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By NICHOLAS ST. FLEUR Neuroscientists have developed a way to turn an entire mouse, including its muscles and internal organs, transparent while illuminating the nerve paths that run throughout its body. The process, called uDisco, provides an alternate way for researchers to study an organism’s nervous system without having to slice into sections of its organs or tissues. It allows researchers to use a microscope to trace neurons from the rodent’s brain and spinal cord all the way to its fingers and toes. “When I saw images on the microscope that my students were obtaining, I was like ‘Wow, this is mind blowing,’” said Ali Ertürk, a neuroscientist from the Ludwig Maximilians University of Munich in Germany and an author of the paper. “We can map the neural connectivity in the whole mouse in 3D.” They published their technique Monday in the journal Nature Methods. So far, the technique has been conducted only in mice and rats, but the scientists think it could one day be used to map the human brain. They also said it could be particularly useful for studying the effects of mental disorders like Alzheimer’s disease or schizophrenia. Dr. Ertürk and his colleagues study neurodegenerative disorders, and are particularly interested in diseases that occur from traumatic brain injuries. Researchers often study these diseases by examining thin slices of brain tissue under a microscope. “That is not a good way to study neurons because if you slice the brain, you slice the network,” Dr. Ertürk said. “The best way to look at it is to look at the entire organism, not only the brain lesion but beyond that. We need to see the whole picture.” To do this, Dr. Ertürk and his team developed a two-step process that renders a rodent transparent while keeping its internal organs structurally sound. The mice they used were dead and had been tagged with a special fluorescent protein to make specific parts of their anatomy glow. © 2016 The New York Times Company
Keyword: Brain imaging
Link ID: 22590 - Posted: 08.23.2016
Scientists and clinicians have long dreamed of helping the injured brain repair itself by creating new neurons, and an innovative NIH-funded study published today in Nature Medicine may bring this goal much closer to reality. A team of researchers has developed a therapeutic technique that dramatically increases the production of nerve cells in mice with stroke-induced brain damage. The therapy relies on the combination of two methods that show promise as treatments for stroke-induced neurological injury. The first consists of surgically grafting human neural stem cells into the damaged area, where they mature into neurons and other brain cells. The second involves administering a compound called 3K3A-APC, which the scientists have shown helps neural stem cells grown in a petri dish develop into neurons. However, it was unclear what effect the molecule, derived from a human protein called activated protein-C (APC), would have in live animals. A month after their strokes, mice that had received both the stem cells and 3K3A-APC performed significantly better on tests of motor and sensory functions compared to mice that received neither or only one of the treatments. In addition, many more of the stem cells survived and matured into neurons in the mice given 3K3A-APC. “This USC-led animal study could pave the way for a potential breakthrough in how we treat people who have experienced a stroke,” added Jim Koenig, Ph.D., a program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which funded the research. “If the therapy works in humans, it could markedly accelerate the recovery of these patients.”
By Clare Wilson Taking a daily vitamin or mineral supplement is widely seen as a common-sense way of looking after yourself – a kind of insurance, like wearing a seat belt. But evidence is growing that it might not be such a healthy habit after all. The latest finding is that calcium supplements, taken by many women after the menopause to strengthen their bones, are linked to dementia. Among women who have had a stroke, taking calcium was associated with a seven-fold rise in the number who went on to have dementia. Calcium was also linked with a smaller, non-statistically significant, rise in dementia in women who had not had a stroke. The finding emerged from a study that was not a randomised trial, so it is not the most robust type of medical evidence. The researchers merely counted dementia cases in people who had chosen whether to take calcium, and so the data could be biased. But the results are striking and come on the heels of a previous study that was a randomised trial, which found a link between calcium supplements and a modestly higher risk of heart attacks – suggesting that caution over calcium is indeed warranted. If future research confirms the association with dementia, women would face a horrible dilemma: should they continue to take calcium, staving off bone weakness that can lead to fatal hip fractures, while running an increased risk of one of the most dreaded illness of ageing? So what’s going on? Team member Silke Kern at the Sahlgrenska Academy Institute of Neuroscience and Physiology in Gothenburg, Sweden, says that taking a calcium pill triggers a rapid surge in the mineral’s levels in the blood, one that you wouldn’t get from calcium in food. © Copyright Reed Business Information Ltd.
Link ID: 22588 - Posted: 08.23.2016
By GINA KOLATA Shena Pearson nearly froze in her seat, terrified, as she stared at a power-point slide. She was at her first meeting of an epilepsy foundation, seeking help for her 12-year-old son Trysten, when a neurologist flashed the slide about something called Sudep. It stands for sudden unexpected death in epilepsy. Her son’s neurologist had never mentioned it. “Oh dear God, my child is at risk, seriously at risk,” Ms. Pearson thought to herself. Sudden death in epilepsy is a little-known and seldom-mentioned phenomenon, but now, after a push by advocates, the federal government has begun a concerted program to understand it. Yet a question remains: When, if ever, should patients be warned? In a way, the extreme reticence of many neurologists to mention sudden unexpected death to epilepsy patients harks back to the days when doctors and families often did not tell people they had cancer — too terrifying. But today, patients learn not just about cancer but about many other potentially fatal conditions, like an inoperable brain aneurysm that could burst at any time and kill a person. So the quiet about the epilepsy death risk appears to be an anomaly. Sudep’s name pretty much explains what it is: Someone with epilepsy — unprovoked seizures, which are electrical surges in the brain — dies, and there is no apparent cause. Often a person with epilepsy goes to bed and is found in the morning, unresponsive. In some cases, there is indirect evidence of a seizure, like urine on the sheets, bloodshot eyes or a severely bitten tongue, leading to the suggestion that preventing seizures as much as possible with medications could lower patients’ risks. But so much about the syndrome remains unknown. © 2016 The New York Times Company
Link ID: 22587 - Posted: 08.23.2016
By Daniel Barron After prepping for the day’s cases, “Mike Brennan,” a 63-year-old cardiology technician, sat down for his morning coffee and paper. On the front page, he discovered something troubling: he could no longer read. No matter how long he stared at a word, its meaning was lost on him. With a history of smoking and hypertension, he worried that he might have had a stroke. So, leaving his coffee, he walked himself down the hall to the emergency department, where neurologists performed a battery of tests to tease out what had happened. Mike still recognized individual letters and, with great difficulty, could sound out small words. But even some simple vocabulary presented problems, for example, he read “desk” as “dish” or “flame” as “thame.” Function words such as prepositions and pronouns gave him particular trouble. Mike couldn’t read, but there was nothing wrong with his eyes. Words heard were no problem. He could recognize colors, faces, and objects. He could speak, move, think and even write normally. Mike had “pure alexia,” meaning he could not read but showed no other impairments. An M.R.I. scan of Mike’s brain revealed a pea-sized stroke in his left inferior occipitotemporal cortex, a region on the brain’s surface just behind the left ear. © 2016 Scientific American
Link ID: 22586 - Posted: 08.23.2016
By Lydia Pyne | On August 3, 1908, the first near-complete Neanderthal skeleton was discovered in a cave near the village of La Chapelle-aux-Saints in south central France, during a survey of the region’s Paleolithic archaeological sites. For decades prior, prehistorians had collected bits and pieces of curious but not-quite-human fossils from museums and excavations alike—the odd skull here, a scrap of tooth there. In 1863, the mélange of bones was finally given its own species designation, Homo neanderthalensis. Forty-five years later, the La Chapelle discovery was the first Neanderthal specimen found in an original archaeological context and the first to be expertly excavated and carefully studied. Because the body was arranged in a flexed, fetal position and carefully placed in the floor of the cave, excavators argued that fossil—nicknamed the Old Man—had been purposefully buried by his Neanderthal contemporaries. More than any other single individual, the Old Man of La Chapelle has shaped the way that science and popular culture have thought about Neanderthals. But why? What is it about this Neanderthal’s story that is so special? In short, the Old Man was the right fossil found at the right time. He was—and still is—offered as a key bit of evidence in debates about evolution and human origins. He quickly became a scientific touchstone, an archetype for how science and popular culture create celebrity fossils. I explore the stories of similarly spectacular paleoanthropological finds in my new book Seven Skeletons: The Evolution of the World’s Most Famous Human Fossils. © 1986-2016 The Scientist
Link ID: 22585 - Posted: 08.23.2016
Sara Reardon Neuroscientists have invented a way to watch the ebb and flow of the brain's chemical messengers in real time. They were able to see the surge of neurotransmitters as mice were conditioned — similarly to Pavlov's famous dogs — to salivate in response to a sound. The study, presented at the American Chemical Society’s meeting in Philadelphia, Pennyslvania, on 22 August, uses a technique that could help to disentangle the complex language of neurotransmitters. Ultimately, it could lead to a better understanding of brain circuitry. The brain’s electrical surges are easy to track. But detecting the chemicals that drive this activity — the neurotransmitters that travel between brain cells and lead them to fire — is much harder. “There’s a hidden signalling network in the brain, and we need tools to uncover it,” says Michael Strano, a chemical engineer at the Massachusetts Institute of Technology in Cambridge. In many parts of the brain, neurotransmitters can exist at undetectably low levels. Typically, researchers monitor them by sucking fluid out from between neurons and analysing the contents in the lab. But that technique cannot measure activity in real time. Another option is to insert a metal probe into the space between neurons to measure how neurotransmitters react chemically when they touch metal. But the probe is unable to distinguish between structurally similar molecules, such as dopamine, which is involved in pleasure and reward, and noradrenaline which is involved in alertness. © 2016 Macmillan Publishers Limited
Laura Sanders Fractions of a second after food hits the mouth, a specialized group of energizing nerve cells in mice shuts down. After the eating stops, the nerve cells spring back into action, scientists report August 18 in Current Biology. This quick response to eating offers researchers new clues about how the brain drives appetite and may also provide insight into narcolepsy. These nerve cells have intrigued scientists for years. They produce a molecule called orexin (also known as hypocretin), thought to have a role in appetite. But their bigger claim to fame came when scientists found that these cells were largely missing from the brains of people with narcolepsy. People with narcolepsy are more likely to be overweight than other people, and this new study may help explain why, says neuroscientist Jerome Siegel of UCLA. These cells may have more subtle roles in regulating food intake in people without narcolepsy, he adds. Results from earlier studies hinted that orexin-producing nerve cells are appetite stimulators. But the new results suggest the opposite. These cells actually work to keep extra weight off. “Orexin cells are a natural obesity defense mechanism,” says study coauthor Denis Burdakov of the Francis Crick Institute in London. “If they are lost, animals and humans gain weight.” Mice were allowed to eat normally while researchers eavesdropped on the behavior of their orexin nerve cells. Within milliseconds of eating, orexin nerve cells shut down and stopped sending signals. |© Society for Science & the Public 2000 - 2016
Link ID: 22583 - Posted: 08.22.2016
By KATHERINE KINZLER You may not be surprised to learn that food preference is a social matter. What we choose to eat depends on more than just what tastes good or is healthful. People in different cultures eat different things, and within a culture, what you eat can signal something about who you are. More surprising is that the sociality of food selection, it turns out, runs deep in human nature. In research published this month in the Proceedings of the National Academy of Sciences, my colleagues and I showed that even 1-year-old babies understand that people’s food preferences depend on their social or cultural group. Interestingly, we found that babies’ thinking about food preferences isn’t really about food per se. It’s more about the people eating foods, and the relationship between food choice and social groups. While it’s hard to know what babies think before they can talk, developmental psychologists have long capitalized on the fact that babies’ visual gaze is guided by their interest. Babies tend to look longer at something that is novel or surprising. Do something bizarre the next time you meet a baby, and you’ll notice her looking intently. Using this method, the psychologists Zoe Liberman, Amanda Woodward, Kathleen Sullivan and I conducted a series of studies. Led by Professor Liberman, we brought more than 200 1-year-olds (and their parents) into a developmental psychology lab, and showed them videos of people visibly expressing like or dislike of foods. For instance, one group of babies saw a video of a person who ate a food and expressed that she loved it. Next they saw a video of a second person who tried the same food and also loved it. This second event was not terribly surprising to the babies: The two people agreed, after all. Accordingly, the babies did not look for very long at this second video; it was what they expected. © 2016 The New York Times Company
Laura Sanders For some people, fentanyl can be a life-saver, easing profound pain. But outside of a doctor’s office, the powerful opioid drug is also a covert killer. In the last several years, clandestine drugmakers have begun experimenting with this ingredient, baking it into drugs sold on the streets, most notably heroin. Fentanyl and closely related compounds have “literally invaded the entire heroin supply,” says medical toxicologist Lewis Nelson of New York University Langone Medical Center. Fentanyl is showing up in other drugs, too. In San Francisco’s Bay Area in March, high doses of fentanyl were laced into counterfeit versions of the pain pill Norco. In January, fentanyl was found in illegal pills sold as oxycodone in New Jersey. And in late 2015, fentanyl turned up in fake Xanax pills in California. This ubiquitous recipe-tinkering makes it impossible for users to know whether they’re about to take drugs mixed with fentanyl. And that uncertainty has proved deadly. Fentanyl-related deaths are rising sharply in multiple areas. National numbers are hard to come by, but in many regions around the United States, fentanyl-related fatalities have soared in recent years. Maryland is one of the hardest-hit states. From 2007 to 2012, the number of fentanyl-related deaths hovered around 30 per year. By 2015, that number had grown to 340. A similar rise is obvious in Connecticut, where in 2012, there were 14 fentanyl-related deaths. In 2015, that number was 188. |© Society for Science & the Public 2000 - 2016.
By Andrea Anderson When we bed down in a new locale, our sleep often suffers. A recent study finds that this so-called first-night effect may be the result of partial wakefulness in one side of the brain—as if the brain is keeping watch. Researchers at Brown University and the Georgia Institute of Technology used neuroimaging and a brain wave–tracking approach called polysomnography to record activity in four brain networks in 11 individuals as they slept on two nights about a week apart. The subjects nodded off at their normal bedtimes, and their brain was scanned for about two hours—the length of a sleep cycle. As participants slept, right hemisphere regions showed consistent slow-wave activity regardless of the night. Yet average slow-wave activity was shallower in their left hemisphere during the first night—an asymmetry that was enhanced in those who took longer to fall asleep. The results, published in May in Current Biology, suggest systems in one side of the brain remain active as people venture into unfamiliar sleep situations—an apparent survival strategy reminiscent of the unihemispheric sleep reported in certain animals. Because the results represent just one sleep cycle, however, it is unclear whether the left side of the brain is always tasked with maintaining attentiveness, explains the study's senior author Yuka Sasaki, a cognitive, linguistic and psychological sciences researcher at Brown. It is possible the right hemisphere takes over guard dog duties at some point in the night. © 2016 Scientific American
Link ID: 22580 - Posted: 08.22.2016
By Virginia Morell Scientists have long worried whether animals can respond to the planet’s changing climate. Now, a new study reports that at least one species of songbird—and likely many more—already knows how to prep its chicks for a warming world. They do so by emitting special calls to the embryos inside their eggs, which can hear and learn external sounds. This is the first time scientists have found animals using sound to affect the growth, development, behavior, and reproductive success of their offspring, and adds to a growing body of research revealing that birds can “doctor” their eggs. “The study is novel, surprising, and fascinating, and is sure to lead to much more work on parent-embryo communication,” says Robert Magrath, a behavioral ecologist at the Australian National University in Canberra who was not involved in the study. The idea that the zebra finch (Taeniopygia guttata) parents were “talking to their eggs” occurred to Mylene Mariette, a behavioral ecologist at Deakin University in Waurn Ponds, Australia, while recording the birds’ sounds at an outdoor aviary. She noticed that sometimes when a parent was alone, it would make a rapid, high-pitched series of calls while sitting on the eggs. Mariette and her co-author, Katherine Buchanan, recorded the incubation calls of 61 female and 61 male finches inside the aviary. They found that parents of both sexes uttered these calls only during the end of the incubation period and when the maximum daily temperature rose above 26°C (78.8°F). © 2016 American Association for the Advancement of Scienc
By Diana Kwon When glial cells were discovered in the 1800s, they were thought to be passive, supporting structures—the “glue”—as their Greek name implies—that holds neurons together in the brain and throughout the nervous system. In recent years, however, neuroscientists have discovered that far from being passive, these small cells play an astonishing variety of roles in both the development and functioning of the brain. Some of the latest discoveries suggest that glia play complex roles in regulating appetite and metabolism, making them a possible target for treating obesity. Signs that glia might play such roles were first identified in the 1980s. Neuroscientist Pierre Magistretti and his colleagues found evidence that neurotransmitters could promote the release of glucose reserves stored in astrocytes, a star-shaped type of glial cell. Other studies revealed that obesity leads to increased activation of glial cells in the hypothalamus—the key area of the brain for controlling metabolic processes. This was despite the fact that, for a long time, “neurons were considered the only players in the control of energy metabolism,” says Cristina García-Cáceres, a neurobiologist at the Helmholtz Diabetes Center in Germany. Two recent studies add new evidence that glia play a key role in metabolism. In one study, published last week in Cell, García-Cáceres, together with Matthias Tschöp, the director of the Helmholtz Diabetes Center and colleagues, reported that insulin acts on astrocytes to regulate sugar intake in the brain. © 2016 Scientific American,
Researchers may have discovered a method of detecting changes in the eye which could identify Parkinson's disease before its symptoms develop. Scientists at University College London (UCL) say their early animal tests could lead to a cheap and non-invasive way to spot the disease. Parkinson's affects 1 in 500 people and is the second most common neurodegenerative disease worldwide. The charity Parkinson's UK welcomed the research as a "significant step". The researchers examined rats and found that changes could be seen at the back of their eyes before visible symptoms occurred. Professor Francesca Cordeiro who led the research said it was a "potentially revolutionary breakthrough in the early diagnosis and treatment of one of the world's most debilitating diseases". "These tests mean we might be able to intervene much earlier and more effectively treat people with this devastating condition." Symptoms of Parkinson's include tremors and muscle stiffness, slowness of movement and a reduced quality of life. These symptoms usually only emerge after brain cells have been damaged. But there is currently no brain scan, or blood test, that can definitively diagnose Parkinson's disease. Parkinson's does not directly cause people to die, but symptoms do get worse over time. © 2016 BBC
Link ID: 22577 - Posted: 08.20.2016
By Emily Underwood In 2010, neurobiologist Beth Stevens had completed a remarkable rise from laboratory technician to star researcher. Then 40, she was in her second year as a principal investigator at Boston Children’s Hospital with a joint faculty position at Harvard Medical School. She had a sleek, newly built lab and a team of eager postdoctoral investigators. Her credentials were impeccable, with high-profile collaborators and her name on an impressive number of papers in well-respected journals. But like many young researchers, Stevens feared she was on the brink of scientific failure. Rather than choosing a small, manageable project, she had set her sights on tackling an ambitious, unifying hypothesis linking the brain and the immune system to explain both normal brain development and disease. Although the preliminary data she’d gathered as a postdoc at Stanford University in Palo Alto, California, were promising, their implications were still murky. “I thought, ‘What if my model is just a model, and I let all these people down?’” she says. Stevens, along with her mentor at Stanford, Ben Barres, had proposed that brain cells called microglia prune neuronal connections during embryonic and later development in response to a signal from a branch of the immune system known as the classical complement pathway. If a glitch in the complement system causes microglia to prune too many or too few connections, called synapses, they’d hypothesized, it could lead to both developmental and degenerative disorders. © 2016 American Association for the Advancement of Science.
Meghan Rosen Zika may harm grown-up brains. The virus, which can cause brain damage in infants infected in the womb, kills stem cells and stunts their numbers in the brains of adult mice, researchers report August 18 in Cell Stem Cell. Though scientists have considered Zika primarily a threat to unborn babies, the new findings suggest that the virus may cause unknown — and potentially long-term — damage to adults as well. In adults, Zika has been linked to Guillain-Barré syndrome, a rare neurological disorder (SN: 4/2/16, p. 29). But for most people, infection is typically mild: a headache, fever and rash lasting up to a week, or no symptoms at all. In pregnant women, though, the virus can lodge in the brain of a fetus and kill off newly developing cells (SN: 4/13/16). If Zika targets newborn brain cells, adults may be at risk, too, reasoned neuroscientist Joseph Gleeson of Rockefeller University in New York City and colleagues. Parts of the forebrain and the hippocampus, which plays a crucial role in learning and memory, continue to generate nerve cells in adult brains. In mice infected with Zika, the virus hit these brain regions hard. Nerve cells died and the regions generated one-fifth to one-half as many new cells compared with those of uninfected mice. The results might not translate to humans; the mice were genetically engineered to have weak immune systems, making them susceptible to Zika. But Zika could potentially harm immunocompromised people and perhaps even healthy people in a similar way, the authors write. © Society for Science & the Public 2000 - 2016.
Keyword: Development of the Brain
Link ID: 22575 - Posted: 08.20.2016
By Nicholas Bakalar Taking antipsychotic medicines during pregnancy does not increase the risk for birth defects, a large new study has found. Antipsychotics are used to treat schizophrenia, bipolar disorder, depression and other psychiatric disorders. Previous studies of their use during pregnancy have been small and have had mixed results. This study, in JAMA Psychiatry, reviewed records of 1,341,715 pregnant women, of whom 9,258 filled prescriptions for the newer atypical antipsychotics like quetiapine (Seroquel) or aripiprazole (Abilify), and 733 for older typical antipsychotics such as haloperidol (Haldol). All prescriptions were filled in the first trimester of pregnancy. After controlling for race, number of pregnancies, smoking, alcohol use, psychiatric conditions, additional medications and other variables, there was no difference in the risk for birth defects between those who took the drugs and those who did not. One possible exception was a marginal increase in risk with one drug, risperidone (Risperdal), which the authors said will require further study. “These findings suggest that the use of antipsychotics during the first trimester does not seem to increase congenital malformation,” or birth defects, said the lead author, Krista F. Huybrechts, an assistant professor of medicine at Harvard. But, she added, “we only looked at congenital malformation, not other possible negative outcomes for women and their children.” © 2016 The New York Times Company
SINCE nobody really knows how brains work, those researching them must often resort to analogies. A common one is that a brain is a sort of squishy, imprecise, biological version of a digital computer. But analogies work both ways, and computer scientists have a long history of trying to improve their creations by taking ideas from biology. The trendy and rapidly developing branch of artificial intelligence known as “deep learning”, for instance, takes much of its inspiration from the way biological brains are put together. The general idea of building computers to resemble brains is called neuromorphic computing, a term coined by Carver Mead, a pioneering computer scientist, in the late 1980s. There are many attractions. Brains may be slow and error-prone, but they are also robust, adaptable and frugal. They excel at processing the sort of noisy, uncertain data that are common in the real world but which tend to give conventional electronic computers, with their prescriptive arithmetical approach, indigestion. The latest development in this area came on August 3rd, when a group of researchers led by Evangelos Eleftheriou at IBM’s research laboratory in Zurich announced, in a paper published in Nature Nanotechnology, that they had built a working, artificial version of a neuron. Neurons are the spindly, highly interconnected cells that do most of the heavy lifting in real brains. The idea of making artificial versions of them is not new. Dr Mead himself has experimented with using specially tuned transistors, the tiny electronic switches that form the basis of computers, to mimic some of their behaviour. © The Economist Newspaper Limited 2016.
By Jef Akst ANDRZEJ KRAUZEAs a psychiatrist at Western University in London, Ontario, Lena Palaniyappan regularly sees patients with schizophrenia, the chronic mental disorder that drastically affects how a person thinks, feels, and behaves. The disorder can be devastating, often involving hallucinations and delusions. But one thing Palaniyappan and other mental health professionals have noticed is that, unlike those with degenerative neurological disorders such as Alzheimer’s disease, Huntington’s, or Parkinson’s, sometimes schizophrenia patients eventually start to improve. “In the clinic we do actually see patients with schizophrenia having a very relentless progress in early years,” Palaniyappan says. “But a lot of them do get better over the years, or they don’t progress as [quickly].” So far, most research has focused on the neurological decline associated with schizophrenia—typically involving a loss of brain tissue. Palaniyappan and his colleagues wondered whether there might be “something happening in the brain [that] helps them come to a state of stability.” To get at this question, he and his colleagues performed MRI scans to assess the cortical thickness of 98 schizophrenia patients at various stages of illness. Sure enough, the researchers noted that, while patients who were less than two years removed from their diagnosis had significantly thinner tissue than healthy controls, those patients who’d had the disease for longer tended to show less deviation in some brain regions, suggesting some sort of cortical amelioration (Psychol Med, doi:10.1017/S0033291716000994, 2016). “Some brain regions are regaining or normalizing while other brain regions continue to show deficits,” Palaniyappan says. © 1986-2016 The Scientist
By Jessica Hamzelou JACK NICHOLSON has a lot to answer for. One of the knock-on effects of hit 1975 movie One Flew Over the Cuckoo’s Nest was a public backlash against electroconvulsive therapy (ECT). The treatment, used since the 1930s for a wide range of mental health conditions, delivers a jolt of electricity to the brain big enough to trigger a seizure. The film’s brutal depiction of ECT and lobbying helped it fall out of favour in the 1980s and 1990s. But ECT may now be undergoing a revival, led by psychiatrists who champion it because of its success rate. “It’s the most effective treatment we have in psychiatry,” says George Kirov at Cardiff University, UK, who oversees ECT treatments in the area. A report from the UK Royal College of Psychiatrists last September showed that three-quarters of people with mental health problems felt improvement after having ECT. And psychiatrists say that a similar percentage of people who have schizophrenia that doesn’t respond to drug treatment find ECT effective. “I’ve never seen an ECT treatment that doesn’t work,” says Helen Farrell, a psychiatrist at the Beth Israel Deaconess Medical Center in Boston. “People have such a skewed view of electroconvulsive therapy. It is seen as primitive and horrific“ Mounting evidence has convinced the US Food and Drug Administration (FDA) to consider reclassifying ECT devices to make the technology more accessible for people with depression or bipolar disorder. The public will still take some convincing, however. In a 2005 survey in Switzerland, for example, 56 per cent were against ECT, while just 1 per cent said they were in favour. © Copyright Reed Business Information Ltd.
Link ID: 22571 - Posted: 08.18.2016