Most Recent Links
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By JAMES GORMAN SAN DIEGO — Dr. Karl Deisseroth is having a very early breakfast before the day gets going at the annual meeting of the Society for Neuroscience. Thirty thousand people who study the brain are here at the Convention Center, a small city’s worth of badge-wearing, networking, lecture-attending scientists. For Dr. Deisseroth, though, this crowd is a bit like the gang at Cheers — everybody knows his name. He is a Stanford psychiatrist and a neuroscientist, and one of the people most responsible for the development of optogenetics, a technique that allows researchers to turn brain cells on and off with a combination of genetic manipulation and pulses of light. He is also one of the developers of a new way to turn brains transparent, though he was away when some new twists on the technique were presented by his lab a day or two earlier. “I had to fly home to take care of the kids,” he explained. He went home to Palo Alto to be with his four children, while his wife, Michelle Monje, a neurologist at Stanford, flew to the conference for a presentation from her lab. Now she was home and, here he was, back at the conference, looking a bit weary, eating eggs, sunny side up, and talking about the development of new technologies in science. A year ago, President Obama announced an initiative to invest in new research to map brain activity, allocating $100 million for the first year. The money is a drop in the bucket compared with the $4.5 billion the National Institutes of Health spends annually on neuroscience, but it is intended to push the development of new techniques to investigate the brain and map its pathways, starting with the brains of small creatures like flies. Cori Bargmann of Rockefeller University, who is a leader of a committee at the National Institutes of Health setting priorities for its piece of the brain initiative, said optogenetics was a great example of how technology could foster scientific progress. © 2014 The New York Times Company
Keyword: Brain imaging
Link ID: 19520 - Posted: 04.22.2014
by Bethany Brookshire Many of us have experienced that depressing sight: The bottom of the ice cream pint. You get to the end of your favorite movie and suddenly realize the ice cream is gone — and you’re far too full for comfort. We’re left wondering why we did it. But when it comes to forgetting ourselves and bingeing on the pint, the power of habit can be strong. It could be that our previous eating experiences make us helpless to our habits. A new study in rats, published April 2 in the Journal of Neuroscience, shows that long-term exposure to bursts of sweet, fatty foods produces animals that appear to seek food not out of hunger, but out of habit. And neural changes associated with habit formation accompany the behavioral changes. The results suggest that repeated binges on sugar and fat could tilt the neural balance from taking a few scoops of Cherry Garcia toward mindlessly reaching the bottom of the bowl. But while the results show us the power of habit, bad habits don’t necessarily make us food addicts. Teri Furlong and her colleagues at the University of Sydney in Australia were interested in how animals control behaviors. Some behaviors are goal-directed, while others are more efficiently taken care of with habits. Furlong describes habits as “behaviors where we are not thinking about the consequences as we do them.” Many habits can be useful things to develop — eating breakfast daily or brushing your teeth, for example. But other habits can become maladaptive, such as drug abuse — or binge eating. © Society for Science & the Public 2000 - 2013.
It looks like a standardized test question: Is the sum of two numbers on the left or the single number on the right larger? Rhesus macaques that have been trained to associate numerical values with symbols can get the answer right, even if they haven’t passed a math class. The finding doesn’t just reveal a hidden talent of the animals—it also helps show how the mammalian brain encodes the values of numbers. Previous research has shown that chimpanzees can add single-digit numbers. But scientists haven’t explained exactly how, in the human or the monkey brain, numbers are being represented or this addition is being carried out. Now, a new study helps begin to answer those questions. Neurobiologist Margaret Livingstone of Harvard Medical School in Boston and her colleagues had already taught three rhesus macaques (Macaca mulatta) in the lab to associate the Arabic numbers 0 through 9 and 15 select letters with the values zero through 25. When given the choice between two symbols, monkeys reliably chose the larger to get a correspondingly larger number of droplets of water, apple juice, or orange soda as a reward. To test whether the monkeys could add these values, the researchers began giving them a choice between a sum and a single symbol rather than two single symbols. Within 4 months, the monkeys had learned how the task worked and were able to effectively add two symbols and compare the sum to a third, single symbol. To ensure that the monkeys hadn’t simply memorized every possible combination of symbols and associated a value with the combination—this wouldn’t be true addition—Livingstone’s team next taught the animals an entirely new set of symbols —Tetris-like blocks rather than letters and numbers. With the new symbols, the monkeys were again able to add—this time calculating the value of combinations they’d never seen before and confirming the ability to do basic addition, the team reports online today in the Proceedings of the National Academy of Sciences. © 2014 American Association for the Advancement of Science.
Link ID: 19518 - Posted: 04.22.2014
Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair, according to a study funded by the National Institutes of Health. In research conducted with rats, scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle regeneration. “The finding gives insight into why chronic heavy drinking often saps muscle strength and it could also lead to new targets for medication development,” said Dr. George Koob, director of the National Institute on Alcohol Abuse and Alcoholism, the NIH institute that funded the study. The study is available online in the April issue of the Journal of Cell Biology. It was led by Dr. Gyorgy Hajnoczky, M.D., Ph.D., director of Thomas Jefferson University’s MitoCare Center, Philadelphia, and professor in the Department of Pathology, Anatomy and Cell Biology. Mitochondria are cellular structures that generate most of the energy needed by cells. Skeletal muscle constantly relies on mitochondria for power. When mitochondria become damaged, they can repair themselves through a process called mitochondrial fusion — joining with other mitochondria and exchanging material such as DNA. Although well known in many other tissues, the current study is the first to show that mitochondria in skeletal muscle are capable of undergoing fusion as a repair mechanism. It had been thought that this type of mitochondrial self-repair was unlikely in the packed fibers of the skeletal muscle cells, as mitochondria have little opportunity to interact in the narrow space between the thread-like structures called myofilaments that make up muscle.
By Floyd Skloot, March 27, 2009. I was fine the night before. The little cold I’d had was gone, and I’d had the first good night’s sleep all week. But when I woke up Friday morning at 6:15 and got out of bed, the world was whirling counterclockwise. I knocked against the bookcase, stumbled through the bathroom doorway and landed on my knees in front of the sink. It was as though I’d been tripped by a ghost lurking beside the bed. Even when I was on all fours, the spinning didn’t stop. Lightheaded, reaching for solid support, I made it back to bed and, showing keen analytical insight, told my wife, Beverly, “Something’s wrong.” The only way I could put on my shirt was to kneel on the floor first. I teetered when I rose. Trying to keep my head still, moving only my eyes, I could feel my back and shoulders tightening, forming a shell. Everything was in motion, out of proportion, unstable. I barely made it downstairs for breakfast, clutching the banister, concentrating on each step and, when I finally made it to the kitchen, feeling too aswirl to eat anyway. I didn’t realize it at the time, but those stairs would become my greatest risk during this attack of relentless, intractable vertigo. Vertigo — the feeling that you or your surroundings are spinning — is a symptom, not a disease. You don’t get a diagnosis of vertigo; instead, you present with vertigo, a hallmark of balance dysfunction. Or with dizziness, a more generalized term referring to a range of off-kilter sensations including wooziness, faintness, unsteadiness, spatial disorientation, a feeling akin to swooning. It happens to almost everyone: too much to drink or standing too close to the edge of a roof or working out too hard or getting up too fast. © 1996-2014 The Washington Post
Link ID: 19516 - Posted: 04.22.2014
By JAMES GORMAN As the Brain Initiative announced by President Obama a year ago continues to set priorities and gear up for what researchers hope will be a decade-long program to understand how the brain works, two projects independent of that effort reached milestones in their brain mapping work. Both projects, one public and one private, are examples of the widespread effort in neuroscience to create databases and maps of brain structure and function that can serve as a foundation for research. While the Obama initiative is concentrating on the development of new tools, that research will build on and use the data being acquired in projects like these. One group of 80 researchers, working as part of a consortium of institutions funded by the National Institute of Mental Health, reported that it had mapped the genetic activity of the human fetal brain. Among other initial findings, the map, the first installment of an atlas of the developing human brain called BrainSpan, confirmed the significance of areas thought to be important in the development of autism. A group of 33 researchers, all but one at the Allen Institute for Brain Science, announced an atlas of the mouse brain showing the connections among 295 different regions. Ed Lein, an investigator at Allen, was the senior author on the fetal brain paper. He said the research required making sections only 20 microns thick, up to 3,500 for each of four brains, two from fetuses at 15 weeks of development and two from about 21 weeks. The researchers measured the activity of 20,000 genes in 300 different brain structures. One interesting finding, Dr. Lein said, was that “95 percent of the genome was used,” meaning almost all of the genes were active during brain development, significantly more than in adult brains. The team also found many differences from the mouse brain, underscoring the findings that, despite the many similarities in all mammalian brains, only so much can be extrapolated to humans from other animals. © 2014 The New York Times Company
Forget cellphones; rambunctious friends may be the riskiest driver distraction for teens, according to a new study. Researchers installed video and G-force recorders in the vehicles of 52 newly licensed high school students for 6 months. They found that certain distractions, such as fiddling with the car’s controls and eating, were not strongly related to serious incidents, which included collisions and evasive maneuvers. However, when passengers in the car were engaged in loud conversation, teen drivers were six times more likely to have a serious incident. What’s more, horseplay increased risk by a factor of three whereas cellphone use only doubled it, the team reported online this week in the Journal of Adolescent Health. Forty-three states restrict newly licensed drivers from having more than one other teen in the car, and the study authors say their data suggest that's good policy. © 2014 American Association for the Advancement of Science.
The negative social, physical and mental health effects of childhood bullying are still evident nearly 40 years later, according to research by British psychiatrists. In the first study of its kind to look at the effects of childhood bullying beyond early adulthood, the researchers said its impact is "persistent and pervasive", with people who were bullied when young more likely to have poorer physical and psychological health and poorer cognitive functioning at age 50. "The effects of bullying are still visible nearly four decades later ... with health, social and economic consequences lasting well into adulthood," said Ryu Takizawa, who led the study at the Institute of Psychiatry at King's College London. The findings, published in the American Journal of Psychiatry on Friday, come from the British National Child Development Study which includes data on all children born in England, Scotland and Wales during one week in 1958. It included 7,771 children whose parents gave information on their child's exposure to bullying when they were aged 7 and 11. The children were then followed up until they reached 50. Bullying is characterized by repeated hurtful actions by children of a similar age, where the victim finds it difficult to defend themselves. More than a quarter of children in the study — 28 per cent — had been bullied occasionally, and 15 per cent were bullied frequently - rates that the researchers said were similar to the situation in Britain today. The study, which adjusted for other factors such as childhood IQ, emotional and behavioural problems and low parental involvement, found people who were frequently bullied in childhood were at an increased risk of mental disorders such as depression, anxiety and experiencing suicidal thoughts. © CBC 2014
By CLYDE HABERMAN Her surname in Italian means “slave,” and is pronounced skee-AH-vo. Grim as it may be, the word could apply to Theresa Marie Schiavo, even with its Americanized pronunciation: SHY-vo. For 15 years, Terri Schiavo was effectively a slave — slave to an atrophied brain that made her a prisoner in her body, slave to bitter fighting between factions of her family, slave to seemingly endless rounds of court hearings, slave to politicians who injected themselves into her tragedy and turned her ordeal into a national morality play. To this day, the name Schiavo is virtually a synonym for epic questions about when life ends and who gets to make that determination. It would be nice to believe that since Ms. Schiavo’s death nine years ago, America has found clear answers. Of course it has not, as is evident in Retro Report’s exploration of the Schiavo case, the latest video documentary in a weekly series that examines major news stories from the past and their aftermath. Ms. Schiavo, a married woman living in St. Petersburg, Fla., was 26 years old when she collapsed on Feb. 25, 1990. While her potassium level was later found to be abnormally low, an autopsy drew no conclusion as to why she had lost consciousness. Whatever the cause, her brain was deprived of oxygen long enough to leave her in a “persistent vegetative state,” a condition that is not to be confused with brain death. She could breathe without mechanical assistance. But doctors concluded that she was incapable of thought or emotion. After her death on March 31, 2005, an autopsy determined that the brain damage was irreversible. Between her collapse — when she “departed this earth,” as her grave marker puts it — and her death — when she became “at peace” — the nation bore witness to an increasingly acrimonious battle between her husband, Michael Schiavo, and her parents, Robert and Mary Schindler. Mr. Schiavo wanted to detach the feeding tube that gave her nourishment. Terri never would have wanted to be kept alive that way, he said. The Schindlers insisted that the tube be kept in place. That, they said, is what their daughter would have wanted. To Mr. Schiavo, the woman he had married was gone. To the Schindlers, a sentient human was still in that body. © 2014 The New York Times Company
Link ID: 19512 - Posted: 04.21.2014
By Melissa Healy The nature of psychological resilience has, in recent years, been a subject of enormous interest to researchers, who have wondered how some people endure and even thrive under a certain amount of stress, and others crumble and fall prey to depression. The resulting research has underscored the importance of feeling socially connected and the value of psychotherapy to identify and exercise patterns of thought that protect against hopelessness and defeat. But what does psychological resilience look like inside our brains, at the cellular level? Such knowledge might help bolster peoples' immunity to depression and even treat people under chronic stress. And a new study published Thursday in Science magazine has made some progress in the effort to see the brain struggling with -- and ultimately triumphing over -- stress. A group of neuroscientists at Mount Sinai's Icahn School of Medicine in New York focused on the dopaminergic cells in the brain's ventral tegmentum, a key node in the brain's reward circuitry and therefore an important place to look at how social triumph and defeat play out in the brain. In mice under stress because they were either chronically isolated or rebuffed or attacked by fellow littermates, the group had observed that this group of neurons become overactive. It would logically follow, then, that if you don't want stressed mice (or people) to become depressed, you would want to avoid hyperactivity in that key group of neurons, right? Actually, wrong, the researchers found. In a series of experiments, they saw that the mice who were least prone to behave in socially defeated ways when under stress were actually the ones whose dopaminergic cells in the ventral tegmental area displayed the greatest levels of hyperactivity in response to stress. And that hyperactivity was most pronounced in the neurons that extended from the tegmentum into the nearby nucleus accumbens, also a key node in the brain's reward system.
Scientists have traced vulnerability to depression-like behaviors in mice to out-of-balance electrical activity inside neurons of the brain’s reward circuit and experimentally reversed it – but there’s a twist. Instead of suppressing it, researchers funded by the National Institutes of Health boosted runaway neuronal activity even further, eventually triggering a compensatory self-stabilizing response. Once electrical balance was restored, previously susceptible animals were no longer prone to becoming withdrawn, anxious, and listless following socially stressful experiences. “To our surprise, neurons in this circuit harbor their own self-tuning, homeostatic mechanism of natural resilience,” explained Ming-Hu Han, Ph.D External Web Site Policy., of the Icahn School of Medicine at Mount Sinai, New York City, a grantee of the NIH’s National Institute of Mental Health (NIMH) and leader of the research team. Han and colleagues report on their discovery April 18, 2014 in the journal Science. Prior to the new study, the researchers had turned resilience to social stress on and off by using pulses of light to manipulate reward circuit neuronal firing rates in genetically engineered mice – optogenetics. But they didn’t know how resilience worked at the cellular level. To find out, they focused on electrical events in reward circuit neurons of mice exposed to a social stressor. Some mice that experience repeated encounters with a dominant animal emerge behaviorally unscathed, while others develop depression-like behaviors.
By Bill Briggs A Vietnam veteran swoops his hand through a row of baby vegetables, caressing the peppers on down to the kale. The plants are aligned in tidy, military order atop his backyard fence. He could spend hours describing his first garden. But he cannot utter a word. He can’t even eat his eventual harvest. So, Bob Hoaglan, 71, simply stands and grins at the spouts behind his Oxnard, Calif., home. Then, he grabs his primary communication tool, an LCD tablet, scribbling a stylus across the screen. He displays his words with a silent chuckle: “I don’t have a green thumb.” With a button click, he erases that sentence before composing another. His daily aim is to throw his body and brain into new pursuits. The crops — fresh life for a man facing mortality — help shove his disease to the back of his mind. He admits, though, he can’t keep it there: “I try,” he writes, “Sometimes it creeps up on me.” As he shows that message, the smile vanishes. Hoaglan was diagnosed with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, nearly a year ago. Inside a malady that offers no cure or explanation, he embodies two intriguing clues that, a top researcher says, may whisper answers: Hoaglan served in the military, and he is a nice man. U.S. veterans carry a nearly 60 percent greater risk of contracting ALS than civilians, according to a white paper published in 2013 by the ALS Association, citing Harvard University research that tracked ex-service members back to 1910.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 19509 - Posted: 04.19.2014
By David Z. Hambrick and Christopher Chabris The College Board—the standardized testing behemoth that develops and administers the SAT and other tests—has redesigned its flagship product again. Beginning in spring 2016, the writing section will be optional, the reading section will no longer test “obscure” vocabulary words, and the math section will put more emphasis on solving problems with real-world relevance. Overall, as the College Board explains on its website, “The redesigned SAT will more closely reflect the real work of college and career, where a flexible command of evidence—whether found in text or graphic [sic]—is more important than ever.” A number of pressures may be behind this redesign. Perhaps it’s competition from the ACT, or fear that unless the SAT is made to seem more relevant, more colleges will go the way of Wake Forest, Brandeis, and Sarah Lawrence and join the “test optional admissions movement,” which already boasts several hundred members. Or maybe it’s the wave of bad press that standardized testing, in general, has received over the past few years. Critics of standardized testing are grabbing this opportunity to take their best shot at the SAT. They make two main arguments. The first is simply that a person’s SAT score is essentially meaningless—that it says nothing about whether that person will go on to succeed in college. Leon Botstein, president of Bard College and longtime standardized testing critic, wrote in Time that the SAT “needs to be abandoned and replaced,” © 2014 The Slate Group LLC.
Link ID: 19508 - Posted: 04.19.2014
by Ashley Yeager A nerve cell's long, slender tentacle isn’t evenly coated with an insulating sheath as scientists had thought. Instead, many nerve cells in the brains of mice have stretches of these tentacles, called axons, that are naked, researchers report April 18 in Science. The unsheathed feeler can be as long as 80 micrometers. Nerve cells can also have specific patterns in the gaps of the insulating layer, called myelin. The differences in the thickness of that coating may control how fast signals travel between nerve cells, the scientists suggest. The finding could have implications for understanding nerve-based diseases, such as multiple sclerosis, and improve scientists’ understanding of how signals are transmitted in the brain. © Society for Science & the Public 2000 - 2013.
By David Brown, At the very least, the new experiment reported in Science is going to make people think differently about what it means to be a “rat.” Eventually, though, it may tell us interesting things about what it means to be a human being. In a simple experiment, researchers at the University of Chicago sought to find out whether a rat would release a fellow rat from an unpleasantly restrictive cage if it could. The answer was yes. The free rat, occasionally hearing distress calls from its compatriot, learned to open the cage and did so with greater efficiency over time. It would release the other animal even if there wasn’t the payoff of a reunion with it. Astonishingly, if given access to a small hoard of chocolate chips, the free rat would usually save at least one treat for the captive — which is a lot to expect of a rat. The researchers came to the unavoidable conclusion that what they were seeing was empathy — and apparently selfless behavior driven by that mental state. “There is nothing in it for them except for whatever feeling they get from helping another individual,” said Peggy Mason, the neurobiologist who conducted the experiment along with graduate student Inbal Ben-Ami Bartal and fellow researcher Jean Decety. “There is a common misconception that sharing and helping is a cultural occurrence. But this is not a cultural event. It is part of our biological inheritance,” she added. The idea that animals have emotional lives and are capable of detecting emotions in others has been gaining ground for decades. Empathic behavior has been observed in apes and monkeys, and described by many pet owners (especially dog owners). Recently, scientists demonstrated “emotional contagion” in mice, a situation in which one animal’s stress worsens another’s. © 1996-2014 The Washington Post
Everything we do — all of our movements, thoughts and feelings – are the result of neurons talking with one another, and recent studies have suggested that some of the conversations might not be all that private. Brain cells known as astrocytes may be listening in on, or even participating in, some of those discussions. But a new mouse study suggests that astrocytes might only be tuning in part of the time — specifically, when the neurons get really excited about something. This research, published in Neuron, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For a long time, researchers thought that the star-shaped astrocytes (the name comes from the Greek word for star) were simply support cells for the neurons. It turns out that these cells have a number of important jobs, including providing nutrients and signaling molecules to neurons, regulating blood flow, and removing brain chemicals called neurotransmitters from the synapse. The synapse is the point of information transfer between two neurons. At this connection point, neurotransmitters are released from one neuron to affect the electrical properties of the other. Long arms of astrocytes are located next to synapses, where they can keep tabs on the conversations going on between neurons. In recent years, it has been shown that astrocytes may also play a role in neuronal communication. When neurons release neurotransmitters, levels of calcium change within astrocytes. Calcium is critical for many processes, including release of molecules from the cell, and activation of a host of proteins within the cell. The role of this astrocytic calcium signaling for brain function remains a mystery.
Link ID: 19505 - Posted: 04.17.2014
By Melissa Hogenboom Artists have structurally different brains compared with non-artists, a study has found. Participants' brain scans revealed that artists had increased neural matter in areas relating to fine motor movements and visual imagery. The research, published in NeuroImage, suggests that an artist's talent could be innate. But training and environmental upbringing also play crucial roles in their ability, the authors report. As in many areas of science, the exact interplay of nature and nurture remains unclear. Lead author Rebecca Chamberlain from KU Leuven University, Belgium, said she was interested in finding out how artists saw the world differently. "The people who are better at drawing really seem to have more developed structures in regions of the brain that control for fine motor performance and what we call procedural memory," she explained. In their small study, researchers peered into the brains of 21 art students and compared them to 23 non-artists using a scanning method called voxel-based morphometry. Detail of 'Giant Lobster' from NHM specimen collection One artist who has practised for many years is Alice Shirley - here is a detail of her Giant Lobster These detailed scans revealed that the artist group had significantly more grey matter in an area of the brain called the precuneus in the parietal lobe. "This region is involved in a range of functions but potentially in things that could be linked to creativity, like visual imagery - being able to manipulate visual images in your brain, combine them and deconstruct them," Dr Chamberlain told the BBC's Inside Science programme. BBC © 2014
BY Ellen Rolfes Rebecca Kamen’s sculptures appear as delicate as the brain itself. Thin, green branches stretch from a colorful mass of vein-like filaments. The branches, made from pieces of translucent mylar and stained with diluted acrylic paint, are so delicate that they sway slightly when mounted to the wall. Perched on various parts of the sculpture are mylar butterflies, whose wings also move, as if fluttering. One of Kamen's influences is the writing of Santiago Ramon y Cajal, who is called the "father of modern neuroscience." Cajal once said: “Like the entomologist in search of colorful butterflies, my attention has chased in the gardens of the grey matter cells with delicate and elegant shapes, the mysterious butterflies of the soul, whose beating of wings may one day reveal to us the secrets of the mind." One of Kamen’s artistic influences is the writing of Santiago Ramon y Cajal, who is called the “father of modern neuroscience.” The work, called “Butterflies of the Soul” was inspired by neuroscientist Santiago Ramon y Cajal, who won the 1906 Nobel Prize, for his groundbreaking work on the human nervous system. Kamen’s sculpture is a nod to his work and the development of modern neuroscience. Cajal’s observation of the cells under the microscope radically changed how scientists study the brain and its functions, Kamen said. And the butterflies in her sculpture represent Cajal’s drawings of Purkinje cells, which are found in the cerebellar cortex at the base of the brain. Purkinje cells play an important role in motor control and in certain cognitive functions, such as attention and language. And attention and language are skills of great interest to Kamen, who has dyslexia. Her fascination with the brain and its structure deepened when she discovered that she was dyslexic later in life. © 1996 - 2014 MacNeil / Lehrer Productions.
Link ID: 19503 - Posted: 04.17.2014
By DORIS IAROVICI, M.D. “I think our experiment failed,” the young graduate student told me, referring to our attempt to take her off the antidepressant she’d been on for seven years. She was back in my campus office after a difficult summer break, and as she talked about feeling unsettled and upset, I wondered about the broader experiment playing out on college campuses across the country. Antidepressants are an excellent treatment for depression and anxiety. I’ve seen them improve — and sometimes save — many young lives. But a growing number of young adults are taking psychiatric medicines for longer and longer periods, at the very age when they are also consolidating their identities, making plans for the future and navigating adult relationships. Are we using good scientific evidence to make decisions about keeping these young people on antidepressants? Or are we inadvertently teaching future generations to view themselves as too fragile to cope with the adversity that life invariably brings? My patient had started medication as a college freshman, after she’d become depressed and spent much of her time in bed. She was forced to take a medical leave but improved quickly, returned to school and graduated. She married soon after and worked for a few years, feeling well all the while. Professional guidelines recommend six to nine months of medicine for first episodes of depression. But my patient had never been advised to stop taking it. She reluctantly agreed to my recommendation to taper off her antidepressant. © 2014 The New York Times Company
Link ID: 19502 - Posted: 04.17.2014
On Wednesday morning we woke to the news that a passenger ferry had sunk off the coast of South Korea, with at least four people confirmed dead and 280 unaccounted for. Meanwhile, though the search has continued for the missing Malaysia Airlines plane, relatives' hopes of a safe landing have long since been extinguished. Human tragedies like these are the stuff of daily news, but we rarely hear about the long-term psychological effects on survivors and the bereaved, who may experience the symptoms of post-traumatic stress disorder for years after their experience. Although most people have heard of PTSD, few will have a clear idea of what it entails. The American Psychiatric Association's Diagnostic and Statistical Manual (DSM) defines a traumatic event as one in which a person "experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others". PTSD is marked by four types of responses to the trauma. First, patients repeatedly relive the event, either in the form of nightmares or flashbacks. Second, they seek to avoid any reminder of the traumatic event. Third, they feel constantly on edge. Fourth, they are plagued with negative thoughts and low mood. According to one estimate, almost 8% of people will develop PTSD during their lifetime. Clearly trauma (and PTSD) can strike anyone, but the risks of developing the condition are not equally distributed. Rates are higher in socially disadvantaged areas, for instance. Women may be twice as likely to develop PTSD as men. This is partly because women are at greater risk of the kinds of trauma that commonly produce PTSD (rape, for example). Nevertheless – and for unknown reasons – when exposed to the same type of trauma, women are more susceptible to PTSD than men. © 2014 Guardian News and Media Limited