctum for confidential communications. They were told about the noises and the symptoms and were offered the opportunity to be tested if they had concerns. Nearly all of those present, as well as some family members, soon asked to be evaluated.

Keyword: Emotions
Link ID: 26244 - Posted: 05.17.2019

By Jessica Wright, Clinicians can reliably diagnose autism in some toddlers roughly two years earlier than the typical age of diagnosis, a new study suggests. The researchers assessed more than 1,200 toddlers for autism at least twice using standard diagnostic tools. They diagnosed roughly one in three with the condition by age 2; 84 percent of these toddlers retained the label at their last visit, which was at age 3 on average. The finding suggests clinicians should take autism traits in toddlers seriously, says co-lead researcher Karen Pierce, professor of neurosciences at the University of California, San Diego. “If children meet criteria and they do show signs and symptoms, don’t wait; let’s get them the help and the treatment that they need,” Pierce says. Experts are divided on whether autism can reliably be diagnosed before age 3. The American Academy of Pediatrics recommends screening for autism starting at 18 months. However, the U.S. Preventive Services Task Force—a government panel that makes recommendations about preventive medicine—has said there is insufficient evidence to recommend universal screening before 3. The new study suggests that early screening and diagnosis may benefit some proportion of children: It indicates that some toddlers are likely to have clear enough signs of autism to warrant a diagnosis before 2 years of age, says Zachary Warren, associate professor of pediatrics, psychiatry and behavioral sciences at Vanderbilt University in Nashville, Tennessee. “The study shows that well-trained, expert teams evaluating young kids with autism are able to pick up concerns at fairly young ages for some kids,” says Warren, who was not involved in the work. “It’s an interesting and creative approach to understanding screening and diagnosis.” © 2019 Scientific American

Keyword: Autism
Link ID: 26243 - Posted: 05.17.2019