By Helen Thomson Do you find it difficult to spot a face in the crowd? Now we know why: people with face blindness seem to have a missing “hub” of brain connections. The discovery could be used to diagnose children with the condition, and teach them new ways to identify faces. People with prosopagnosia, which often runs in families, cannot easily tell faces apart. This can have a significant impact on people’s lives. People with the condition rely heavily on voice recognition, clothes, hairstyle and gait to identify people, but can still fail to recognise family and friends. It can lead to social anxiety and depression, and can often go undiagnosed for many years. Face processing isn’t a function of a single brain region, but involves the coordinated activity of several regions. To investigate what might be causing the problem, Galia Avidan at Ben-Gurion University of the Negev, Israel, and her colleagues scanned the brains of 10 adults who have reported life-long problems with face processing. They also scanned 10 adults without the condition. During the scan, participants were shown sets of images of emotional, neutral, famous and unfamiliar faces. During the task they were asked to press a button when two consecutive images were identical. Some of the images also included buildings, which people with face blindness do not have any trouble identifying – these acted as a control. © Copyright New Scientist Ltd.

Keyword: Attention
Link ID: 24281 - Posted: 11.03.2017

By Jocelyn Kaiser CENTREVILLE, VIRGINIA—Nothing unusual jumps out upon meeting Evelyn, a bubbly almost-3-year-old with red curls—except that she should not be here, chatting with a visitor in her family’s living room, twirling in her tights to the Pharrell Williams song “Happy.” Evelyn’s older sister Josephine had spinal muscular atrophy type 1 (SMA1), a genetic disease that gradually paralyzes babies. She died at 15 months. Evelyn was an unexpected pregnancy, but her parents decided to have the baby despite one-in-four odds of a second tragedy. Soon after Evelyn was born in December 2014, they were devastated to learn from genetic testing that she, too, had SMA1. “We knew what we were dealing with: We’ll love her for as long as we can,” says her father, Milan Villarreal. But that same night, frantically searching the internet, they learned about a clinical trial in Ohio and sent an email. At 8 weeks old, Evelyn received a gene therapy treatment that gave her body a crucial missing protein. And now here she is, not so different from any healthy toddler. Although she has weak thighs and can’t run normally or jump, she can walk quickly, dance, trace letters, toss foam blocks, carry a small chair, and climb onto her mother Elena’s lap. After the heartbreak of losing their first baby, the Villarreals have watched in amazement as Evelyn has crawled, walked, and talked. “It was just a miracle. Every milestone was like a celebration. We opened a bottle of wine for every little thing she did,” Milan says. © 2017 American Association for the Advancement of Science.

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

Alison Abbott The first controlled, but controversial and small, clinical trial of giving young blood to people with dementia has reported that the procedure appears safe. It has also hinted that it may even produce modest improvements in the daily lives of people who have Alzheimer's disease. Researchers who conducted the trial and others caution that the results are based on just 18 people and therefore are only a first step in exploring this type of treatment. “This is a really very small trial and the results should not be over-interpreted,” says Tony Wyss-Coray, a neurologist at Stanford University in California who led the study. The trial was conducted by his start-up company Alkahest, which is based in San Carlos, California. The results suggest the procedure is safe and hint that it could even boost the ability of people with dementia to undertake everyday skills, such as shopping or preparing a meal. The team plans to present the results on 4 November at the 10th Clinical Trials on Alzheimer’s Disease conference in Boston, Massachusetts. Wyss-Coray and his colleagues tested people aged between 54 and 86 with mild to moderate Alzheimer's disease. The team gave the 18 subjects weekly infusions for four weeks. They received either a saline placebo or plasma — blood from which the red cells have been removed — from blood donors aged 18–30. During the study, the team monitored the patients to assess their cognitive skills, mood and general abilities to manage their lives independently. The study detected no serious adverse reactions. It saw no significant effect on cognition, but two different batteries of tests assessing daily living skills both showed significant improvement. © 2017 Macmillan Publishers Limited,

Keyword: Alzheimers; Hormones & Behavior
Link ID: 24279 - Posted: 11.02.2017

By SHEILA KAPLAN WASHINGTON — Everyday Advanced Hemp Oil, Bosom Lotion and CBD Edibles Gummie Men may have their fans, but the Food and Drug Administration is not among them. Four companies selling those and dozens of other marijuana-derived dietary supplements have been warned by the F.D.A. to stop pitching their products as cures for cancer, a common but unproven claim in the industry. “Substances that contain components of marijuana will be treated like any other products that make unproven claims to shrink cancer tumors,” said Dr. Scott Gottlieb, the agency’s commissioner, in a news release on Wednesday. “We don’t let companies market products that deliberately prey on sick people with baseless claims that their substances can shrink or cure cancer.” The businesses — Stanley Brothers Social Enterprises, Green Roads of Florida, That’s Natural and Natural Alchemist — each sell products that falsely claim to cure cancer, Alzheimer’s disease or other illnesses, the agency said. The supplements allegedly contain cannabidiol (CBD), a component of the marijuana plant that is not approved by the F.D.A. for any use. Unlike medical marijuana, CBD contains only a fraction of the tetrahydrocannabinol, known as THC, needed to cause a high, according to the manufacturers. The companies sell CBD over the internet in a wide range of oil drops, capsules, syrups, teas and creams. The websites feature endorsements from people — generally identified only by first names and last initials — who claim that they or their loved ones have been miraculously cured of terminal diseases and other illnesses. “There are a growing number of effective therapies for many cancers,” said Dr. Gottlieb, a cancer survivor himself. “When people are allowed to illegally market agents that deliver no established benefit, they may steer patients away from products that have proven, anti-tumor effects that could save lives.” © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 24278 - Posted: 11.02.2017

By NICHOLAS BAKALAR Chronic inflammation in middle age may be associated with an increased risk for brain shrinkage and Alzheimer’s disease later in life. A new study, published in Neurology, looked at 1,633 people whose average age was 53 in 1987-89, measuring white blood cell count and various blood proteins that indicate inflammation. They followed the participants for 24 years. In 2011-13, when the subjects’ average age was 77, the scientists measured their brain volume using M.R.I. and tested their mental agility with a word-memorization task. They found that the greater the number of elevated inflammatory markers earlier in life, the smaller the volume of several parts of the brain, including those associated with Alzheimer’s disease. Higher levels of inflammation were also associated with poorer performance on the memory test. The authors acknowledge that they had blood tests for only one point in time, and that they are assuming that brain loss occurred in the years after the inflammatory markers were assessed. “It’s important early in life that we prevent diseases like diabetes, heart disease or hypertension that cause systemic inflammation,” said the lead author, Keenan A. Walker, a postdoctoral fellow at Johns Hopkins. “This study shows a temporal relationship between early inflammation and later brain volume loss.” © 2017 The New York Times Company

Keyword: Alzheimers; Neuroimmunology
Link ID: 24277 - Posted: 11.02.2017

By Emily Underwood In 2003, neurologist Helen Mayberg of Emory University in Atlanta began to test a bold, experimental treatment for people with severe depression, which involved implanting metal electrodes deep in the brain in a region called area 25. The initial data were promising; eventually, they convinced a device company, St. Jude Medical in Saint Paul, to sponsor a 200-person clinical trial dubbed BROADEN. This month, however, Lancet Psychiatry reported the first published data on the trial’s failure. The study stopped recruiting participants in 2012, after a 6-month study in 90 people failed to show statistically significant improvements between those receiving active stimulation and a control group, in which the device was implanted but switched off. Although that decision was “game over” for BROADEN, the story wasn’t finished for some 44 patients who asked to keep the implants in their brains, and the clinicians responsible for their long-term care, Mayberg explained last week to colleagues at a meeting on the ethical dilemmas of brain stimulation research at the National Institutes of Health (NIH) in Bethesda, Maryland. The episode highlights a tricky dilemma for companies and research teams involved in deep brain stimulation (DBS) research: If trial participants want to keep their implants, who will take responsibility—and pay—for their ongoing care? And participants in last week’s meeting said it underscores the need for the growing corps of DBS researchers to think long-term about their planned studies. © 2017 American Association for the Advancement of Science.

Keyword: Depression
Link ID: 24276 - Posted: 11.01.2017

Rachael Lallensack It takes a village to teach a bat how to communicate. Baby Egyptian fruit bats learn calls from their mothers, but research now shows that they can learn new dialects, or the pitch of their vocalizations, from the colony members around them. Learning to communicate by repeating the noises that others make is something only a few mammal groups — including humans, whales and dolphins — are known to do. Researchers call this vocal learning, and it's something that they're starting to study in bats. Findings published on 31 October in PLOS Biology1 show that bats can also pick things up from the group around them, a process that the authors dub crowd vocal learning. Bats are becoming the best organism to use in studies of how mammals learn to vocalize, because they’re more easily manipulated in the lab than whales or dolphins. The latest research underscores their importance, says neuroscientist Michael Yartsev of the University of California, Berkeley, who was not involved with the work. Egyptian fruit bats (Rousettus aegyptiacus) are highly social and live in colonies with dozens to thousands of other bats. To see how the pups learn dialects, researchers caught 15 pregnant Egyptian fruit bats and took them into the lab. To control for potential genetic effects, they ensured that the mothers weren't closely related. The team then split the mothers into three groups of five and put each group into one of three chambers, where the mothers gave birth to their young. The scientists used recordings of wild Egyptian fruit bat colonies that were low in frequency, high or a mix of both frequencies, and then piped one pitch into each chamber. © 2017 Macmillan Publishers Limited,

Keyword: Animal Communication; Language
Link ID: 24275 - Posted: 11.01.2017

Using an innovative “NeuroGrid” technology, scientists showed that sleep boosts communication between two brain regions whose connection is critical for the formation of memories. The work, published in Science, was partially funded by the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a project of the National Institutes of Health devoted to accelerating the development of new approaches to probing the workings of the brain. “Using new technologies advanced by the BRAIN Initiative, these researchers made a fundamental discovery about how the brain creates and stores new memories,” said Nick Langhals, Ph.D., program director at NIH’s National Institute of Neurological Disorders and Stroke. A brain structure called the hippocampus is widely thought to turn new information into permanent memories while we sleep. Previous work by the new study’s senior author, New York University School of Medicine professor György Buzsáki, M.D., Ph.D., revealed high-frequency bursts of neural firing called ripples in the hippocampus during sleep and suggested they play a role in memory storage. The current study confirmed the presence of ripples in the hippocampus during sleep and found them in certain parts of association neocortex, an area on the brain’s surface involved in processing complex sensory information. “When we first observed this, we thought it was incorrect because it had never been observed before,” said Dion Khodagholy, Ph.D., the study’s co-first author and assistant professor at Columbia University in New York.

Keyword: Learning & Memory
Link ID: 24274 - Posted: 11.01.2017

Teens are getting less sleep than they did before smartphones became commonplace, prompting concerns about potentially serious health consequences, researchers say. A study published in the current issue of the journal Sleep Medicine examined data from two surveys of U.S. adolescents conducted over many years and including questions about how many hours of sleep they got. Almost 370,000 adolescents participated. The researchers focused on how much sleep teens reported getting in the years from 2009 to 2015, "when the mobile technology really saturated the market among adolescents," said Zlatan Krizan, a psychologist specializing in sleep and social behaviour at Iowa State University and co-author of the study. Zlatan Krizan, a psychology researcher specializing in sleep, personality and social behaviour at Iowa State University, was one of the authors of a recent study that showed a trend of teens getting less sleep over the years they started using smartphones. (Iowa State University) Krizan and his colleagues found that teens were 16 to 17 per cent more likely to report getting less than seven hours of sleep a night in 2015 than they were in 2009. The recommended amount of sleep for 13 to 18-year-olds is eight to 10 hours per night, according to the U.S. Centers for Disease Control and Prevention. ©2017 CBC/Radio-Canada.

Keyword: Sleep; Development of the Brain
Link ID: 24273 - Posted: 11.01.2017

By Dr Michael Mosley BBC Thanks to the clocks going back, many of us managed to grab a little bit of extra shut-eye over the weekend. And that's no bad thing because, as a country, we seem to be chronically sleep-deprived. According to the Sleep Council, the average Briton gets six-and-a-half hours sleep a night, which for most people is not enough. Lots of studies have shown that cutting back on sleep, deliberately or otherwise, can have a serious impact on our bodies. A few nights of bad sleep can really mess with our blood sugar control and encourage us to overeat. It even messes with our DNA. A few years ago, Trust Me I'm a Doctor did an experiment with Surrey University, asking volunteers to cut down on their sleep by an hour a night for a week. Dr Simon Archer, who helped run the experiment, found that getting an hour's less sleep a night affected the activity of a wide range of our volunteers' genes (around 500 in all) including some which are associated with inflammation and diabetes. Disturbed nights So the negative effects on our bodies of sleep deprivation are clear. But what effect does lack of sleep have on our mental health? To find out Trust Me teamed up with sleep scientists at the University of Oxford to run a small experiment. This time, we recruited four volunteers who normally sleep soundly. We fitted them with devices to accurately monitor their sleep and then, for the first three nights of our study, let them get a full, undisturbed eight hours. For the next three nights, however, we restricted their sleep to just four hours.

Keyword: Sleep
Link ID: 24272 - Posted: 11.01.2017

Susan Milius Kleptopredation klep-toe-preh-day-shun n. A food-gathering strategy of eating an organism and the meal it just ate. A wily sea slug has a way to get two meals in one: It gobbles up smaller predators that have recently gulped in their own prey. “Kleptopredation” is the term Trevor Willis of the University of Portsmouth in England and his colleagues propose for this kind of food theft by well-timed predation. Researchers knew that the small Mediterranean nudibranch Cratena peregrina, with a colorful mane of streamers rippling off its body, climbs and preys on pipe cleaner‒skinny, branched colonies of Eudendrium racemosum hydroids, which are distant relatives of corals. The nudibranchs devour the individual hydroid polyps and, new tests show, prefer them well fed. In experimental buffets with fed or hungry polyps, the nudibranchs ate faster when polyps were fat with just-caught plankton. In this way, at least half of a nudibranch’s diet is plankton. This quirk explains why some biochemical signatures that distinguish predators from prey don’t work out clearly for nudibranchs and hydroids, the researchers report November 1 in Biology Letters. A weird echo of this meal-stealing strategy shows up in certain jumping spiders. The arachnids don’t have the biology to drink vertebrate blood themselves. Instead, they catch a lot of female mosquitoes that have just tanked up (SN: 10/15/05, p. 246). |© Society for Science & the Public 2000 - 2017. All rights reserved.

Keyword: Aggression
Link ID: 24271 - Posted: 11.01.2017

Sara Reardon Human genome databases are enabling researchers to take a deeper dive into the evolution of psychiatric disorders. Psychiatric disorders can be debilitating and often involve a genetic component, yet, evolution hasn’t weeded them out. Now, recent work is beginning to reveal the role of natural selection — offering a peek at how the genetic underpinnings of mental illness has changed over time. Many psychiatric disorders are polygenic: they can involve hundreds or thousands of genes and DNA mutations. It can be difficult to track how so many genetic regions evolved, and such studies require large genome data sets. But the advent of massive human genome databases is enabling researchers to look for possible connections between mental illnesses and the environmental and societal conditions that might have driven their emergence and development. Others are looking to Neanderthal genetic sequences to help inform the picture of these disorders, as well as cognitive abilities, in humans. Several of these teams presented their findings at the American Society of Human Genetics (ASHG) meeting in Orlando, Florida, in late October. One project found that evolution selected for DNA variants thought to protect against schizophrenia. The study, led by population geneticist Barbara Stranger of the University of Chicago in Illinois, looked at hundreds of thousands of human genomes using a statistical method that identified signals of selection over the past 2,000 years1. There were no signs of selection in genetic regions associated with any other mental illness. Many of schizophrenia's symptoms, such as auditory hallucinations and jumbling sentences, involve brain regions tied to speech, says Bernard Crespi, an evolutionary biologist at Simon Fraser University in Burnaby, Canada. Over the course of hominid evolution, he says, the ability to speak could have outweighed the small, but unavoidable risk that the genes involved in language could malfunction and result in schizophrenia in a small percentage of the population. © 2017 Macmillan Publishers Limited

Keyword: Schizophrenia; Depression
Link ID: 24270 - Posted: 10.31.2017

Jon Hamilton People who are thinking about killing themselves appear to have distinctive brain activity that can now be measured by a computer. In these people, words like "death" and "trouble" produce a distinctive "neural signature" not found in others, scientists report in the journal Nature Human Behavior. More than 44,000 people commit suicide in the U.S. each year. "There really is a difference in the way [suicidal] people think about certain concepts," says Marcel Just, an author of the paper and the D. O. Hebb professor of cognitive neuroscience at Carnegie Mellon University. That difference allowed a computer program to distinguish people who thought about suicide from people who did not more than 90 percent of the time. It also allowed the computer program to distinguish people who had attempted suicide from people who had only thought about it. The results come from a study of just 34 young adults and will need to be replicated, says Barry Horwitz, chief of brain imaging and modeling at the National Institute on Deafness and Other Communication Disorders. But he says they hint at a future in which brain scans and computers can help assess a person's mental health. Horwitz was not involved in the study. "Just looking at behavior is probably inadequate for a lot of purposes," he says. "It's much better to be able to see what the brain is doing." © 2017 npr

Keyword: Depression
Link ID: 24269 - Posted: 10.31.2017

Christopher French, Alice M Gregory and Dan Denis Of all the sleep disorders, “exploding head syndrome” (EHS) has arguably the most intriguing name. EHS has been described as “a sensory parasomnia characterised by the perception of loud noises and/or a sense of explosion in the head when transitioning to or from sleep. These noises are not associated with significant pain, but lead to abrupt arousal and feelings of fright”. Although this phenomenon was first described as long ago as 1876, it was not given its colourful title until 1988. Despite its long history, it has received very little systematic research attention, with most of our knowledge being based upon small samples of case histories as opposed to large-scale investigations. We, the authors of this piece, along with the world’s leading authority on EHS, Dr Brian Sharpless of Argosy University, Northern Virginia, are hoping to rectify that situation by carrying out a large-scale survey of EHS. We’re also interested in the equally intriguing phenomenon of sleep paralysis, which involves a temporary period of paralysis occurring between sleep and wakefulness, often accompanied by hallucinations. If you have ever experienced either EHS or sleep paralysis, or even if you haven’t, we would love to hear from you. In addition to explosions, other types of loud noise perceived during episodes of EHS include gunshots, fireworks, thunder, doors slamming, clapping, shouting, and the clash of cymbals. There can also be beeps, buzzing and video static. This may be accompanied by “electrical” sensations, palpitations, breathing difficulties, sweating, seeing a flash of light, and twitching. Perhaps unsurprisingly, intense fear caused by the belief that something is seriously wrong is often reported. © 2017 Guardian News and Media Limited

Keyword: Sleep
Link ID: 24268 - Posted: 10.31.2017

By GINA KOLATA It is a question that plagues all who struggle with weight: Why do some of us manage to keep off lost pounds, while others regain them? Now, a study of 14 participants from the “Biggest Loser” television show provides an answer: physical activity — and much more of it than public health guidelines suggest. On average, those who managed to maintain a significant weight loss had 80 minutes a day of moderate activity, like walking, or 35 minutes a day of vigorous exercise, like running. The researchers conducting the new study did not distinguish between purposeful exercise, like going to the gym and working out, and exercise done over the course of the day, like walking to work or taking the stairs. Guidelines from the Centers for Disease Control and Prevention, by comparison, call for at least 150 minutes a week of moderate exercise, or 75 minutes a week of vigorous exercise for healthy adults. The study was published on Tuesday in the journal Obesity. The lead author, Kevin Hall, chief of the Integrative Physiology Section at the National Institute of Diabetes and Digestive and Kidney Diseases, and his colleagues also presented their work at the Obesity Society’s annual meeting. Although the study is very small and must be replicated, Dr. Hall said, it is the first to assess obese people years after they lost weight with state-of-the-art methods to measure the calories they had consumed and the amount of exercise they had done. The researchers did their measurements when the contestants were chosen, and again at six weeks, thirty weeks and six years after the contest began. “The findings here are important,” said Rena Wing, a psychiatry professor at Brown University and a founder of the National Weight Control Registry, which includes more than 10,000 people. The food eaten “is the key determinant of initial weight loss. And physical activity is the key to maintenance,” she said. © 2017 The New York Times Company

Keyword: Obesity
Link ID: 24267 - Posted: 10.31.2017

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

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

There is no good evidence that a nutrient drink being sold online in the UK to "help" people with early Alzheimer's actually slows the disease, say experts. Latest trial results in patients who took Souvenaid did not find it preserves memory and thinking. The authors say in Lancet Neurology that bigger studies are needed to show if the product can work as hoped. And consumers should be aware that the £3.49 per bottle drink "is not a cure". Manufacturer Nutricia says its drink should only be taken under the direction of a doctor, specialist nurse or pharmacist. Souvenaid comes in strawberry or vanilla flavour and contains a combination of fatty acids, vitamins and other nutrients. Taken once daily, the idea is that the boost of nutrients it provides will help keep Alzheimer's at bay in people with the earliest signs of this type of dementia. But the latest phase two clinical trial results do not prove this. What the trial found The study involved 311 patients with very early Alzheimer's or mild cognitive impairment. All of them were asked to take a daily drink, but only half were given Souvenaid - the other half received one with no added nutrients. After two years of participating, the patients were reassessed to see if there was any difference between the two groups in terms of dementia progression, measured by various memory and cognitive tests. The treatment did not appear to offer an advantage, although patients in the Souvenaid group did have slightly less brain shrinkage on scans, which the researchers say is promising because shrinkage in brain regions controlling memory is seen with worsening dementia. But experts remain cautious. Prof Tara Spires-Jones, a dementia expert at the University of Edinburgh, said: "Some of the other tests of brain structure and function were promising, but overall this study indicates that a specific change in nutrition is unlikely to make a large difference to people with Alzheimer's, even in the early stages. © 2017 BBC.

Keyword: Alzheimers
Link ID: 24265 - Posted: 10.31.2017

By Nicholas Kristof The colored parts of the image above, prepared by Columbia University scientists, indicate where a child’s brain is physically altered after exposure to this pesticide. This chemical, chlorpyrifos, is hard to pronounce, so let’s just call it Dow Chemical Company’s Nerve Gas Pesticide. Even if you haven’t heard of it, it may be inside you: One 2012 study found that it was in the umbilical cord blood of 87 percent of newborn babies tested. And now the Trump administration is embracing it, overturning a planned ban that had been in the works for many years. The Environmental Protection Agency actually banned Dow’s Nerve Gas Pesticide for most indoor residential use 17 years ago — so it’s no longer found in the Raid you spray at cockroaches (it’s very effective, which is why it’s so widely used; then again, don’t suggest this to Dow, but sarin nerve gas might be even more effective!). The E.P.A. was preparing to ban it for agricultural and outdoor use this spring, but then the Trump administration rejected the ban. That was a triumph for Dow, but the decision stirred outrage among public health experts. They noted that Dow had donated $1 million for President Trump’s inauguration. So Dow’s Nerve Gas Pesticide will still be used on golf courses, road medians and crops that end up on our plate. Kids are told to eat fruits and vegetables, but E.P.A. scientists found levels of this pesticide on such foods at up to 140 times the limits deemed safe. © 2017 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 24264 - Posted: 10.30.2017

Nick Fraser I was just finishing a talk about documentaries I was giving in Soho. I’d been asked a question about why so many films are seriously depressing. I remember that I talked about the great neurosurgeon Henry Marsh and the documentary about him, The English Surgeon. The film followed him to Ukraine as he helped and taught the local surgeons, who often resorted to using rusty domestic power tools to work on their patients’ skulls. I’d talked about him for some time, enthusiastically explaining how awed Henry said he felt every time he opened a patient’s head, and about how beautiful the brain is. I wanted to say more – but suddenly I sat down, and couldn’t say or think anything. Something had happened to me. I had gone into a different world of not making sense. I was taken by ambulance to University College hospital and given a head CT scan. There was a blood clot on my brain. I’d had a stroke, a brain attack. Time is all-important to stroke patients, and fortunately I was within the time frame to be given serious clot-busting drugs. There was something else they could do, the doctor said, a procedure called a thrombectomy. UCH offered the procedure up until 6pm. The time was then around 8pm, but the doctor heroically fought through NHS protocols and secured me a trip to St George’s hospital in south-west London, the only UK location open 24/7 for thrombectomies. I was lucky. I remember meeting the neuro-radiologist who, after putting me under mild sedation, performed the extraordinary procedure that involved sending a very thin wire from my groin to my brain, and removing one small clot and one larger one from the left side of my brain. I could understand the details of the operation, but I couldn’t say anything. I wondered if I would be all right. © 2017 Guardian News and Media Limited o

Keyword: Stroke; Language
Link ID: 24263 - Posted: 10.30.2017

By KYLE SPENCER As other college students head out to party on a Saturday night, Julie Linneman, a sophomore at Villanova University, rides the subway to a small rowhouse in West Philadelphia to meet with “her people,” a posse of students who understand what it’s like to be taken down by opioids. Ms. Linneman is a bespectacled 22-year-old who favors shredded jeans. She is a fan of cooking shows, fantasy fiction and Paul McCartney. She spent her first attempt at sophomore year — the one at Northern Kentucky University — in her dorm room, high on heroin. Coming to terms with a habit that nearly killed her, she has found support at the Haven at Drexel, Drexel University’s housing for students in recovery. Seven students from colleges in the Philadelphia area — including the University of Pennsylvania, Temple and Villanova — live, eat and socialize here, where they can abstain without temptation. More converge during these Saturday night meetings. “Sometimes you just need to be around other students who know what you have gone through,” Ms. Linneman said. They share snacks, drink water instead of beer, and talk about their life-threatening addictions. Ms. Linneman, who agreed to be named because she hopes to pursue a career in recovery advocacy, got her first pills — Vyvanse and Adderall, stimulants for attention deficit hyperactivity disorder — in high school from the boy with the locker next to hers. She soon moved on to prescription painkillers like Percocet. The “warm blanket” effect alleviated debilitating anxiety and loneliness. Once at college, she replaced pills with bags of cheap heroin. Her roommate moved out. The drug rendered her friendless. “It was one of the most lonely times of my life,” she recalled. She grew thin and pale. She would sit in the cafeteria alone, barely eating, occasionally nodding off. The workers would ask, “Are you O.K.?” © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 24262 - Posted: 10.30.2017